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BDS2; CHHD > Interactive oral manifestations of systemic disease > Flashcards

Interactive oral manifestations of systemic disease Flashcards

1
Q

What are Campbell de Morgan sports

A

= Cherry red haemangiomas

  • firm red, blue/ purple papule 0.1-1cm diameter
  • when thromboses they can appear black and under dermatoscope they will appear red/ purple
  • these can develop anywhere but common in scalp, face, lips and trunk
  • occur more frequently after 40
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2
Q

How are Campbell de Morgan spots diagnosed

A

Clinically, characterised by red-clod or lobular pattern on dermatoscopy ‘lacunar pattern’ due to static blood in lesions; a biopsy can be taken if the diagnosis is unclear

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3
Q

What are the potential differentials for Campbell de Morgan spots

A
  1. Angiokeratoma = benign cutaneous lesion of capillaries
  2. Spider telangiectasis
  3. Nodular basal cell carcinoma (single isolated lesion)
  4. Amelanotic melanoma
  5. Pyogenic granuloma = reactive proliferation of capillary blood vessels
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4
Q

What is Hereditary Haemorrhagic Telangiectasia

A

= Osler-Weber-Rendu syndrome

  • autosomal dominant condition
  • characterised by telangiectasia on skin/mucosa
  • multiple purpuric spots may get traumatised and bleed
  • typically associated with nose bleeds
  • GIT: bleeding and iron deficiency anaemia
  • lung, liver and cerebral arteriovenous malformations are associated with HHT
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5
Q

What is Spider naevi

A

Numerous vessels radiating from central arteriole filling from the centre outwards

  • skin drained by superior vena cava affected
  • <5 is normal and common in females
  • > 5 is associated with liver disease, oral contraception and pregnancy
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6
Q

What is telangiectasia

A

= Widened venues resulting in threadlike red lines/ patterns on skin which form gradually and in clusters

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7
Q

What is ecchymosis

A

= Bruises

  • tend to be red-blue in colour
  • often follow a history of trauma
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8
Q

What can cause ecchymosis

A
  • sun damage causing weakened collagen can make skin more prone to bruising
  • XS cortisol use can thin skin causing easy bruising
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9
Q

What are spontaneous ecchymosis lesions suggestive of

A

These can occur as blood blisters and may represent underlying platelet/ coagulation disorders or over-anticoagulation with warfarin

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10
Q

What can cause xerostomia

A

= Oral dryness that is age related and associated with poly pharmacy can be caused by

  • tobacco smoking
  • alcohol ingestion
  • caffeine (diuretic)
  • drugs
  • non-insulin dependant DM because XS glucose in the blood acts as a plasma diuretic increasing water excretion
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11
Q

What is Sjogren’s syndrome

A

Chronic systemic autoimmune exocrinopthy involving salivary, lacrimal, sweat and GU glands

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12
Q

Why does Sjogren’s syndrome occur

A

Due to infiltration by lymphocytes and plasma cells causing xerostomia and xerophthalmia and is a result of either primary of secondary Sjogren’s syndrome

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13
Q

What is the difference between primary and secondary Sjogren’s syndrome

A

Primary Sjögren syndrome occurs in the absence of another underlying rheumatic disorder

Secondary Sjögren syndrome is associated with another underlying rheumatic disease (CT disease) e.g. systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), scleroderma, polymyositis and progressive SS

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14
Q

Outline the impact of Sjogren’s syndrome

A
  • Oral discomfort, fatigue, low mood, irritability, headache, impaired cognitions
  • Arthralgia, Raynauds, fatigue, vaginal dryness, pancreatic insufficiency

Decreases QoL and is non-curable; early diagnosis can minimise gross dental caries and corneal damage

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15
Q

Outline swellings occurring in patients with Sjogren’s syndrome

A
  1. Inflammatory duct obstruction with secondary infection causes intermittent moderately painful swelling
  2. Benign lymphoproliferation of mucosa associated with lymphoid tissue (MALT) lymphoma
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16
Q

Which classifications of drugs are most commonly implicated in xerostomia

A
  1. Antidepressants (SSRIs, tricyclics)
  2. Antipsychotics (lithium, phenothiazines, loratadine)
  3. Benzodiazepines (diazepam)
  4. Antihistamines
  5. Proton pump inhibitors (omeprazole, lansoprazole)
  6. Opioids (morphine, tramadol)
  7. Diuretics (amiloride, furosemide)
  8. Antihypertensive agents (methyldopa)
  9. Hypnotics (zopiclone)
  10. Bronchodilators (ipratropium)
  11. Recreational drugs (amphetamines, cannabis, ecstasy)
  12. Vit A analogues (isotretinoin)
  13. Antiparkinsons agents (L-dopa, selegiline)
  14. Decongestants (ephedrine)
  15. Agents for bladder overactivity (tamsulosin)
  16. Didanosine and protease inhibitors
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17
Q

What are the psychogenic causes of xerostomia

A

Anxiety and depression due to hyperventilation and so increased mouth breathing associated with anxiety

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18
Q

Interruption in which pathway causes drug induced xerostomia

A

Anticholinergic activity involving M3 muscarinic receptors

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19
Q

How does the tongue appear in a xerostomic patient

A

Smooth and depopulated ; commonly with infections e.g candidiasis

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20
Q

What is Behcet’s disease

A

Multisystem disease involving vasculitis with recurrent orogenital ulceration which affects young adult males (20-40) from East-Middle East and there is a strong genetic component with HLA B51

21
Q

Outline the major diagnostic criteria for Behcet’s disease

A
  1. Recurrent orogenital ulceration
  2. Typical ocular lesions; anterior uveitis, recurrent hypopion, iritis, chorioretinitis
  3. Skin lesions; erythema nodosum, thrombophlebitis
22
Q

Outline the minor diagnostic criteria for Behcet’s disease

A
  • Arthralgia/arthritis
  • Vascular lesions - thrombosis
  • Central nervous system involvement
  • Gastrointestinal lesions
23
Q

What is erythema nodosum

A

Purple/red tender papules typically presenting on the shins which tend to regress over a few weeks to leave bruises

24
Q

What is erythema nodosum associated with

A
  • Behcet’s disease
  • Crohn’s
  • Ulcerative colitis
  • Sarcoidosis
25
Q

How is Behcet’s disease managed

A

It is difficult to diagnose as there is no diagnostic test, but recurrent oral ulcerations are the first manifestation - this requires systemic medication and if left untreated it can cause visual loss (Japanese young males = commonest cause of visual loss)

26
Q

What is gingival hypertrophy

A

= Enlargement of the gingival tissues

Has a multifactorial aetiology including plaque accumulation, dose and duration of therapy of drugs

27
Q

What is gingival hypertrophy caused by

A

Proliferation of selected fibroblast population and inflammatory infiltrate of B lymphocytes

28
Q

How is gingival hypertrophy managed

A
  • Meticulous plaque control
  • Professional hygiene therapy (scale + polish)
  • Changing medication
29
Q

Which drugs can cause gingival hypertrophy

A
  1. Calcium channel antagonists
    - nifedipine
    - verapamil
    - felodipine, diltiazem, amlodipine
  2. Ciclosporin (immunosupressant for renal transplant)
  3. Anticonvulsants (used for trigeminal neuralgia)
    - phenytoin
    - sodium valporate
    - vigabatrin, phenobarbitone
  4. Oral contraceptive pill
30
Q

What is the potential differential for gingival hypertrophy

A

Acute myeloid leukaemia causing generalised hyperplasia and easy bruising

Other symptoms of AML can relate to infection, anaemia, bleeding, hepatosplenomegaly

31
Q

What is syphilis

A

Gram negative STD caused by spirochete Treponema palladium

32
Q

What is primary syphilis

A

Incubation period of 10-90 days before a painless papule (chancre) appears at site of inoculation (genitalia or oral mucosa) - this can be intrarectal, perianal or oral and can also cause regional lymphadenopathy

There is no pyrexia and the lesion may go un-noticed and resolve in 2-6 weeks without treatment

33
Q

Describe oral lesions of primary syphilis

A
  • Firm, painless nodules
  • Breaks down to form indurated ulcer
  • Resemble oral squamous cell carcinoma
  • Enlarged rubbery lymph nodes
  • Heals over 8-9 weeks without scarring
34
Q

What is secondary syphilis

A

Occurs 4-8 weeks after chancre appearance and in the secondary stage it causes

  • low grade fever, generalised lymphadenopathy
  • headache
  • malaise
  • mucocutaneous rash
35
Q

Describe the mucocutaneous rash occurring in secondary syphilis

A

Non-puritic (non-itchy) covering entire body in symmetric pattern, the skin is indurated with superficial scale on the lesions which can appear like psoriasis

36
Q

Describe the oral lesions of secondary syphilis

A

Variable and nonspecific but typically painful and more extensive than primary syphilis which will resolve in 2-12 weeks; untreated patients experience recurrences of secondary disease

  1. Mucosal patches = multiple slightly raised grey-white pseudomembranes with surrounding erythema, soft palate and pillars, tongue and vestibular mucosa
  2. Snail tract ulcers = flat ulcers with linear outline in posterior part of mouth
  3. Condylomata lata = Broad based, moist triable warty growths (skin folds, genital, anal or oral)
37
Q

Outline the risk factors for oral syphilis

A

> 60% new cases in MSM with strong HIV confection and high risk sexual behaviour; oral sex transmission of syphilis

38
Q

What is oral hairy leukoplakia

A

Corrugated hyperkeratotic lesions usually involving the lateral borders of the tongue in HIV positive and immunocompromised individuals - this is asymptomatic and benign

Generally associated with CD4 count <300/mm^3 and due to EBV infection in keratinocytes

39
Q

How is AIDS diagnosed

A

CD4 count <200cells/mL or occurrence of specific HIV associated conditions (PCP chest infection, oesophageal candidiasis, HIV wasting disease, HIV associated tumours - Kaposi’s sarcoma)

40
Q

What oral lesions are associated with HIV

A
  1. Candidiasis
    - pseudomembranous
    - erythematous
    - hyperplastic
  2. Oral hairy leukoplakia
  3. Kaposi’s sarcoma
  4. Lymphoma
  5. Periodontal disease
  6. Oral ulcers
  7. Diffuse infiltrative lymphocytosis syndrome (DILS)
41
Q

Outline candidosis presentation in HIV disease

A
  • common
  • reduced by HAART (highly active antiviral therapy)
  • may involve drug resistant strains/species
  • presentations = pseudomembranous, erythematous and angular chelitis
42
Q

Describe oral ulceration in HIV disease

A

Infective causes are common (HSV, HZV, CMV)

  • occasionally unusual bacterial/fungal infections e.g. tuberculosis
  • severe recurrent oral ulceration my present following seroconversion (may respond to thalidomide)
  • ulceration causes pain and difficulty eating
43
Q

What are the HPV related lesions

A
  1. Papillomas (on palate/gingivae) = cauliflower-like
  2. Condyloma acuminatum = orogenital contact and association with HIV
  3. Focal epithelial hyperplasia (Heck’s disease) HPV 13/32 in Eskimos/North American Indians
44
Q

What is Diffuse infiltrative lymphocytosis syndrome

A

DILS has an increasing prevalence with HAART and gives a Sjogren’s syndrome-like picture with salivary gland enlargement and xerostomia

It is characterised by CD8+ T-cells and absence of typical autoantibodies

45
Q

What oral tumours occur in HIV infection

A
  1. Kaposi’s sarcoma
  2. Non-Hodgkin’s lymphoma
  3. Oral squamous cell carcinoma
46
Q

What is oral kaposi’s sarcoma

A

Associated with human herpes virus 8 = HHV8 (t is the most common skin cancer in HIV occurring in the late stage) and typically affects palate and periodontal tissues causing red-blue/purple patches/nodules which can ulcerate - it can also affect nose

It is pathognomonic of AIDS-mouth

47
Q

What is the treatment for oral kaposi’s sarcoma

A
  • Alitretinoin gel
  • Liposomal daunorubicin/ oloxorubicin
  • Paclitaxel
  • IFN-a
  • Thalidomide
48
Q

How does Non-Hodgkin’s Lymphoma present in the mouth

A

High grade B-cell NHL is recognised as a manifestation if HIV infection commonly with EBV positive

In the mouth it presents as rapidly progressive lesions which mimic tuberculous ulcers and these can go deeper and affect the bone

BDS2; CHHD (32 decks)

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