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Pathology Term 2 > Week 1 - HEAD & NECK > Flashcards

Week 1 - HEAD & NECK Flashcards

URTIs, Oral Lesions, Influenza, Salivary Glands, Others

1
Q

What is the most common oral lesion and describe it?

A

Aphthous Ulcers (Canker Sores)

  • common, young age (<20)
  • self-limited
  • painful, superficial ulcers of unknown etiology
  • covered by thin exudate
  • surrounded by hyperemia
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2
Q

What is a fibroma?

A
  • firm nodular swelling of fibrous/scar tissue (healing tissue)
  • chronic irritation –> common on buccal mucosa along bite lines
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3
Q

What is the commonest oral cancer?

A

Squamous cell carcinoma

-95%

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4
Q

What are the common locations and etiologies of oral cancers?

A

Location:
-lips, tongue, floor, oropharynx (HPV)

Etiology:
-tobacco, alcohol, sunlight (lips), HPV

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5
Q

What is the pathogenesis of oral cancers?

A

-from precursor lesions (leukoplakia/erythroplakia)
-injury due to tobacco, alcohol, HPV, sunlight, etc.
-hyperplasia
metaplasia
-dysplasia (leukoplakia/erythroplakia)
-carcinoma in situ –> CARCINOMA

  • HPV 16 –> loss of E1/E2 tumour suppressor genes
  • spread to cervical lymph nodes –> distant organs
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6
Q

Compare leukoplakia vs. erythroplakia

A

Leukoplakia:

  • asymptomatic, chronic, white
  • tobacco, irritation, infection (EBV, HIV, HPV)
  • thick keratinised epidermis
  • less vascular submucosa
  • micro: –> 10% dysplastic cells
  • decreased risk of malignancy

Erythroplakia:

  • asymptomatic, chronic, red
  • tobacco, alcohol (inflammation)
  • thin, dysplastic epidermis
  • more vascular submucosa
  • micro: –> 90% dysplastic cells
  • increased risk of malignancy
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7
Q

What are the microscopic features of oral squamous cell carcinoma?

A
  • pleomorphic pink cells forming irregular clusters
  • keratin pearls and keratinisation of cells
  • increased inflammatory infiltrate
  • haemorrhage
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8
Q

What is verrucous carcinoma?

A
  • warty, exophytic white lesion (“cauliflower-like”)
  • hard, keratin-producing tumour
  • low grade/well-differentiated
  • buccal mucosa, vestibule, gingiva
  • marked continual keratosis WITHOUT infiltration
  • -> papillary hyperkaratosis over dysplastic epithelial growth
  • no/rare metastases –> wide excision –> good prognosis
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9
Q

What is hairy leukoplakia?

A
  • irregular, rough-surfaced leukoplakia-like patch
  • white patches of fluffy, hairy hyperkeratotic thickenings
  • lateral side of tongue
  • some times with candidiasis too
  • increase in EBV/immunocompromised (AIDS) pts.
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10
Q

What is the microscopy of hairy leukoplakia?

A
  • acanthosis

- balloon cells (loaded with EBV)

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11
Q

What are balloon cells?

A

Cells loaded with EBV on microscopy of hairy leukoplakia

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12
Q

What is EBV?

  • symptoms?
  • IP?
  • transmission?
A

AKA infectious mononucleosis/glandular fever
IP = 1-2 months; self-limited after 4-6wks
Transmission = spread in youth, close contacts, saliva (“kissing disease”)
Symptoms:
-URTI Sx.
-lymphadenopathy
-splenomegaly
-hepatitis
-(pneumonitis, meningitis, encephalitis)

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13
Q

What is the pathogenesis of EBV?

A
  • EBV infects epithelium + B lymphocytes

- EBV-specific CD8 T cells –> defense (destroy cells containing EBV

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14
Q

What are complications of EBV?

A
  • hepatitis
  • spleen rupture due to splenomegaly –> youth death
  • organ failure
  • meningitis
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15
Q

How is coxsackie virus transmitted and what do each of its 2 types cause?

A

-faeco-oral transmission

Coxsackie A = herpangina, HFM disease
Coxsackie B = myocarditis, pericarditis

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16
Q

What is herpangina?

A
  • fever
  • sore throat
  • oral tiny papulovesicles –> ulcers
  • caused by coxsackie virus (A)
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17
Q

What are the risk factors for URTIs and which is the most important?

A

CONTACT = most important
-crowding, school, kindergarten, travel, congregations

Others:

  • immunity
  • nutrition
  • age
  • smoking
  • carrier states (e.g. GAS)
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18
Q

What are the common pathogens for URTIs in:

  • nasopharynx?
  • oropharynx?
  • epiglottitis?
  • larynx –> tachea?
  • bronchi?
A 
Nasopharynx --> rhinoviruses 
Oropharynx --> GAS
Epiglottitis --> H. influnzae (rare)
Larynx - Trachea --> parainflunza, S. aureus
Bronchi --> S. pnuemoniae, H. influenzae
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19
Q

What is the commonest URTI and its most common cause?

A

Rhinitis –> “The Common Cold”

  • rhinovirus
  • other causes = influenza, parainfluenza, SARS, adenovirus, RSV
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20
Q

True or False?

Secondary bacterial infections are uncommon in rhinitis

A

False

-v. common

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21
Q

Describe transmission of rhinitis

A

Highly contagious

-droplets spread by sneezing, coughing, or hand contact with nose, eyes or face

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22
Q

What is the incubation period and symptoms of rhinitis?

A
  • IP = 2-4 days
  • sneezing, coughing and malaise for 3-6 days
  • recovery after approx. 7 days w/without Tx. (VIRAL)
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23
Q

What is meant by rhinitis being catarrhal inflammation?

A

-excess mucous production

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24
Q

What are complications of rhinitis?

A
  • sinusitis
  • pharyngitis
  • tonsillitis
  • otitis media
  • septicemia
  • nasal polyps –> inflammatory (allergy/hypersensitivity) –> inflamm. tissue occurs under mucosa
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25
Q

What is the common cause of pharyngitis?

A

GAS

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26
Q

What is centor criteria

A
  1. Fever
  2. Tonsillar exudate
  3. Anterior lymphadenopathy
  4. NO cough
  • criteria used to diagnose pharyngitis
  • 0=unlikely, 4 = likely (^each Sx. = 1 point)
27
Q

Why is epiglottitis not common nowadays?

A
  • can be in children

- not common due to vaccine against Hib

28
Q

What are the Sx. of epiglottitis?

A
  • fever
  • dysphagia
  • drooling
  • hoarseness
  • stridor

*complete obstruction = urgent endotracheal intubation

29
Q

What is chronic rhinosinusitis?

A

Inflammation of paranasal/maxillary sinuses for >12 wks

30
Q

What are the 3 types of sinusitis and what are the symptoms?

A
  1. with polyps
  2. without polyps
  3. allergic

Sx. –> fecer, pain, nasal discharge, hyposmia/anosmia

31
Q

What is the causative organism of diptheria and why is it rare nowadays?

A

Corynebacterium diptheriae

  • gram + pleomorphic bacilli (‘chinese letter pattern’)
  • rare due to DPT vaccine
32
Q

What are the Sx. of diptheria?

A

-high fever
-SOB
-sore throat, cough
hoarseness
-nausea and vomiting
-marked neck lymphadenopathy (“Bull Neck”)
-pseudomembrane formation –> mucosal necrosis with fibropurulent exudate

33
Q

What are complications of diptheria?

A
  • aspiration of pseudomembrane + airway obstruction
  • spread of exotoxin –> myocarditis, heart failure/death, peripheral neuritis
  • cutaneous diptheria –> non-healing ulcer
34
Q

What is the IP and mode of transmission of influenza?

A
  • IP = 1-5 days

- person to person spread (crowd, school, aged-care, etc.)

35
Q

What are clinical symptoms of influenza and how is it diagnosed?

A

Clinical:

  • mild URTI –> high fever
  • chills
  • headache/muscle aches
  • dry cough
  • abdo. pain + diarrhoea (esp. in children)

Diagnosis:

  • nasopharyngeal swab for a rapig Ag test or PCR
  • serum Abs develop later
36
Q

What are the 2 main surface Ags of influenza A?

A

500 surface molecules of hemagglutinin (H)
100 surface molecules of neuraminidase (N)

  • influenza = orthomyxovirus
  • types A, B, C
37
Q

Which strain(s) of influenza is there a vaccine for? And what are the 2 available types of vaccines?

A
  • type A + B
  • type C = rare (no vaccine)

Vaccine = purified, inactivated Fluvac

  1. Trivalent* –> commonest (2A + 1B)
  2. Quadrivalent (2A + 2B)
38
Q

How is Influenza B named?

A

according to LOCATION

-e.g. Influenza Brisbane

39
Q

What is the most common influenza strain nationally?

A

Influenza A (H3N2)

40
Q

Commonly prescribed trivalent vaccine in Australian Fluvac has this type?

A

B Phuket

41
Q

What is SARS?

A

Severe Acute Respiratory Syndrome

  • severe pneumonia
  • high morbidity/mortality
42
Q

What is atrophic rhinitis?

-symptoms + etiology?

A
  • rhinitis sicca/dry nose
  • chronic atrophy of nasal mucosa + turbinates

Sx.
-nasal crusting, fetor, widening of space, ANOSMIA

Etiology:

  • primary –> unknown - immune/hereditary?
  • secondary –> chronic sinusitis, trauma, surgery, granulomatous disease
43
Q

What bacteria is commonly isolated from the greenish pus produced in atrophic rhinitis?

A

coccobacillus

44
Q

What are the major and minor salivary glands and which type are each?

A

Major:

  1. Parotid - serous (enzyme-rich)
  2. Submandibular - mixed
  3. Sublingual - mucinous (for lubrication)

Minor:
-hundreds of small widespread glands all over oral cavity

45
Q

How are salivary glands linked to the pancreas?

A
  • they have acini and ducts

- difference is that the salivary glands have mucinous acini as well

46
Q

What are the functions of saliva?

A
  • lubrication (mucous
  • digestion (enzymes)
  • mineralisation of teeth
  • speech
47
Q

What is the commonest tumour of salivary glands?

A

Pleomorphic adenoma

  • benign
  • commonest carcinoma = mucoepidermoid carcinoma
  • Warthins tumour = #2
48
Q

Which glands are commonly affected in sialadenitis and what is the pathogenesis?

A
  • parotid + submandibular
  • parotid sialadenitis identified clinically by raising of earlobes

Pathogenesis:

  • dry mouth (xerostomia) –> drying of secretions –> ductal block –> inflammation and infection
  • mumps –> bacterial infection of salivary glands
  • Sjogren’s syndrome –> autoimmune sialadenitis (parotitis)
49
Q

What is chronic sialadenitis?

A
  • total atrophy/fibrosis of the gland
  • common in submandibular
  • drying up of secretions –> stone formation of ducts (sialolithiasis)
50
Q

What is xerostomia?

  • causes?
  • clinical features?
  • complications?
A

-dry mouth –> “decreased saliva”

Causes:

  • drugs, stress, fever, anticholinergics, antipsychotics, sedatives, antihistamines, Vit. C
  • autoimmune –> Sjogren + SICCA syndrome

Clinical Features:
-dry mouth, atrophy of papillae of tongue with fissuring, ulcerations

Complications:
-caries, candidiasis, dysphagia, speaking difficulty

51
Q

What are the 2 types of Sjogren’s syndrome?

A

AUTOIMMUNE SIALADENITIS

  1. Primary (SICCA syndrome): (50%)
    - systemic
    - T cell mediated –> ducts
  2. Secondary (with other disorders): 50%
    - RA, SLE, SS, etc
52
Q

What are the clinical features of Sjogren’s syndrome?

A
  • dry eyes (conjunctivitis)
  • dry mouth (xerostomia)
  • caries
  • speech/taste abnormalities
  • dysphagia
53
Q

What antibodies are involved in Sjogren’s syndrome?

A

Anti-SS-A/SS-B (anti-Ro + La)

*used to confirm diagnosis

54
Q

What type of virus is Mumps and what is the ‘good’ thing about mumps?

A
  • paramyxovirus

- single serotype –> therefore infects only ONCE with subsequent lifelong immunity

55
Q

What are the clinical features of mumps and what other diseases can it cause?

A

Clinical features:

  • fever
  • swollen, painful parotids
  • orchitis

Can cause:

  • aseptic meningitis
  • orchitis
  • acute pancreatitis
56
Q

Why is there an increased likelihood of recurrence of pleomorphic adenomas?

A
  • often involve extensions into surrounding tissue

- therefore difficult to excise adequately –> increase recurrence

57
Q

What 2 tissues is pleomorphic adenomas comprised of?

A
  • epithelial and connective tissues

- benign mixed tumour

58
Q

What are the gross and microscopic features of pleomorphic adenoma?

A

Gross:

  • solid grey/white tumour
  • translucent blue areas of cartilage + myxoid tissue

Micro:

  • epithelial + CT
  • cartilage common
  • glandular structures
59
Q

From what do pleormphic adenomas typically arise from?

A

Myoepithelial cells

-of the salivary ducts

60
Q

What is carcinoma ex pleomorphic adenoma?

A
  • carcinoma that arises after many years in a pleomorphic adenoma
  • 10% at 10yrs
  • highly aggressive
  • mortality = 50% at 5yrs
61
Q

What is Warthin’s tumour?

A
  • benign tumour due to the inclusion of lymphoid tissue into the gland
  • no damage/inflammation
  • ONLY in parotid glands
  • morphology = double layer of neoplastic epithelium folded around dense lymphoid tissue with cystic spaces
62
Q

What salivary glands do adenoid cystic carcinomas affect?

A

Minor salivary glands

-palate, cheeks, lips

63
Q

What are 2 key points for nasopharyngeal carcinomas?

A
  1. common in Asian people

2. strong link to EBV infection

64
Q

What is the common CT element associated with pleomorphic adenomas?

A

Cartilage

Pathology Term 2 (6 decks)

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