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M4: Oral cancer > Aetiology: infectious agents > Flashcards

Aetiology: infectious agents Flashcards

1
Q

What are the key viruses that can present as oral lesion?

A

Human papilloma virus (HPV)
Epstein-barr virus (EBV or HHV 4)
HIV
Human herpes virus (HHV 1&2)
Paramyxovirus (mumps)

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2
Q

Five types of Human papilloma virus

A
  1. Alpha
  2. Beta
  3. Gamma
  4. Mu
  5. Nu
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3
Q

HPV - alpha

A

warts

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4
Q

HPV - beta

A

oral

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5
Q

Papilloma

A

Small raised white lesion - benign.
Treated by excision

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6
Q

High risk types of HPV

A

Cancer causing.

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7
Q

What is an unusual candidate that have been seen to present with oropharyngeal cancer?

A

White, non-smoking males age 35 to 55 are most at risk, 4:1 over females.

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8
Q

Epitheliatrophic

A

mucosal targeting

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9
Q

Features of HPV

A
  • Small, non-enveloped DNA viruses of a symmetrical icosahedral shape.
  • Important ones in the head and neck cancer are type 16 and 18.
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10
Q

HPV type 16

A

Made up of 6 early genes (E1, 2, 4, 5, 6 & 7) and 2 late genes (L1 and 2).

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11
Q

What aspects of HPV 16 make it carcinogenic?

A

Early genes: E6 and E7

They target tumour suppressor genes and knock out their function. They take over cellular proliferation and DNA synthesis.

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12
Q

How is HPV infectious/spread to others?

A

Capsid proteins L1 and L2 accumulate in the mature epithelial cells before they are shed, then there is assembly of the infectious virions takes place in the upper epithelial barrier layers.

These layers are then shed (natural process within the mucosa every 21 days) into the environment and thus transferred to other people.

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13
Q

How does HPV initially approach the cell?

A

It initially binds with heparin sulphate proteoglycan (HSPGs) before becoming endocytose (entering the cell), now being referred to as an endosome.

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14
Q

What happens to HPV once it has entered the cell?

A

Goes from an early endosome to a late endosome when the viral genome uncoats and the viral complex with L2 is released. Then attaches to the cells nucleus (complexing with ND10) and then RNA transcription begins.

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15
Q

How long does it take for the HPV to attach to the cell’s nucleus from the point of entry to the cell?

A

24 hours

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16
Q

What cell type does HPV targeted initially and how does it then move through the cells?

A

Basal cells –> stratum basal to stratum spinosum all the way to the superficial layer (which is shed into the environment).

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17
Q

What types of HPV might you see in a latency in the nucleus?

A

HPV -6 and -11 as these are “low-risk”

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18
Q

What are the tumour suppressor genes targeted by E6 and E7?

A

p53 and pRB (retinoblastoma gene)

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19
Q

How is p53 targeted by HPV?

A

E6 binds and marks it for destruction (by ubiquitin pathway)

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20
Q

How is pRB targeted by HPV?

A

E7 binds and inactivates it.

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21
Q

Why is high-risk HPV more likely going to lead to an abnormal growth?

A

E6 is present to knock out p53 and thus the apoptosis pathway, this means the process that would usually allow destruction of the abnormal cells is no longer there.

22
Q

Oral HPV lesions : benign

A

Papilloma or Condylomata

23
Q

Oral HPV lesions: malignant

A

Cancer - SCC

24
Q

What is this and treatment?

A

Common papilloma (benign) lesion caused by low-risk HPV.

Treatment: surgical excision

Sexual related

25
Q

What is this ?

A

Condylomata (benign) lesion caused by low-risk HPV.

Different from papilloma as there are usually multiple lesions.

Sexual related

26
Q

What is this?

A

Cancer - a keratinised (white) lesion

Site: lingual gutter (under the tongue) is a high risk site.

27
Q

What is this?

A

Cancer - could be painless and asymptomatic. Teeth become very mobile (wobbly).

28
Q

What is this?

A

Cancer - all white/red patch, raised, ulcerated (need further investigation).

29
Q

exophytic

A

Abnormal growth is growing outwards and

30
Q

exophytic

A

Abnormal growth is growing outwards and

31
Q

endophytic

A

abnormal growth is growing inwards (breaks down and ulcerates)

32
Q

HPV has a role to play in what percentage of oral cancers?

A

25%

33
Q

What percentage of oropharyngeal cancers are related to HPV?

A

80%

34
Q

Key risk factors for HPV

A

Number of sexual partners

Weakened immune systems

35
Q

How can you know if a lesion in cancerous?

A

Incisional biopsy

36
Q

Investigations that can be done on a biopsy for HPV?

A

P16 staining (immunohistochemical staining)

In-situ hybridisation (ISH) this is the one more commonly used.

37
Q

How is HPV controlled?

A

Vaccination

38
Q

What are the three HPV vaccinations

A
  1. Quadrivalent Gardasil (6, 11, 16, 18)
  2. Bivalent cervarix (16, 18)
  3. Nonvalent Gardasil 9 (16, 18, 31, 33, 45, 52, and 58)
39
Q

Who gets the HPV vaccine?

A

UK girls and boys 11-12 and 13-26

Men who have sex with men; up to and including the age of 45

40
Q

How did vaccination impact HPV cases when introduced in Australia?

A

The risk of cervical cancer in women decreased by 50%.

41
Q

EBV?

A

Epstein-Barr Virus (type of herpes virus)

42
Q

What can EBV cause?

A

Mononucleosis (glandular fever), lymphoma, nose and throat cancers.

43
Q

EBV action

A

It latently infects B-lymphocytes.

44
Q

What is this?

A

Infectious mononucleosis (glandular fever) caused by EBV.

Usually will be systemically unwell.

45
Q

What is this?

A

Burkitt’s lymphoma (cancer from EBV) more common in Africa.

46
Q

HIV patient oral symptoms

A

Oral candidiasis, hairy leukoplakia, kaposis’s sarcoma.. etc

47
Q

What is this?

A

Pseudomembranous candidiasis (thrush) in an immunocompromised patent.

48
Q

Two biggest groups at risk of HIV

A

Men who have unprotected sex with other men.
People who share needles for injection drug use.

49
Q

How is HIV managed?

A

Highly effective anti-viral treatment (HAART)

50
Q

HHV-8

A

Kaposi sarcoma-associated herpes virus (KSHV)

51
Q

What is this?

A

Kaposi’s sarcoma: Red, purple, or brown patches, plaques, or nodules on the skin. Abnormal growth of small blood vessels just below the skin gives the lesions their purplish hue.

M4: Oral cancer (12 decks)

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