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omopor > L8: viral infections pt 2 > Flashcards

L8: viral infections pt 2 Flashcards

1
Q

what kind of cells does EBV affect

A

immortalises b cells and remains in host for life (latent)

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2
Q

ebv is hhv what

A

hhv 4

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3
Q

how does ebv spread?

A

via bodily fluids (saliva, blood, semen)

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4
Q

what is known as the kissing disease?

A

infectious mononuleosis, which is brought about by ebv (hhv4)

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5
Q

what are the symptoms of infectious mononucleosis?

A

person infected with ebv wil have infectious mononucleosis
- lymphadenopathy, hepatosplenomegaly, thrombocytopenia, aplstic anemia
- pharyngitis, rhinitis, cough, rash
- fatigue, malaise

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6
Q

symptoms of infectious mononucleosis is more pronounced in who

A

older px

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7
Q

associated conditions with ebv infection:

A
  • OHL
  • lymphoproliferative disroders eg burkitts lymphoma
  • nasopharyngeal carcinoma
  • salivary lymphoepithelial carcinoma
  • sarcoma
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8
Q

what is an eg of lymphoproliferative disorder?

A

burkitts lymphoma

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9
Q

oral presentation of ebv

A
  • necrotizing ulcerative gingivitis (NUG)
  • mucosal petechiae
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10
Q

how to dx ebv?

A
  • full blood cell count - if got lymphocytosis (increase in absolute lymphocyte count)
  • clinically
  • serology (paul bunnell test to detect heterophil antibodies)
  • serology (indirect immunofluorescent test for ebv specific AB - done if the PB test is negative)
  • ELISA and recombinant DNA derived Ag test
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11
Q

what is the paul bunnell test used to detect and what infection does it detect?

A

detects heterophil antibodies which are Ig that agglutinate sheep erythrocytes
used as a rapid test for ebv

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12
Q

tx for ebv

A

supportive care via:
- antipyretics
- non aspirin nsaid
- not rec to use AB in cases with tonsilitis
- not rec to use corticosteroid unless there is life threatening symptoms like airway obstruction (due to enlarged tonsils and adenoids)
- antiviral agents (but only temporary resolution of OHL)

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13
Q

primary cmv infection is mostly in what type of ppl

A

infancy – through placenta, breastfeeding

adolescence - sexual activity

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14
Q

recurrent cmv infection is mostly in what types of ppl

A

immunocompromised

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15
Q

cmv lies latent in what

A

endothelial cells mainly, also got lymphocytes, macrophages and salivary glands

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16
Q

cmv spreads via what

A

body fluids like saliva and blood

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17
Q

which virus is present in 40% of 30 year olds, and 80-100% of 60 year olds?

A

cmv

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18
Q

tx of cmv

A
  • most resolve spontaneously
  • symptomatic relief can be provided by NSAIDs
  • immunocompromised px: give anti virals like ganciclovir and valganciclovir
  • in immunocompromised, can also give cART (combination antiretroviral therapy) to improve immune status
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19
Q

histopatho findings of cmv

A

owl eye cells (swollen infected cells)
aka reed sternberg cells

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20
Q

in what type of infection do we see owl eye cells

A

cmv

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21
Q

what types of cells do hhv 6, 7, 8 target?

A

6 and 7 target t lymphocytes
8 targets b lymphocytes and endothelial cells

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22
Q

which virus is a common cause of childhood acute febrile illness?

A

hhv 6

23
Q

what are the types of enteroviruses?

A
  • coxsackie virus (type A and B)
  • echo virus
24
Q

characteristics of enteroviruses:
- is it widespread and contagious?
- what kind of outbreak does it cause?
- what kind of diseases caused?

A
  • widespread and highly contagious
  • cause epidemic outbreaks
  • wide spectrum of diseases but mostly self limiting
25
Q

where are the lesions of hfmd?

A
  • hand and foot: around fingers toes and heel margins
  • oral lesions in labial and buccal mucosa, vestibules, tongue, palate
26
Q

which lesions are painless and which are painful in hfmd?

A

those on hands and feet are painless, those in oral cavity are mild to moderate pain

27
Q

what are the descriptions of lesions of hfmd on the skin and the oral lesions?

A

skin is firm raised NODULES, painless
oral lesions are multiple small ULCERS, mild to moderate pain

28
Q

how to dx hfmd?

A

clinical presentation: will have prodromal flu like symptoms before lesions develop
- immunofluorescence or culture

29
Q

mx of hfmd?

A

supportive and palliative ** (these are KEYWORDS)
- give lots of fluids, can give anesthetics and analgesics
- monitor for systemic complications/ systemic disease

30
Q

how long does hfmd last

A

usual course is 7-10 days

31
Q

hfmd caused by what kind of virus

A

enterovirus - coxsackie A16

32
Q

how does hfmd spred?

A

via faecal oral route

33
Q

herpangina caused by what virus?

A

enterovirus – coxsackie A1-6, A8, A10, A22

34
Q

what are some systemic symptoms of herpangina?

A

sore throat, dysphagia, fever, malaise, headahce

35
Q

description of herpangina lesions

A

multiple small 2-3mm ulcers
red macules -> fragile vesicles then rapidly ulcerate

36
Q

how long do herpangina lesions take to heal?

A

7-10 days

37
Q

location of herpangina lesions

A

posterior oral cavity/ oropharynx
if we see some lesions elsewhere, it is unlikely herpangina

38
Q

how to dx herpangina?

A
  • clinical presentation
  • viral culture, immunofluoresnce
39
Q

mx of herpangina?

A
  • supportive and palliative for symptomatic cases
  • can give anesthetics and analgesics
40
Q

histo patho findings of herpangina

  • _____ and _______ oedema that form intraepithelial ______
  • vesicle enlarges and ruptures through ________ layer to form _______ vesicle
  • epithelial ____ and ______
  • inclusion bodies and multinucleated epithelial cells _______
A
  • intracellular and intercellular oedema that form intraepithelial vesicle
  • vesicle enlarges and ruptures through epithelial basal cell layer to form subepithelial vesicle
  • epithelial necrosis and ulceration
  • inclusion bodies and multinucleated epithelial cells absent
41
Q

histopatho findings of herpangina

  • intracellular and intercellular _____ that form ______
  • vesicle enlarges and _____ through epithelial basal cell layer to form _____
  • _______ _____ and ulceration
  • ________ bodies and _______ epithelial cells absent
A
  • intracellular and intercellular oedema that form intraepithelial vesicle
  • vesicle enlarges and ruptures through epithelial basal cell layer to form subepithelial vesicle
  • epithelial necrosis and ulceration
  • inclusion bodies and multinucleated epithelial cells absent
42
Q

ddx of herpangina?

A

hfmd (similar clinical findings)

to differentiate, hfmd usually has more lesions and involve anterior oral cavity more, whereas herpangina is posterior oral cavity

43
Q

what type of virus got more than 100 strains identified but we only need to focus on a few?

A

hpv

need to focus on
hpv 6 and 11 (benign )
hpv 13, 32 (focal epithelial hyperplasia)
and 16, 18, 31, 33 and 35 (squamous cell carcinoma)

44
Q

are the hpv oral lesions contagious?

A

mildly contagious, require direct mucosal contact

45
Q

hpv lies latent in what cells

A

epithelial cells

46
Q

hpv infect what type of cells? how?

A

infect keratinocytes via
- viral DNA incorporation into host DNA
- E6&7 genes induce transformation of cell

47
Q

what HPV associated with focal epithelail hyperplasia?

A

hpv 13, 32

48
Q

what HPV associated with SCC?

A

16, 18, 31, 33 and 35

49
Q

what HPV associated with proliferative verrucous leukoplakia (benign)?

A

6, 11

50
Q

verruca vulgaris is which hpv?

A

2,4

51
Q

mx of hpv?

A
  • biopsy to identify virus is recommended before removal
  • removal of hpv lesions can be done by:
    conservative surgical excision,
    co2 laser (which vaporises lesion)
    cryotherapy (liquid nitrogen)
    electrosurgery
    chemical tx

but there will be high rate of recurrence of lesions

52
Q

what are the chemical tx avail for hpv lesions? -

A
  • podophyllotoxin 0.5% gel
  • interferon alpha (INF-a) * rmb this one, is an intra lesional injection
  • imiquimod cream/ soln
53
Q

histopatho findings of HPV

  • proliferation of _____ arranged in ____ like projections, with ________ CT cores
  • ______ (viral altered epithelial cells) present in spinous cell layer
A
  • proliferation of keratinised squamous epithelium arranged in finger like projections, with fibrovascular CT cores
  • koilocytes (viral altered epithelial cells) present in spinous cell layer
54
Q

histopatho findings of HPV

  • proliferation of ______ squamous epithelium arranged in finger like projections, with __________
  • koilocytes (_______ cells) present in ______ ___ layer
A
  • proliferation of keratinised squamous epithelium arranged in finger like projections, with fibrovascular CT cores
  • koilocytes (viral altered epithelial cells) present in spinous cell layer

omopor (11 decks)

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