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Stage 4 OD > OD part 2 > Flashcards

OD part 2 Flashcards

1
Q

Explain macule and plaque

A

-Spot (aka macule)=flat lesion with a colour change. Smooth or finely granular
-Patch (aka plaque)= thickened solid lesion (~1-4mm thick) with slightly rough surface

can vary in colour: white, red, brown, grey, black

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2
Q

Explain erosion and ulceration. Main difference

A

-Erosions: involve epithelium ONLY. More superficial.
-Ulcer: much deeper loss of tissue than erosions -the epithelium and lamina propria is breached. More commonly seen in cancer. Lost layers from basement membrane upwards

-Clinically, may be difficult to distinguish between the 2

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3
Q

List types of acute and chronic oral ulcers

A

-Acute
Herangina
Primary herpetic ginigivostomatitis
Hand foot and mouth disease
Necrotising ulcerative gingivostomatitis
Traumatic ulcers
Hypersensitivity reactions
Erythema multiform

-Chronic
pemphigus vulgaris
Mucous membrane pemphigoid
TB ulcer
Lichen plenus

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4
Q

Difference betweeen bullae and vesicle

A

Both elevated fluid filled lesions.

-Bullae (blisters) are larger than vesicles (>1cm). Single or multiple but usually not in greater numbers. In the mouth they burst easily giving way to erosions
-Vesicles: <1cm. Usually numerous (tens, hundred)

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5
Q

With pemphigus and pemphiogid, which is intra-epithelial and which is sub epithelial blistering. Which affects keratinocytes, which basement membrane

A

-pemphigus- an intra-epithelial blister - altered adhesion between keratinocytes

-pemphigoid – sub-epithelial blister. Altered adhesion at basement membrane

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6
Q

What are verrucous papillary lesions

A

-Raised growth on the mucosa
-can be sessile or pedunculated, red or white
-range from benign (Papilloma) to malignant (verrucous carcinoma)

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7
Q

List hyperplastic oral lumps

A

-fibroepithelial polyp
-pyogenic granuloma
-Epulides
-gingival hyperplasia
-Denture granuloma
-Squamous cell papilloma
-Mucoceles

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8
Q

list hyperkeratosis oral conditions

A

white sponge naevus
frictional keratosis
leukoplakia
lichen planus
Smoker’s keratosis

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9
Q

Difference between Oral lichen planus and oral lichenoid lesions

A

OLP= bilateral
OLL= not OLL if bilateral, desquamative gingivitis, tongue involvement, skin involvement, papule and striae. It is Unilateral, Contact and drug types

Both type IV hypersensitivity

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10
Q

Viruses that cause oral hairy leukoplakia

A

EBV (HHV4)
HIV

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11
Q

Causes of macroglossia

A

-acromegaly
-hypothyroidism (myxoedema)
-amyloidosis
-vit B12 deficiency
-seen in Beckwith-Wiedemann syndrome and Down syndrome

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12
Q

Which areas of the mouth have masticatory and lining mucosa

A
  1. Masticatory mucosa (Keratinised epithelium): Gingiva
    Hard palate
  2. Lining mucosa (non-keratanised)
    Labial and buccal mucosa
    Ventrum of tongue (dorsum is specialised with papillae)
    FOM
    Soft palate
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13
Q

What are the 4 cell layers of keratinised epithelium

A

Keratin layer
Granular cell layer
Prickle cell layer (stratum spinosum)
Basal cell layer

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14
Q

What is oral epithelial dysplasia. What are some features

A

-Term used to describe histological changes that suggest increased risk of malignant transformation
-graded as mild, moderate and severe dysplasia

-features of cytological atypia (abnormal nuclear size and shape), altered proliferation (increased mitotic activity), altered maturation (premature keratinisation), loss of epithelial organisation (drop-shaped rete processes, verrucous papillary architecture, disorganised basal cells, irregular stratification, reduced keratinocyte adhesion)

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15
Q

What are oral potentially malignant disorders. Do they have dysplasia

A

associated with an increased risk of occurrence of cancer of the lip or oral cavity

Important to note that not all OPMDs exhibit epithelial dysplasia. They range from hyperkeratosis to different degrees of dysplasia

eg. leukoplakia, erythroplakia, lichen planus

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16
Q

Which sites of leukoplakia have highest risk of malignant transformation. More risk if homogenous or non-homogenous

A

-Site: tongue and FOM (10-30% risk)
-Non-homogenous - Red or speckled

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17
Q

Candida facts (where, types of oral infections)

A

-yeast found in digestive and vaginal tracts
-Dimorphous fungus = proliferates in either yeast or hyphal form
-opportunistic= live communally but can cause disease when host defences compromised
-dorsum of tongue most common site
-Candida-related disorders: denture induced stomatitis, median rhomboid glossitis, angular cheilitis

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18
Q

Risk factors for candida

A

-disease of the diseased
-decreased saliva, smoking, decreased blood supply, poor OH, dental prostheses, altered oral flora, immunosupression (HIV, corticosteroids), malnutrition, malignancies, broad spectrum antibiotic therapy, steroid inhalers, anaemia

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19
Q

Which viruses are associated with cervical cancer, oropharyngeal cancer, Kaposi’s sarcoma and Burrit’s lymphoma

A

HHV8, HIV= Kaposi’s sarcoma
HPV=cervical cancer, head and neck cancer (Oropharyngeal)
EBV= burkitt’s lymphoma

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20
Q

Oral manifestations of HSV1&2, HHV3,4,5, measles, mumps, coxsackie, HIV, HPV

A

-HSV1 = herpetic gingivostomatitis, herpetic whitlow
-Recurrent HSV1&2= herpes labials (cold sores)
-Coxsackie: Herpangina (white vesicles on soft palate). Hand foot and mouth disease
-Epstein Barr virus (HHV4) = oral hairy leukoplakia, glandular fever
-HIV= oral hairy leukoplakia, increased infections, Kaposi’s sarcoma
-HPV = benign oral warts -
-HHV3 reactivation = shingles and oral lesions
-Measles virus= koplik’s spots (white surrounded by red patches on buccal mucosa)
-Mumps=swelling of salivary glands
-HHV5 cytomegalovirus - palate ulceration, glandular fever

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21
Q

What is anaemia, macrocytic v microcytic. General and oral signs of anaemia

A

-Reduced haemoglobin
-High and low mean cell volume
-Lethargy, pallor, brittle nails, sore mouth, glossitis, ulcers, angular chelitis, acute pseudomembranous candidosis

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22
Q

Levels of platelets in thrombocytopenia. Causes. Features

A

< 150,000 platelets per microliter of circulating blood.
<100 = INCREASED BLEEDING
<50 = DANGEROUS

Due to marrow disease, liver disease, cytotoxic drugs, radiotherapy.

(thrombocytosis= too many platelets)

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23
Q

Different types/ causes of anaemia

A
  1. Acute excess loss
  2. Genetic failure of of production of RBCs
  3. B12 Deficiency anaemia (PERNICIOUS ANAEMIA (too little IF, lack of absorption)
  4. Folate deficiency anaemia
  5. Fe deficiency anaemia -chronic blood loss, lack in diet, periods, pregnancy
  6. Marrow disease (Leukaemia, Aplastic anaemia)
  7. Excess destruction – haemolytic anaemia
  8. Sickle cell anaemia
  9. Thalassaemia – no haemaglobin production
24
Q

Explain acute, chronic, lymphoid and myeloid leukaemia

A

Abnormal immature leukocytes suppressing the amount of normal ones

*Acute – primitive blast cells (immature WBCs) released into blood
*Chronic – abnormal cells which retain most of morphological features of normal counterparts
*Lymphoid – lymphocyte lineage of the malignant cells
*Myeloid – granulocyte/monocyte lineage of the malignant cells

Acute lymphoblastic, acute myeloid, chronic lymphoblastic, chronic myeloid

25
Q

Difference between Hodgkin and non-hodgkin lymphoma. Which is more common

A

-HL: Reed-Sternberg lymphocyte cell is present. Affects younger patients. Better prognosis. Affects lymph nodes in upper body (neck, chest, armpits) - presents usually with neck swelling.
NHL: cell is not present. More common. Arises in lymph nodes anywhere in the body.

26
Q

List causes of sialadenitits

A

inflammation of the salivary gland. Due to:
-Bacterial (infection due to reduced salivary flow)
-Viral (Mumps from paramyxovirus)
-HIV

27
Q

Causes of Xerostomia and its effects

A

-dehydration, diabetes, renal failure, head and neck radiotherapy, Sjögren’s syndrome
-medications: anticholinergic agents (atropine), antidepressants, carbemazepine, diuretics (furosemide), anxiolytics

-thirst, difficulty eating, swallowing, talking, taste disturbance, increased caries and perio disease, candida, bacterial sialadenitis, cobblestone appearance, poor denture retention

28
Q

Management for Xerostomia

A

-Frequent sips of water
-Lubricants (oralube, xerostom, biotene)
-Olive oil on surface of tooth
-Stimulate secretion – pilocarpine (Muscarinic agonist)
-Sugar free gum, lozenges, mints
-Prevent oral disease: OHI, Chx rinse 0.2%, Diet, Fluoride, Anti-fungals, Denture hygiene

29
Q

Functions of saliva

A

-Mechanical washing
-Anti-microbial activities
o Enzymes - lysozyme
o Antibodies- IgA
o Lactoferrin
o Bacterial aggregation [mucin]
o Sialoperoxidase
-Remineralisation of dental tissues
-Buffer acid
-Lubrication – mucin
-Digestion [amylase]

-Lysozyme= breaks peptidoglycan cell wall
-Lactoperoxidase=converts H2O2 into hypothiocyanous acid
-Lactoferrin-hides iron from bacteria

30
Q

Sjögren’s syndrome: difference between primary and secondary, exclusion criteria

A

-Autoimmune disease
-Primary: dry eyes and mouth for > 3 months. Secondary is associated with other autoimmune diseases (SLE, RA, scleroderma)

-Exclusion: Head and neck radiotherapy, Hep C, AIDs, History of Sarcoidosis, GvHD, Use of anticholinergic drugs. Pre-existing lymphoma for primary but not secondary

31
Q

Diagnosing sjogren’s syndrome -antibodies, eye tests

A

-AECG criteria
-Histology shows lymphoid infiltrate around ducts which causes destruction and fibrous gland
-Ultrasound of glands
-Schirmer’s filter paper test: <5mm in 5 mins of tears
-Rose Bengal staining
-Anti-Ro or Anti-La
-Rheumatoid factor
-ESSDAI questionnaire
-Salivary proteonomics

32
Q

What antibody is specific in sjogren’s syndrome

A

Anti-Ro or Anti- La

33
Q

What is the most common benign salivary gland tumour. What about malignant. What % of salivary tumours are benign

A

-Pleomorphic adenoma
-Mucoepidermoid carcinoma

80% benign

34
Q

Features of a malignant salivary gland neoplasm

A

-Firm fixed lump (Indurated = rock hard)
-Fixed as eating into the tissues deeply
-Poorly demarcated
-Rapid growth
-Pain
-Skin/mucosal ulceration
-If in parotid gland: potential facial nerve palsy
-Bone invasion

35
Q

What muscle does the parotid duct pierce, what muscle does the submandibular gland wrap around, what muscle does the sublingual gland sit above.

A

1.Parotid – duct though buccinator
2.Submandibular – deep part wraps posterior border of mylohyoid and duct goes through sublingual gland orifices
3.Sublingual – above mylohyoid

36
Q

Causes of acute inflammatory salivary swellings. And recurrent swellings

A

-Acute= bacterial sialadenitis, mumps, HIV related
-Recurrent= salivary calculi, papillary obstruction, duct stricture, punctuate sialectasis (present in Sjogren’s)

37
Q

What tumour has a characteristic out pouching on the salivary capsule, requiring extra capsular dissection

A

pleomorphic salivary adenoma

38
Q

What does sialography involve

A

-put cannula in entrance to duct, inject radiopaque dye and use scanner to see where dye goes – shows blockages or narrowing
-stones are usually radiopaque

39
Q

Pro and con of using ultrasound for investigating salivary gland blockages

A

non-ionising -but cannot examine deep parotid

MRI good for imaging soft tissue, but less readily available

40
Q

List types of salivary gland surgery

A

1.Removal of calculi
2.Ductal dilatation/repositioning – saliva flows out better
3.Excision of sublingual gland, or sublingual
4. Removal of minor salivary gland tumours
5.Parotidectomy - superficial or total
6.Extracapsular dissection
7.Minimally invasive surgery

41
Q

3 nerves that can be damaged in submandibular gland removal

A
  1. FACIAL NERVE CERVICAL BRANCH – droopy lower lip
  2. LINGUAL NERVE – associated with deep part of gland
  3. HYPOGLOSSAL NERVE – lies deep to fascia where SM gland is removed
42
Q

What structures run through parotid gland

A

-auriculotemporal nerve, external carotid, retromandibular vein
-facial nerve divides it into superficial and deep lobes

43
Q

Risks of parotidectomy

A

-Pain, swelling
-damaging facial nerve= facial palsy
-damage to auriculotemporal nerve= numb ear lobe
-sialocele= secretion of saliva which can’t get out causing skin swelling
-Frey’s syndrome = sweating when eating

44
Q

Cause of Frey’s syndrome

A

-occurs in ~1/3 parotid operations
-Postganglionic parasympathetic fibres connect to sympathetic instead so impulses which would have led to saliva flow causes sweating instead.
-Common, but most patients unaware they have it.
-Botox injections help

45
Q

Is upper or lower lip swelling more likely to be benign or malignant

A

-UPPER LIP = more likely MALIGNANT (eg. canalicular adenoma)
-LOWER LIP =more likely MUCOCELE (trauma from biting causes accumulation of mucous in tissue)

46
Q

Reasons for doing an incisional and excisional biopsy

A

-Incisional – don’t know what something is to find out what it is. Premalignancies. Take affected and unaffected tissue. Use LA, 15 blade scalpel
-Excisional – definitely know it is benign, through examination or further investigation. Or if unsure but so small (<1cm) so may as well take it all out

47
Q

What does skin patch testing involve and what oral disease is it useful for diagnosing

A

-apply allergens to skin and wait for an inflammatory reaction. Apply for 3-4 days
-test for type IV hypersensitivity
-Oral lichenoid reactions

48
Q

What oral conditions can exfoliative cytology be used for diagnosing

A

-Examination of cells scraped from surface of a lesion or material aspirated from a cyst
-Advantages = QUICK/ EASY/ NO LA/ can be immune-stained
-Most useful for detecting virally damaged cells, pemphigus or candida hyphae

49
Q

Indications for taking a biopsy

A

-Neoplastic/ premalignant features
-Persistent lesions of unknown aetiology
-Persistent lesions which not responsive to treatment
-Confirmation of clinical diagnosis

50
Q

Possible reasons for failure in histological diagnosis when taking a biopsy

A

-Specimen poorly fixed or damaged during removal -poor handling
-Specimen unrepresentative of lesion/ too small
-Disease does not have diagnostic histological features (eg. aphthous ulcers)
-Histological features have several possible causes (eg. Granulomas)
-Histological features are difficult to interpret
-Inflammation may mask correct diagnosis

51
Q

Dos and don’ts of taking a biopsy. What an Ideal sample looks like

A

-Don’t inject LA directly into lesion
-Don’t apply pressure- this creates damage/artefacts
-Include some healthy tissue in biopsy
-Must not be wedge shaped-only small amount of lamina propria and basal layer
-Deep enough to allow study of interface between epithelium & connective tissue
- 4-5mm large
-Don’t squeeze/ crush tissue with forceps
-Put sample on the paper with epithelium facing up
-Immediate fix sample in formalin
-Suture using vicryl 3-4/0 or silk 3-4/0

52
Q

What is a biopsy sample fixed in. Why is a biopsy not wedge shaped (narrow at bottom)

A

-formalin
-if wedge shaped then not enough lamina propria and basal layer

53
Q

What is direct and indirect immunofluorescence

A

-labeling antibodies or antigens with fluorescent dyes
1.Direct = detect antibodies against IgG, IgM, IgA, C3, fibrinogen in skin or mucous membrane
2. Indirect = detect circulating autoantibodies bound to skin/mucous components

54
Q

How immunofluorescence helps diagnose pemphigus, pemphigoid and lichen planus

A

-Pemphigoid= IgG and C3 at basement membrane
-Oral lichen planus= shaggy fibrinogen deposits along basement membrane
-Pemphigus= intercellular space deposition with IgG. Circulating anti-epithelial antibodies

55
Q

Why punch biopsy not ideal for bullous diseases. Why need to be careful with biopsy

A

-Punch biopsies not preferred because twisting motion used in taking the specimen may dislodge the epithelium

-Carried out where epithelium present
-Avoid the epithelium-connective tissue split during removal of specimen
-Advised to capture the edge of lesions where the mucosa appears to be healthy

Stage 4 OD (2 decks)

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