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Oral Medicine > Clinical > Flashcards

Clinical Flashcards

1
Q

Which groups of viruses cause infection in the oral cavity?

A

Herpesviruses
Papillomaviruses
Coxsackie viruses
Paramyxoviruses

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2
Q

List all the herpesviruses

A 
herpes simplex 1
herpes simplex 2
varicella zoster (chicken pox)
Epstein Barr virus
Cytomegalovirus
HHV-6 (not well known)
HHV-8 (causes Kaposi sarcoma)
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3
Q

List 3 triggers for secondary herpes simplex 1 infection.

A
  1. Sunlight
  2. Immunosuppression
  3. Stress
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4
Q

Who gets herpes zoster (shingles)?

A

Usually immunosuppressed individuals, who are often very old and have significant systemic illnesses: Malignancy (lymphoma/leukemia), Drugs (corticosteroids) and AIDS.

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5
Q

List the different proteins that are attacked in pemphigus vulgaris and mucous membrane pemphigoid.

A

Pemphigus vulgaris - desmoglein 3

MMP - laminin 5 BP180

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6
Q

How do you diagnose pemphigus vulgarise and MMP?

A

Biopsy (from non-ulcerated mucosa)

Confirm with immunofluorescence -

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7
Q

What causes/triggers recurrent aphthae?

A

Syndromes - Behcet syndrome, PFAPA (periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis) syndrome

  • Associated with coeliac disease and ulcerative colitis
  • Triggers - stress, trauma, diet, hormones, depressed immunity
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8
Q

Describe the 3 types of recurrent aphthous ulcers.

A
  1. Minor ~5mm in diameter
  2. Major 10+mm
  3. Herpetiform - coalesced ulcers with irregular margins
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9
Q

Outline non-pharmacologic and pharmacologic management of RAS

A

Non-pharmacologic - control of predisposing factors: trauma, deficiency states, certain triggering foods, hormone therapy (in pts that get ulcers related to menstrual cycle), stress management counselling

Pharmacologic - CHX mouthwash, topical anaesthetic gels, topical corticosteroid (if in prodromal stage –> can hasten recovery), corticosteroid mouthwash (for widespread ulceration), systemic corticosterids (severe cases)

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10
Q

What is Erythema Multiforme

A

Inflammatory (type 4 cell-mediated hypersensitivity reaction) muco-cutaneous disease characterised with swelling, redness and blistering/crusting of significant skin/mucosal areas

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11
Q

3 common triggers of Erythema Multiforme

A
  1. Infection by HSV
  2. Drug reactions to NSAIDs or anticonvulsants
  3. Food preservatives - benzoic acid
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12
Q

Prognosis of Erythema Multiforme

A

Self-limiting - resolves over 2-6 weeks depending on severity

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13
Q

Treatment of Erythema Multiforme

A

Supportive in nature - analgesic and antiseptic mouthwashes
Eye involvement - assessed by ophthalmologist
corticosteroids (severe disease)
hospital admission (EM major with dehydration and limitation in drinking)

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14
Q

What is the 5-year survival rate of oral cancer?

A

50%

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15
Q

What is histoplasmosis

A

Deep fungal infection, spread through inhalation of spores. Can cause chronic non healing ulcers in the oral cavity, secondary to lung disease

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16
Q

What is the supposed aetiology of hairy tongue?

A
  • Drugs - antibiotics and systemic corticosteroids
  • Smoking (high intensity)
  • Irradiated patients

There seems to be an alteration of the normal oral microbiota with overgrowth of fungi and certain chromogenic bacteria and concomitant hyperplasia of filliform papilla

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17
Q

Management of hairy tongue

A
  1. Identification/management of predisposing factors (e.g. antibiotics)
  2. Brushing with baking soda
  3. Reassurance
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18
Q

Summarise Erythema migrans

A
  • also called geographic tongue
  • benign condition of unknown aetiology
  • affects tongue, strongly associated with fissured tongue
  • Presents as atrophic (red) patches surrounded by raised hyperkeratotic margins
  • Self-limiting, usually asymptomatic
  • If symptomatic - Good OH, steroids
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19
Q

What is the significance of Oral Lichen planus

A
  1. Relatively common - 2% of population
  2. Potential for malignant transformation - 1% at 5 years
  3. More severe forms can be painful and distressing, requiring steroids
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20
Q

Pathogenesis of OLP

A
  • T-Lymphocytes attack epithelium of mucosa destroying basal keratinocytes via released cytokines (initiate apoptosis)
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21
Q

Histopathology of OLP

A
  • Hyperkeratosis
  • basal layer vacuolisation with apoptotic keratinocytes
  • lymphocytic infiltrate at epithelium-connective tissue interface
  • saw-tooth appearance of rete ridges in skin
22
Q

Diagnosis of OLP

A
  • Based on clinical and history alone usually

- If atypical presentation (plaque form or atrophic/erosive type) –> biopsy to exclude SCC

23
Q

Management of OLP

A

Non-pharmacological

  • Avoidance of irritants (certain foods, sharp cusps etc)
  • good oral hygiene (CHX mouthwash)

Pharmacological

  • Topical corticosteroids
  • Systemic corticosteroids
  • supplemental antifungal agents
24
Q

Describe Lupus Erythematosus

A
  • autoimmune disease, resembles OLP in the oral cavity
  • autoantibodies and antigen-antibody complexes circulate in serum and create problems in various body systems
  • Two main types: discoid, systemic
  • Oral: delicate white striae
25
Q

Candida albicans exists as commensal part of normal oral microflora in many people - how does it then cause disease?

A

We have no tests available currently that can discriminate the transition of candidal saprophytism to pathogenicity.

However, C. albicans is an opportunistic pathogen. When certain predisposing factors are present it can cause disease.

26
Q

List 6 factors that predispose to a candidal infection in the oral cavity

A
  1. Changes in oral microflora - systemic antibotics
  2. Hyposalivation - reduced IgA antibodies and other defensive proteins
  3. Immunosuppression - systemic corticosteroids
  4. Ill-fitting prostheses - trauma
  5. Uncontrolled diabetes
  6. Nutritional deficiencies - may result in reduced host defences and loss of mucosal integrity
27
Q

Diagnosis of Candidosis

A
  • History and clinical findings
  • if hyper plastic lesion present –> biopsy to exclude cancer
  • if initial therapy not successful - direct examination of smear, culture or biopsy
28
Q

Describe steps in Management of Candidosis

A
  1. Manage aetiological & risk factors
  2. Check adequacy of dentures
  3. Exclude deficiency states
  4. Exclude diabetes mellitus
  5. Check drug history - ABs, steroids
  6. Check med history - immunosuppression
  7. Treat with appropriate anti fungal agent
29
Q

Pharmacological Mx of Candidosis

A
  1. Amphotericin (polyene) lozenge (10mg) 4/day
  2. Amphotericin + Miconazole gel (azole) -f denture wearer
  3. Nystatin (polyene) ointment on fitting surface of denture
    Systemic antifungals reserved for debilitated or immunocompromised patients
30
Q

What is median rhomboid glossitis

A
  • An atrophic lesion found in the middle of the tongue, often associated with candidal infection, inhaled steroids and smoking.
31
Q

What is angular cheilitis?

A
  • erythematous fissuring one or both corners of the mouth
  • usually associated with an intra-oral candidal infection, but staphylococci and streptococci also associated
  • facial wrinkling (older people) at corners of mouth leads to chronically moist environment suitable for infection
32
Q

How can you tell that a red-blue lesion is some type of vascular malformation?

A

It blanches when pressure applied to it

33
Q

What is a varix?

A

A type of acquired vascular malformation, typically a focally dilated vein. No treatment necessary unless of cosmetic concern or gets frequently traumatised.

34
Q

Pyogenic granuloma summary

A
  • exuberant tissue response to local irritation/trauma
  • hyperplastic granulation tissue with prominent capillaries.
  • commonly seen in pregnant women
  • commonly become ulcerated due to trauma
  • treatment: excision, occasional recurrence
35
Q

Peripheral Giant Cell Granuloma summary

A
  • hyperplastic connective tissue response to injury of gingival tissues
  • distinctive feature - multinucleate giant cells
  • clinically indistinguishable from pyogenic granuloma
  • treatment - excision (including connective tissue from each it arises - PDL/periosteum)
36
Q

Consequences of VitB deficiency

A
  • glossitis (red, atrophic, pain, tenderness, burning)

- angular cheillitis

37
Q

Pernicious Anaemia summary

A
  • Deficiency of B12 - required for DNA synthesis
  • Results from inability to transport B12 across intestinal mucosa - due to lack intrinsic factor
  • Similar oral manifestation as VitB deficiency
38
Q

Iron-deficiency anaemia

A
  • iron required for haemoglobin molecule in erythrocytes

- similar oral manifestations as other nutritional deficiencies

39
Q

Briefly summarise Burning Mouth Syndrome

A
  • Symptoms of pain and burning (sometimes intense), but without clinically detectable lesions
  • normal appearing oral mucosa
  • normal histopathology
  • many possible causes - in some patients, several factors can be identified, in others none
  • diagnosis by exclusion
40
Q

Mx of Burning Mouth Syndrome

A

Non-pharmacological

  • reassurance
  • Address any detected predisposing factors
  • psychological counselling

Pharmacological

  • topical steroids
  • viscous lidocaine
  • antidepressants
41
Q

What are petechiae and ecchymoses

A

Soft tissue bruises (usually due to trauma/blood dyscrasia)

  • petechiae - pin-point
  • ecchymoses - larger than pin-point
42
Q

Describe Kaposi Sarcoma

A
  • spindle-cell tumour from endothelial cell origin (often seen in HIV pts)
  • caused by HHV-8
  • pulmonary involvement - most common cause of mortality
  • in Oral cavity - bulky tumours may interfere with speech or mastication
  • Poor prognosis in immunodeficiency states
43
Q

What is the most common oral pigmented lesion?

A

Amalgam tattoo

44
Q

How would you classify pigmented lesions?

A

Melanocytic (melanin-containing or intrinsic)
- various conditions ranging from melanotic macule to melanoma
Non-melanocytic (extrinsic)
- Amalgam tatto
Drug-induced pigmentation

45
Q

Which drugs can cause oral pigmentation?

A
  • Minocycline - tetracycline drug
  • Chloroquine - used in malaria t
  • Cyclophosphamide - anti-cancer drug
  • AZT (Zidovudine) - anti-retroviral tx for HIV
46
Q

How is smoking-associated melanosis treated?

A

Smoking cessation –> improvement over months or few years

47
Q

Difference between melanotic macule and melanocytic nevus

A
  • melanotic macule - normal no. of melanocytes, but increases melanin accumulation - no tx necessary. Biopsy if suspecting melanoma
  • melanocytic nevus - collection of nevus cells, seen clinically as a papule or nodule, and thus should be biopsied to exclude melanoma
48
Q

Write short acronym for clinical features suggestive of melanoma

A 
ABCs
A - Asymmetry
B - Borders irregular
C - Colour variable
S - satellite lesions
49
Q

Can tetracycline cause discolouration of soft tissues?

A

Yes - it deposits in underlying bone and in areas of thin epithelium, a greyish-green discolouration may be visible.

50
Q

What are high risk sites for melanoma?

A

Palate and gingiva

51
Q

What is Addison’s disease and it’s relation to oral pigmentation

A
  • Primary adrenocortical insufficiency
  • lack of cortisol stimulates ACTH secretion by pituitary gland
  • Increased ACTH becomes broken down in MSH (melanocyte-stimulating hormone) leading to multiple melanotic macules across the body including the oral cavity

Oral Medicine (2 decks)

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