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Repeating KHIO 1 > 8 Herpes > Flashcards

8 Herpes Flashcards

1
Q

Herpes simplex keratitis:

A

HSV type 1 > most common cause of infectious blindness in developed world
Infects any part of eye (epithelia > stroma > endothelia)
HSV 2 > STD related, keratitis in neonates
Commonly unilateral unless immunocompromised

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2
Q

HSV-1 structure:

A

Alpha subfamily of herpesvirus
dsDNA in icosahedral caspid
Inner mRNA/protein, outer bilayer with glycoproteins

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3
Q

HSV life cycle:

A

Membrane glycoproteins allow penetration of capsid through host membrane
Herpes viral entry mediator (HVEM) or nectin-1 delivers capsid to cytoplasm
DNA polymerase forms virons
Release via host heparanase
Enters latency by moving to trigeminal ganglion via corneal nerves
Exists in CD8+ T cells

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4
Q

HSV epidemiology:

A

50% prevalence in UV > 90% in Africa, decreasing
50% keratitis recurrence 5y > 60% in 20y
Major entry via direct host mucus contact

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5
Q

Herpes keratitis risk:

A

Asthma, cardiovascular disease, corticosteroids
HIV positive

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6
Q

HSV transmission:

A

Children/young adults via mucous membrane contact

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7
Q

HSV reactivation:

A

HSV moves via anterograde axonal transport
Occurs at high sensory tissue (cornea/oral) via ophthalmic branch
Risk decreased by oral acyclovir

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8
Q

HSV reactivation triggers:

A

Stress, fever, UV, allergies, corticosteroids, laser treatment
immunocompromisation

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9
Q

HSV epithelial keratitis clinical presentation:

A

Commonly unilateral, 20% bilateral in immunosuppressed
Pain, tearing, redness, FBS, DED
Dendritic keratitis > bulb-lesions/geographic ulcer (fluroscein)
Corneal denervation > neurotrophic keatopathy > corneal melt

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10
Q

HSV epithelial lesions::

A

Punctate keratopathy > dendritic keratitis (follow nerve plexus) > terminal bulb enlargement > geographic ulcer (central dead cells)

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11
Q

HSV epithelial lesion staining:

A

Fluorescein > central dendritic staining
Rose bengal/lissamine > edge lesion (dead cells)

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12
Q

HSV epithelial keratitis immune function:

A

Infected epithelial cells secrete type 1 interferon (IFN-a/b) and IgG/sigA in tear film limit viral spread.
Contribute to spontaneous lesion resolving
Immunocompromised/corticosteroids > basement membrane invasion

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13
Q

Epithelial Herpetic keratitis DDX:

A

Misdiagnosed as acanthamoeba keratitis
HZO does not have terminal bulbs
Tested with PCR

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14
Q

HSV endothelial keratitis clinical presentation:

A

Disciform> most common, central oedema disc
Diffuse> wide oedema
Linear> limbal oedema

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15
Q

HSV stromal keratitis (HSK) clinical presentation:

A

20-50% of recurrent cases
Corneal vascularisation, stromal oedema/opacity, irreversible scaring
Necrotizing: stromal infiltration/ring, epithelial ulcer > corneal melt
Disciform: stromal oedema > neovascularisation

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16
Q

HSV stromal keratitis treatment

A

Topical corticosteroid Prednefrin Forte 1% (6/day, 10 weeks)
With oral valaciclovir (antiviral)
Dosage increased with epithelial defects
Always tapered

17
Q

HSK immune procedure:

A

Trigeminal virus reactivation > corneal innate immune signalling > cytokine/chemokines from stroma > 24h neutrophil/NK cell aggregation
Dendritic cells phagocytose virus > present antigen to lymph nodes > 7-21d CD4+T cells aggregate > IFN-g / IL-17 secretion
Inflammatory cells > corneal clouding

18
Q

HSV endothelitis / uveitis clinical presentation:

A

Endothelial oedema / precipitates
High IOP (trabeculitis)
Iris atrophy

19
Q

Immune cells in ocular HSV infection

A

Neutrophils > earliest responder, cause corneal opacity
Macrophage, NK cells > innate phagocytes
Dendritic cells > adaptive phagocyte
CD4+T cells > IL2/IFN, drive lesion development
CD8+T cells > controls recurrence via T cell receptor

20
Q

Immune factors in ocular HSV infection:

A

Toll-like receptors > innate PAMP detector, drives cytokine production and opacity
Cytokine/Chemokine > IFN a/b stimulate antiviral genes, IFN y stimulates inflammation
Heparanase > removes harparan sulfate allowing virion release to other cells

21
Q

HSV Corneal neovascularisation pathology:

A

Neutrophils form metalloproteases > extracellular matrix breakdown > vascularisation mediated by VEGF
Infection depletes VEGF receptors > increase in VEGF

22
Q

HSV effect on corneal surface:

A

Loss of sub-basal nerve plexus > desensitisation (neurotrophic keratopathy)
NK > Tear reduction > DED
Frequent recurrence > neuropathic pain, corneal melt, superinfection

23
Q

HSV antiviral treatment:

A

Systemic > acyclovir, valacyclovir, famciclovir
Tropical > acyclovir, trifluridine, ganciclovir

24
Q

Acyclovir HSV treatment:

A

Most common
Nucleoside analog > DNA polymerase inhibition > HSV replication inhibition
HSV enzyme can mutate for resistance
Highest HSV affinity > less toxicity for non-infected cells

25
Q

Anti-inflammatory treatment of HSV:

A

Focused treatment for HSV inflammatory damage
Corticosteroids > endothelitis/uveitis

26
Q

Varicella zoster virus:

A

Contagious DNA virus; causes
Chickenpox (Varicella) > lifelong trigeminal infection
Shingles > reactivation of VZV

27
Q

Varicella zoster epidemiology:

A

3/1000/year > 30% lifetime attack
Increased rate> age (80>50), immunocompromised, HIV

28
Q

Varicella zoster pathophysiology:

A

Enters upper res. > proliferates to pharyngeal lymph > skin (varicella)

29
Q

HZO skin lesions:

A

Vessicle rash, healed in 4 weeks
Upper face lesion > first trigeminal branch
Nose and below lesion > second branch lesion

30
Q

HZO lid manifestations:

A

Hyperemia, oedema > lagophthalmos
Blepharitis (staph)

31
Q

HZO conjunctiva manifestation:

A

Membraneous / follicular response
Hyperemia / oedema
Resolving in 1 week
Antibiotics prevent bacterial infection

32
Q

HZO corneal manifestations:

A

Punctate epithelial keratitis (focal lesions with fluroscein)
Tapered dendritic lesions
Photophobia, pain

33
Q

HZO uvea manifestations

A

Usually unilateral
Iris atrophy/synechiae, IOP increase, cataract formation

34
Q

HZO acute retinal necrosis (ARN):

A

Fast retinal lesion/necrosis progression
Vitreous inflammation
Immunosuppression > Progressive outer retinal necrosis (white retinal patches) > retinal detachment

35
Q

HZV complications:

A

Cutaneous > post-herpetic neuralgia (skin pain following rash)
Visceral
Neurological > neuropathy/palsy
Ocular > superinfection

36
Q

HZV treatment:

A

Antiviral therapy > acyclovir, ganciclovir, famciclovir, (7d for HZ rash)
Analgesics > lidocaine (pain)
Intravenous acyclovir > ARN/PORN, immunocompromised

37
Q

HZV acyclovir treatment procedure:

A

800mg orally 5/day
Administer within 72 hours of rash, for 7 days
Or 3% gel

Repeating KHIO 1 (15 decks)

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