Interactive Oral Manifestations of Systemic Disease Flashcards

1
Q

What are cherry red haemangiomas and where do they normally appear

A
  • Firm red, blue or purple papule
  • 0.1-1cm in diameter
  • May develop on any part of the body - most often appear on the scalp, face, lips and trunk
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2
Q

What are some differential diagnoses for cherry red haemangiomas

A
  • Angiokeratoma
  • Spider telangiectasis
  • Pyogenic granuloma
  • Nodular basal cell carcinoma
  • Amelanotic melanoma
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3
Q

What is hereditary haemorrhagic telangiectasia characterised by

A
  • By telangiectasia on the skin or mucosa
  • Multiple purpuric spots may get traumatised and bleed
  • Typically associated with nose bleeds
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4
Q

What can happen in the GIT is involved in hereditary haemorrhagic telangiectasia

A

May result in bleeding and frequently iron deficiency anaemia

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5
Q

What is hereditary haemorrhagic telangiectasia associated with

A

Lung, liver and cerebral AVMs

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6
Q

What is spider naevi caused by

A
  • Numerous vessels radiating from central arteriole

- fill from centre

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7
Q

What is spider naevi associated with

A

Liver disease, OCP and pregnancy

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8
Q

What is telangiectasia caused by

A

widened venules

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9
Q

How does telangiectasia often present

A

Results in threadlike red lines or patterns on the skin that often form gradually and in clusters

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10
Q

What is ecchymosis

A

bruising

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11
Q

What might spontaneous lesions (blood blisters) associated with ecchymosis represent

A

may represent underlying platelet or coagulation disorders or over anticoagulation with warfarin.

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12
Q

What are some of the risk factors that can lead to xerostemia

A
  • Polypharmacy and so age-related
  • tobacco smoking
  • alcohol ingestion
    drinking caffeine containing bevs
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13
Q

What causes sjogrens syndrome

A

infiltration of the salivary/lacrimal glands with lymphocytes and plasma cells - autoimmune lol

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14
Q

Whats the difference between primary and secondary sjogrens syndrome

A

Primary - happens in isolation

Secondary - associated with CT disease usually RA (SLE as well)

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15
Q

How common is sjogrens?

A

4% of adult population, second most common CT disease

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16
Q

What are the symptoms associated with sjogrens syndrome

A
  • oral discomfort
  • fatigue
  • low mood
  • impaired cognitive function
  • headache
  • variable non-spefici presentation like arthralgia, raynauds, vaginal dryness and pancreatic insufficiency
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17
Q

What swellings can result from sjogrens syndrome

A
  • Inflammatory duct obstruction with secondary infection with intermittent, moderately painful swelling
  • benign lymphoproliferation of mucosa associated lymphoid tissue (MALT)
  • MALT lymphoma
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18
Q

What kinds of drugs are most commonly implicated in xerostemia

A
  • Antidepressants
  • Antipsychotics
  • Benzodiazepines
  • Antihistamines
  • Proton pump inhibitors
  • Opioids
  • Diuretics
  • Antihypertensive agents
  • Hypnotics
  • Bronchodilators
  • Recreational drugs
  • Vitamin A analogues
  • Antiparkinsons agents
  • Decongestants
  • Agents for bladder overactivity
  • Didanosine and protease inhibitors
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19
Q

What is the most common pathway that causes drug related xerostemia

A
  • Anticholinergic activity involving M3 muscarinic receptors
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20
Q

What are the major clinical diagnostic features of behcet’s disease

A
- Recurrent genital ulceration
Typical ocular lesions:
- anterior uveitis
- recurrent hypopion
- iritis
- chorioretinitis
Skin lesions:
- erythema nodosum
- thrombophlebitis 
(pathergy test?)
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21
Q

What are the minor clinical diagnostic features of behcet’s disease

A
  • Arthralgia/arthritis
  • Vascular lesion - thrombosis
  • CNS involvement
  • Gastrointestinal lesions
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22
Q

What is erythema nodosum and where are they normally found

A
  • Painful, purplish nodules
  • Typically found over shins

regresses over a few weeks to leave bruises

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23
Q

What is erythema nodosum typically associated with

A

UC and crohns but also associated with sarcoidosis and some medications

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24
Q

What are the management options for Behcets disease

A
  • Diagnosis difficult
  • No diagnostic test - dependent on history
  • Recurrent orogential ulcerations often the first manifestation
  • multidiscipline management involving systemic medication
  • Most common cause of visual loss in Japanese young males
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25
Q

What are the aetiologies of gingival hypertrophy

A
  • Plaque accumulation, dose and duration of therapy
26
Q

What proliferation does gingival hypertrophy often lead to

A

Proliferation of selected fibroblast populations - inflammatory infiltrate of predominantly B lymphocytes

27
Q

What does management of gingival hypertrophy often involve

A

Meticulous plaque control with professional hygiene therapy and if possible changing medication to an alternative agent

28
Q

What drugs lead to gingival hypertrophy

A
  • Calcium channel antagonists
  • Ciclosporin
  • Anticonvulsants
  • Oral contraceptive pill
29
Q

What is the most common acute leukaemia affecting adults

A

Acute myeloid leukaemia

30
Q

What are the presentations and symptoms of acute myeloid leukaemia

A
  • Infiltration as gingival hypertrophy
  • Hepatosplenomegaly
  • Symptoms related to infection, anaemia and bleeding
31
Q

What pathogen causes syphilis

A
  • Gram negative spirochete: treponema pallidum
32
Q

What tends to be the first manifestation of a primary infection of syphilis

A

Painless papule appears at the site of inoculation, 10-20% of primary lesions are intrarectal, pernianal or oral

33
Q

What are some symptoms of the primary infection of syphilis

A
  • regional lymphadenopathy

- Fever usually absent

34
Q

How long does it take a primary syphilis lesion to resolve without treatment

A

2-6 weeks

35
Q

What are the features of primary oral lesions of syphilis

A
  • Firm, painless nodule
  • Breaks down to form indurated ulcer
  • May resemble OSCC
  • enlarged rubbery lymph nodes
  • heals over 8-9 weeks often without scarring
36
Q

When abouts does secondary syphils develop

A

4-8 weeks after appearance of chancre

37
Q

What are the symptoms/clinical features of secondary syphilis

A
  • Low grade fever
  • Generalised lymphadenopathy
  • Headache
  • Malaise
  • Mucocutaeneous rash
  • Rash usually non-pruritic and covers entire body in a symmetric pattern
  • Skin is indurated often with superficial scale of the lesions that may lead to a misdiagnosis of psoriasis
38
Q

What kinds of secondary syphilis oral lesions are there

A
  • Mucosal patches
  • Snail tract ulcers
  • Condylomata lata
39
Q

What is a general description of secondary syphilis oral lesions

A

Variable and non-specific by typically painful and more extensive than primary syphilis

40
Q

Describe the mucosal patches you get from secondary syphilis oral lesions

A
  • multiple
  • Slightly raised
  • Covered by greyish
  • White pseudomembranes with surrounding erythema
41
Q

Describe the snail trail ulcers you get from secondary syphilis oral lesions

A
  • Flat ulcers with a linear outline in posterior part of the mouth
42
Q

Describe the condylomata lata you get from secondary syphilis oral lesions

A
  • Broad based

- Most friable warty growths (skin folds, genital anal or oral)

43
Q

How long do the lesions of secondary syphilis take to resolve

A
  • Will resolve spontaneously within 3-12 weeks +/- therapy
  • 25% of untreated patients experience recurrences of secondary disease
  • Tertiary disease occurs in ~1/3 of untreated secondary syphilis
44
Q

How does oral hairy leukoplakia present in the mouth

A

Corrugated hyperkeratotic lesion usually involving the lateral borders of the tongue

45
Q

Who is at risk of oral hairy leukoplakia

A

HIV positive and immunocompromised individuals

46
Q

Ay jaws can i abbe de note plz

A

Manifestation of EBV infection in keratinocytes in patients with oral hairy leukoplakia

47
Q

Describe the clinical symptoms of oral hairy leukplakia and how it is resolve when associated with AIDS

A
  • Painless
  • If associated with AIDS resolves with HAART
  • May mimic other oral mucosal diseases
  • Not premalignant
48
Q

What CD4 count is diagnosis for AIDS

A

200 cells/microL

49
Q

What oral lesions are associated with HIV

A
  • Candidiasis: pseudomembranous, erythematous, hyperplastic
  • Oral hairy leukoplakia
  • Kaposi’s sarcoma
  • Lyphoma
  • Periodontal disease
  • Oral ulcers
  • Diffuse infiltrative lymphocytosis syndrome
50
Q

What are the typical presentations of candidosis in HIV disease

A
  • Pseudomembranous

- Erythematous and angular chelitis

51
Q

What reduces Candidosis in HIV disease

A

HAART

52
Q

What can be some of the causes of oral ulceration in HIV disease

A
  • Viral HSV
  • Viral HZV
  • CMV
  • Occasionally from unusual bacterial or fungal infections
53
Q

What HPV-related lesions can a patient present with

A
  • Papillomas
  • Condyloma acuminatum
  • Focal epithelial hyperplasia
54
Q

Describe papillomas that present from HPV-related lesions

A
  • Most common on palate/gingivae
55
Q

What is Diffuse infiltrative lymphocytosis syndrome characterised by

A
  • Similar to sjogren’s syndrome
  • salivary gland enlargement and xerostemia
  • CD8+ T cells and absence of typical autoantibodies.
56
Q

What does oral kapok’s aroma tend to affect

A

the palate but also periodontal tissues

57
Q

How does oral kaposi’s sarcoma present

A
  • Reddy-blue or purple patches or nodules that may ulcerate.
58
Q

What are the treatment options for oral kapok’s sarcoma

A
  • Alitretinoin gel
  • Liposomal daunorubicin/oloxorubicin
  • Paclitaxel
  • IFN-alpha
  • Thalidomide
59
Q

AY BAWS CAN I HABE DE NOTE PLZ

A
  • Kaposi’s sarcoma is the most common skin cancer in HIV

- Typically occurs in late stage disease

60
Q

How does non-hodgkins lymphoma present in the mouth

A

Usually as rapidly progressive lesions that mimic tuberculous ulcers in appearance