Dietary + GI Disease Influence on Oral Mucosa Flashcards

1
Q

What is the integrity of the oral mucosa dependant on?

A

On the interplay between nutritional, metabolic + hormonal factors

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2
Q

What is the epithelial turnover rate of
a) skin?
b) buccal mucosa?

A

Skin = 50-70 days
BM= ~25 days

Therefore, systemic disease presents orally before cutaneously

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3
Q

What are the 3 most common haematinic deficiencies that have oral manifestations?

A

B12
B9 (folic acid)
Iron

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4
Q

What are the oral manifestations of haematinic deficiency? (8)

A

1) Generalised oral epithelial atrophy
2) Depapilation of Dorsum of the tongue
3) Abnormal oral epithelial cell structure + keratinisation
4) Sensitivity of filiform papillae
5) Oral soreness
6) Reduced taste sensation
7) Ulceration
8) Candidosis

(Symptom often precede changes in FBC)

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5
Q

State Oropharyngeal conditions assoc w haematinic deficiencies? (6)

A
  1. Glossitis
  2. Angular Cheilitis
  3. Candidiosis
  4. Recurrent oral ulceration (ROU)
  5. Burning mouth syndrome
  6. Paterson-Kelly syndrome
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6
Q

What is Glossitis?

A

= inflamed tongue

  • smooth depapillated tongue = indicative of IRON DEF
  • Raw, beefy-red tongue = indicative of Vitamin B12 + B9 (folic acid) def
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7
Q

What is the impact of haematinic deficiency on recurrent oral ulceration (ROU)?

A
  • haematinic deficiency reported ~20% of ROU pts
  • More common in middle-late age pts
  • Typically normal Hb but IRON deficiency (altered MCV or MCH)

Management of iron def (supplementation) –> ROU resolution

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8
Q

What does MCV tell you?

A

Mean corpuscular volume (MCV): The average size of your red blood cells.

Therefore:
decreased MCV = microcytic anaemia
increased MCV= macrocytic anaemia

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9
Q

What does MCH tell you?

A

Mean corpuscular hemoglobin (MCH): The average amount of hemoglobin in your red blood cells.

Therefore:
Low MCH = hypochromic anemia, (where RBCs are paler than normal)
High MCH = hyperchromic anemia (dark R
BCs)

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10
Q

What nutritional deficiency is associated w/ Paterson-Kelly Syndrome? (state all key facts about PKS)

A

Assoc w/ IRON DEF ANAEMIA (+ malnutrition)

Who? Females
Symptoms? Glossitis, spoon shaped brittle nails (koilonychia)

If severe, post-cricoid web dysphagia (due to the overgrowth of keratin &
epithelium)

Increased incidence of both pharyngeal & oral carcinoma!

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11
Q

What are the implications of malnutrition on immunity against viral + non-viral infections?

A

–> immunity = IMPAIRED

Vit A/Zinc deficiencies → diminished cell mediated immunity / early break down in oral mucosal integrity

Vit C deficiency → increased blood + saliva levels of free corticosteroids, impaired phagocytosis / altered immune response

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12
Q

What are the oral implications of malnutrition resultant of alcoholism? (4)

A

(Alcoholics often= malnourished), resulting in:

  1. Sialosis (nonspecific salivary gland swelling)
  2. Upper arch dental erosion secondary to acid reflux
  3. Oral SSC risk
  4. Yellow floor of mouth (indicative of liver cirrhosis)
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13
Q

What is Bulimia Nervosa?

A

= repeated bouts of overeating with an excessive preoccupation with control of body weight

Formal diagnosis if >/= twice weekly for 3 months-

Who?
young women (3rd decade)
1/3 pts have had anorexia

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14
Q

What are the IO/EO implications of malnutrition resultant of Bulimia Nervosa?

A

IO:
Sialosis (due to overuse of salivary glands)
Dental erosion
Ulcers of soft palate
Angular cheilitis

EO:
Calluses on dorsum of hand
(after repeated use to cause vomiting - Russell’s sign)

Hypokalaemia
(low K+ due to repeated vomiting)

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15
Q

What role is Vitamin C involved in?

A

Collagen synthesis

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16
Q

What is the clinical presentation of Vit.C deficiency?

A

Initially:
enlargement + keratosis of hair follicles
→ cork screw hairs

Within weeks:
proliferation of blood vessels around hair follicles + interdental papillae
→ gingival hyperplasia w haemorrhage

Later:
Oral: Tooth mobility + exfoliation
Cutaneous: bleeding + purpura (small, flat spots on your skin)

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17
Q

What is Zinc responsible for + sources of it?

A

Function:
Gene expression
Hormonal function
Immunity

Sources:
Meats, fish, dairy

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18
Q

Who does zinc def most commonly affect?

A

the elderly

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19
Q

What are GENERAL clinical features of zinc deficiency? (7)

A

Alopecia
Diarrhoea/ poor appetite
Lethargy/depression
Poor wound healing
Recurrent infections
Pustular bullous dermatitis
Growth retardation

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20
Q

What are ORAL clinical features of zinc deficiency? (6)

A

Reduced taste (hypogeusia)

Angular cheilitis + candidal superinfection

Superficial aphthous-like ulcers

Delayed wound healing

Perioral psoriasis/ mild eczematous eruption

Benign migratory glossitis ( aka erythema
migrans- geographic tongue)

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21
Q

What conditions are associated with causing MODERATE ZINC DEF? (4)

A

Crohn’s disease (malabsorption)
Sickle cell disease
Chronic renal disease
IV feeding

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22
Q

What conditions are associated with causing SEVERE ZINC DEF? (2)

A
  1. Acrodermatitis Enteropathica
    ( is due to an inherited zinc transporter defect, resulting in reduced intestinal absorption of zinc)

OR
2. post penicillamine tx

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23
Q

What is the clinical name for Geographic Tongue?

A

Benign Migratory Glossitis (BMG)

or Erythema Migrans (EM)

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24
Q

What 10 conditions is Benign Migratory Glossitis assoc w/?

A
  1. Allergy
  2. Diabetes
  3. GI disorders
  4. Low Zinc
  5. Pregnancy
  6. Down syndrome
  7. Psoriasis
  8. Seborrheic dermatitis (dry flaky scalp)
  9. Lithium toxicity
  10. Spasmodic bronchitis of childhood
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25
Q

What clinical questions would you ask pt if you suspect BMG?

A

Have you noticed any movements or changes in size of the tongue?

26
Q

What is the IO appearance of the tongue in BMG?

A

loss of superficial keratin & filiform papillae

Resulting in:
irregular shaped patches of erythematous depapillation surrounded by raised white/yellow borders

(when more subtle can just be tongue fissuring)

27
Q

What is the management of BMG?(7)

A
  1. Reassure the pt that it is a benign condition
  2. Difflam (0.15% benzylamine oral rinse)
  3. Investigation to exclude other causes (check haematinics, may need to give zinc supplements)
  4. Avoid foods which cause discomfort (eg spicy foods)
  5. Advice spacer device & rinse after inhaler use
  6. Swab to check if there is superficial candida too
  7. Encourage pt to take pictures of their tongue when it’s symptomatic
28
Q

What is Pemphagus Vulgaris? (PV)

A

= autoimmune blistering condition that can spread to the skin, where IgG autoantibodies attack desmosome leading to INTRAepithelial blisters.

(can be life threatening)

29
Q

Can dietary factors exacerbate Pemphigus Vulgaris?

A

Yes:

thiols - Garlic onion leek chives

isothiocyanates - Mustard horseradish radish turnip cabbage cauliflower
brussels sprouts broccoli

phenols - Mango cashew pistachio black pepper

tannins - teas, Cassava red wine tea red chillies cherries berries

After withdrawal of food, early symptoms of PV stopped

30
Q

What is Acute Necrotizing Ulcerative Gingivitis (ANUG)?

A

= Non-contagious anaerobic infection associated w specific microbes

(Borrelia vincentii, Prevotella
intermedia, Selenomonas & fusiform bacteria)

31
Q

Who does ANUG affect?

A
  • Malnourished
  • Severely immunocompromised

Age: Young adults

32
Q

What are the predisposing factors for ANUG?

A

Malnutrition
Smoking (due to vasoconstriction, reduced blood supply)
Viral respiratory infections
Poor OH
Stress
Immunodeficiency (eg HIV / leukaemias)
Lower socio-economic classes

33
Q

What is the name of the condition called when ANUG spreads to the oral mucosa + skin?

A

Cancrum Oris

34
Q

What are IO clinical features of ANUG?

A
  • Painful sloughing + ulceration of interdental papillae
  • Tendency to gingival bleeding
  • Halitosis (odour of rotting hay)
  • Sialorrhoea (excessive salivation)
  • Occasial spread to periodontal tissues = necrotising ulcerative periodontitis (NUP) w/ rapid periodontal destruction
35
Q

What is the tx for ANUG?

A
  • Metronidazole/ amoxicillin before debridement
  • Periodontal assessment
  • Oral debridement (RSD) + OHI
  • Hydrogen peroxide m/w
  • VBA + malnutrition advice
36
Q

What is Necrotising Stomatitis (NOMA)?

A

= the spread of ANUG to other tissues, characterised by putrid oral malodour/ rapid necrotising destruction involving the soft +hard orofacial tissues

Can be FATAL

37
Q

What is the aetiology + predisposing factors of NOMA?

A

ANUG + other bacterial infections

Predisposing factors:
- poverty
- haematinic def
- malaria
-viral infections
- poor OH

38
Q

Who does NOMA affect most?

A

Most prevalent in Sub-saharan Africa

39
Q

What are two types of NOMA?

A

Acute - oedema, cheek perforation → secondary infection w rapid death

Chronic - fibrous scar, oral strictures, trismus, dental malposition, salivary incontinence

40
Q

What is tx for NOMA?

A

Improve nutrition (+ vit supplements)-
Antibiotics
Oral debridement & OHI
Hydrogen peroxide m/w

41
Q

What is Coeliac disease (gluten sensitive enteropathy)?

A

Genetically determined chronic inflammatory small intestinal disease induced by gluten

42
Q

What is the typical presentation of Coeliac Disease?

A

malabsorption w chronic diarrhoea, weight loss, abdominal distension, fatigue + anaemia in childhood

43
Q

What are the systemic manifestations of Coeliac Disease? / what conditions does it increase risk of?

A

○metabolic bone disease
○iron/folate deficiencies
○infertility
○autoimmune diseases (hypothyroidism, lichen planus)
○GI malignancies (oesophageal + oropharngeal SCC, NHL, small bowel
adenocarcinoma)

44
Q

What are the IO manifestations of Coeliac disease?

A
  • ROU or ulcers affecting the lips
    -Dental hypoplasia
  • Glossitis / burning mouth
  • Angular Cheillitis
    -Exacerbation of Lichen Planus

(oral symptoms may vary depending on how well controlled/ diagnosed CD is)
(iron/folate def/malabsorption so think of IO features of these)

45
Q

How does dental hypoplasia present in Coeliac Disease?

A
  • most have dental defects

-enamel defects obvious:
symmetrical + chronological
mostly mild (rough enamel surface w/ horizontal grooves or shallow pits)

46
Q

Associated diseases of Coeliac Disease?

A

Sjogren’s
Diabetes
DERMATITIS HERPETIFORMIS (middle aged men, pruritic vesiculopapular rash)
Linear IgA disease
Selective IgA def

47
Q

What is Crohn’s disease?

A

= Chronic aggressive inflammatory bowel disease

Discontinuous pattern of transmural inflammation affecting whole GIT
w large ulcerations & occasional granulomata

48
Q

Predisposing factors of Crohn’s disease?

A

Genetic susceptibility

Environmental factors (nutrition & microflora)

Host immune response

49
Q

The most oral feature of Crohn’s disease?

A

Oral ulcerated lesions (reflective of active gut disease)

These ORAL lesions can present in isolation from GI lesions (no haematinic def or GI radiological changes), the pt then has symptomatic Crohn’s years later

50
Q

What are the general IO of Crohn’s disease?

A
  • LIP SWELLING (soft, diffuse, non-tender)
  • Angular Cheilitis
  • Gingival swelling + MUCOSAL TAGS
  • COBBLESTONE of oral mucosa - ulcerated fissures
  • Persistent IRREGULAR ORAL ULCER
  • Generalised ROU or ‘nonspecific stomatitis’
  • PYOSTOMATITIS VEGETANS
  • Dental pulp involvement (rare)
51
Q

Specific oral lesions of Crohn’s disease?

A

Indurated tag-like lesions
Cobblestoning
Mucogingivitis
Lip swelling with vertical fissures
Deep linear ulceration

52
Q

Non-specific oral lesions of Crohn’s disease?

A
  • ROU
  • Pyostomatitis vegetans
  • Angular cheilitis
  • Glossitis
  • Persistent submandibular lymphadenopathy
53
Q

What is Orofacial Granulomatosis?

A

= predominantly labial swelling associated w/ granulomatous inflammation

(often develops to become Crohn’s over time)

54
Q

What are the clinical features of Orofacial granulomatosis?

A

Non-tender, recurrent lip/lower face swelling that eventually become persistent

+/- submandibular +/- cervical lymphadenopathy

Angular cheilitis, mucosal ulceration, vertical labial fissures, mucosal
tags & lingua plicata

55
Q

What is the impact of Orofacial Granulomatosis?

A

Not life threatening but causes ORAL DISCOMFORT, causing:
- reduced food intake (malabsorption + reduced growth)
- facial swelling (psych implications)
-lip swelling

56
Q

Tx of Crohn’s disease/ OFG?

A

Elimination diets (exclusion of benzoates & cinnamon)

Corticosteroids – topical & intralesional

Topical tacrolimus ointment

Thalidomide (also prescribed in graft-versus-host disease)-

Adalimumab (immune suppressant - cancer risk factor)

57
Q

What is Melkerson-Rosenthal syndrome?

A

= subset of orofacial granulomatosis

-Lower motor neuron palsy
- Fissured tongue
- Plicated mucosal swelling

58
Q

What is Peutz-Jeghers syndrome?

A

= rare autosomal dominant condition
Mutation of gene that plays a role in apoptosis

59
Q

What is the presentation of Peutz-Jeghers syndrome? (IO/EO)

A

Multiple small perioral & vermilion freckles (fades w age)

Intraoral: Pigmented spots
+ (On extremities, nasal & rectal mucosa)

60
Q

What are the risks of Peutz-Jeghers?

A
  • Melantotic spots do not require tx + do not transform into melanoma but are markers for: Hamartomatous intestinal
    polyps (abdominal pain + rectal bleeding)
  • Risk of development of internal malignancy (gut, breast + genital)
  • Counselling + monitoring