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
What are the aetiologies of gingival hypertrophy
- Plaque accumulation, dose and duration of therapy
26
What proliferation does gingival hypertrophy often lead to
Proliferation of selected fibroblast populations - inflammatory infiltrate of predominantly B lymphocytes
27
What does management of gingival hypertrophy often involve
Meticulous plaque control with professional hygiene therapy and if possible changing medication to an alternative agent
28
What drugs lead to gingival hypertrophy
- Calcium channel antagonists - Ciclosporin - Anticonvulsants - Oral contraceptive pill
29
What is the most common acute leukaemia affecting adults
Acute myeloid leukaemia
30
What are the presentations and symptoms of acute myeloid leukaemia
- Infiltration as gingival hypertrophy - Hepatosplenomegaly - Symptoms related to infection, anaemia and bleeding
31
What pathogen causes syphilis
- Gram negative spirochete: treponema pallidum
32
What tends to be the first manifestation of a primary infection of syphilis
Painless papule appears at the site of inoculation, 10-20% of primary lesions are intrarectal, pernianal or oral
33
What are some symptoms of the primary infection of syphilis
- regional lymphadenopathy | - Fever usually absent
34
How long does it take a primary syphilis lesion to resolve without treatment
2-6 weeks
35
What are the features of primary oral lesions of syphilis
- 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
When abouts does secondary syphils develop
4-8 weeks after appearance of chancre
37
What are the symptoms/clinical features of secondary syphilis
- 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
What kinds of secondary syphilis oral lesions are there
- Mucosal patches - Snail tract ulcers - Condylomata lata
39
What is a general description of secondary syphilis oral lesions
Variable and non-specific by typically painful and more extensive than primary syphilis
40
Describe the mucosal patches you get from secondary syphilis oral lesions
- multiple - Slightly raised - Covered by greyish - White pseudomembranes with surrounding erythema
41
Describe the snail trail ulcers you get from secondary syphilis oral lesions
- Flat ulcers with a linear outline in posterior part of the mouth
42
Describe the condylomata lata you get from secondary syphilis oral lesions
- Broad based | - Most friable warty growths (skin folds, genital anal or oral)
43
How long do the lesions of secondary syphilis take to resolve
- 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
How does oral hairy leukoplakia present in the mouth
Corrugated hyperkeratotic lesion usually involving the lateral borders of the tongue
45
Who is at risk of oral hairy leukoplakia
HIV positive and immunocompromised individuals
46
Ay jaws can i abbe de note plz
Manifestation of EBV infection in keratinocytes in patients with oral hairy leukoplakia
47
Describe the clinical symptoms of oral hairy leukplakia and how it is resolve when associated with AIDS
- Painless - If associated with AIDS resolves with HAART - May mimic other oral mucosal diseases - Not premalignant
48
What CD4 count is diagnosis for AIDS
200 cells/microL
49
What oral lesions are associated with HIV
- Candidiasis: pseudomembranous, erythematous, hyperplastic - Oral hairy leukoplakia - Kaposi's sarcoma - Lyphoma - Periodontal disease - Oral ulcers - Diffuse infiltrative lymphocytosis syndrome
50
What are the typical presentations of candidosis in HIV disease
- Pseudomembranous | - Erythematous and angular chelitis
51
What reduces Candidosis in HIV disease
HAART
52
What can be some of the causes of oral ulceration in HIV disease
- Viral HSV - Viral HZV - CMV - Occasionally from unusual bacterial or fungal infections
53
What HPV-related lesions can a patient present with
- Papillomas - Condyloma acuminatum - Focal epithelial hyperplasia
54
Describe papillomas that present from HPV-related lesions
- Most common on palate/gingivae
55
What is Diffuse infiltrative lymphocytosis syndrome characterised by
- Similar to sjogren's syndrome - salivary gland enlargement and xerostemia - CD8+ T cells and absence of typical autoantibodies.
56
What does oral kapok's aroma tend to affect
the palate but also periodontal tissues
57
How does oral kaposi's sarcoma present
- Reddy-blue or purple patches or nodules that may ulcerate.
58
What are the treatment options for oral kapok's sarcoma
- Alitretinoin gel - Liposomal daunorubicin/oloxorubicin - Paclitaxel - IFN-alpha - Thalidomide
59
AY BAWS CAN I HABE DE NOTE PLZ
- Kaposi's sarcoma is the most common skin cancer in HIV | - Typically occurs in late stage disease
60
How does non-hodgkins lymphoma present in the mouth
Usually as rapidly progressive lesions that mimic tuberculous ulcers in appearance