Oral mucosa: manifestations of gastrointestinal & haematological disease Flashcards

1
Q

Oral manifestations of GIT disorders - primary effects (2)

A

Part of the disease process e.g. Crohn’s disease

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2
Q

Oral manifestations of GIT disorders - secondary effects (2)

A

Malabsorption, blood loss

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3
Q

Conditions of interest (4)

A
GORD
Coeliac disease 
Idiopathic inflammatory bowel disease
-Crohn's disease (and oro-facial granulomatosis -OFG)
-Ulcerative colitis
Intestinal polyposis syndromes
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4
Q

Risk factors for GORD (3)

A

obesity, smoking, alcohol

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5
Q

Symptoms of GORD (1)

A

Dyspepsia (heart-burn)

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6
Q

Risk from GORD (2)

A

Barrett’s oesophagus (pre-malignant)

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7
Q

Oral effects of GORD (2)

A

Erosion and halitosis

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8
Q

Treatment of GORD (2)

A

PPIs e.g. omeprazole

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9
Q

Features of coeliac disease (4)

A

Intolerance to α-gliadin peptides in gluten found in wheat, rye and barley
Any age
Genetically susceptible individual and families
Prevalence 0.5-1% in general population (probably under-diagnosed)

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10
Q

Pathogenesis of coeliac disease (5)

A
Exposure to gluten
Proliferation of lymphocytes
Oedema
Crypt hyperplasia and sub-total villous atrophy
Mostly in duodenum and jejunum
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11
Q

Coeliac disease - malabsorption (5)

A
Iron (anaemia)
Calcium and vitamin D
Folic acid    	}
Vitamin C	}   more advanced disease
Vitamin B12    }
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12
Q

Clinical features of coeliac disease (9)

A

Diarrhoea and Steatorrhoea
Wasting, (failure to thrive), loss of appetite
Abdominal discomfort / pain
Tiredness and weakness
Peripheral neuropathy and CNS disturbances
Tetany and osteomalacia
Dermatitis herpetiformis
Oral ulceration
Increased risk of intestinal neoplasms (lymphoma

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13
Q

Oral manifestations of coeliac diease (6)

A

Malabsorption gives anaemia resulting in:
Oral ulceration
Glossitis
Candidiasis
Angular cheilitis
Hypoplasia of enamel of permanent teeth-often generalised and symmetrical (secondary to malabsorption)

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14
Q

Diagnosis of coeliac disease (3)

A
History and clinical signs
Blood tests
-FBC and haematinics
-Anti-endomysial antibodies, tissue transglutaminase antibodies anti-gliadin antibodies, anti-reticulin
Endoscopy and jejunal mucosal biopsy.
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15
Q

Treatment for coeliac disease (2)

A

Exclusion diet to remove gluten from diet

Replacement of haematinics (iron and folate)

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16
Q

Increased risk from coeliac disease (1)

A

Increased risk of T-cell lymphoma and other bowel malignancies

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17
Q

Features of Crohn’s disease (5)

A

Young adults; Western world
Any part of GIT
-may affect several separate areas (skip lesions)
-mostly terminal ileum and ascending colon
-can also affect extra-gastrointestinal sites e.g. skin
Transmural inflammation
-granuloma formation - cobblestone appearance
-wall is thickened and lumen narrowed
-aphthous-like ulceration and fissuring
-fistulae and abscesses.
Chronic inflammation
Lymphoid hyperplasia

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18
Q

Clinical features of relapsing and remitting Crohn’s disease (5)

A
Abdominal pain
Diarrhoea
Weight loss
Malabsorption – B12, bile salts
Variable presentation, depends on severity and site(s) and often intermittent
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19
Q

Oral manifestations of Crohn’s disease (8)

A
Ulceration (may be RAS-like)
Glossitis
Lip swelling
Cobblestone mucosa
Tissue tags
Fissures and ulcers
Angular cheilitis
Mucosal inflammation esp attached gingiva
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20
Q

Management of Crohn’s disease (7)

A

Symptomatic relief
Topical measures first for oral manifestations
Immunosuppressives e.g.methotrexate and azathioprine
Replacement therapy
Anti-TNF antibodies, infliximab etc
Elemental diets
Surgery

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21
Q

Diagnosis of Crohn’s disease (4)

A

History
-may have known diagnosis – if not then….
Oral biopsy – include muscle
Blood tests:
-FBC and haematinics
-gut anti-bodies, ACE (to exclude sarcoid)
Onward referral

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22
Q

Features of oro-facial granulomatosis (4)

A

Oral features of Crohn’s disease with no clinical features of gut involvement
Separate entity or Crohn’s disease?
May have an allergic aetiology
Responds to exclusion diet (not all cases)

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23
Q

Other cause of lip swelling need excluding (5)

A
Crohn’s
Sarcoidosis
Foreign-body reactions
Melkerson-Rosenthal syndrome e.g. triad of lip swelling, fissured tongue and facial palsy
Infections (rare): TB, syphilis, leprosy
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24
Q

Management of oro-facial granulomatosis (4)

A
Surgery in severe cases
Topical and intralesional steroids(temporary relief)
Systemic drugs e.g. azathioprine
Exclusion diet:
-chocolate
-crisps
-carbonated drinks
-carvone
-cinnamon
-benzoates - E210-E219
25
Q

Ulcerative colitis features (3)

A

Large intestine + rectum –tends to be a continuous region of variable extent
Inflammation extends no further than lamina propria
-inflamed, bleeds easily – later ulceration develops. -chronic inflammatory infiltrate

26
Q

Ulcerative colitis results in (5)

A
Bloody diarrhoea
Pain
Weight loss
Tiredness
Iritis, ankylosing spondylitis etc etc
27
Q

Oral manifestations of ulcerative colitis (2)

A

Oral ulceration

Pyostomatitis vegetans

28
Q

Oral effects of drugs used to treat GIT disorders (6)

A

Steroids - candidal infection
Immunosuppressants e.g. Azathioprine, Methotrexate –> ulceration and infection
Antispasmodics - dry mouth
H2 receptor antagonists e.g. Ranitidine –> erythema multiforme, discolouration of tongue, dry mouth
PPIs e.g. Omeprazole –> taste disturbance, dry mouth, erythema multiforme, angio-oedema
Cytokine inhibitors e.g. Infliximab –> oral ulceration, taste disturbance

29
Q

Intestinal polyposis syndromes - Gardener’s syndrome - features and causes (3)

A

AD, APC gene mutation: multiple colon polyps, epidermoid cysts, osteomas, thyroid cancer, fibromas
Risk of colon cancer age 21 is 10%, by age 50 it’s 95%!
Oral manifestations: osteomas, odontomes supernumerary teeth. Osteomas develop first, often 10-30yrs…early referral!

30
Q

Types of intestinal polyposis syndromes (5)

A

Peutz Jeghers syndrome
AD
Hamartomatous polyps (only small risk of dveloping cancer)
BUT, have increased risk of cancer in ovaries, pancreas, liver
Pigmented macules lips and oral cavity (develop in childhood before anything else)

31
Q

Haematological conditions causing oral manifestations (6)

A
Anaemias
-iron deficiency anaemia
-macrocytic anaemia
Leukaemias
Multiple myeloma
Neutropenia / agranulocytosis
Stem cell transplants / GVHD
Angina Bullosa Haemorrhagica
32
Q

Anaemia is due to (3)

A

Decreased numbers of RBC
-loss / destruction (Injury, chronic diseases, infections, sickle cell anaemia, hemolytic anaemias e.g. spherocytosis, red cell auto-Abs)
-failure of production (low Fe, folate, B12, aplastic anemia, leukaemia, Thalassemia, renal failure gives decreased erythropoetin)
Reduction of concentration of haemoglobin e.g. blood loss or hypervolaemia
Reduced ability of RBCs to carry oxygen e.g. sickle cell anaemia and Thalassemias

33
Q

Definition of anaemia (2)

A

A decreased ability of blood to carry O2
Hb concentration below normal range
<13.5 g/dl - males
<11.5 g/dl - females

34
Q

Anaemia by morphology of RBC (3)

A

Normocytic anaemia e.g. blood loss
Macrocytic anaemia e.g. B12 or folate deficiency
Microcytic anaemia e.g. iron deficiency

35
Q

Iron deficiency anaemia features (3)

A

Most common type world-wide
30% world population
-inadequate intake – diet / malabsorption (e.g. Coeliac)
-increased loss (e.g.GI bleed)
-increased demand (e.g. pregnancy)
Hypochromic (less Hb) microcytic anaemia (small)

36
Q

Define macrocytosis (1)

A

Rise in mean cell volume above normal range 80-95fl in adults – lower in children

37
Q

Causes of macrocyic anaemias (7)

A
Dietary deficiency of B12 / folate
Alcohol	
Malabsorption			
Liver disease			
Hypothyroidism				
Increased demand e.g. pregnancy			
Drugs e.g. Azathioprin
38
Q

How is Vit B12 absorbed (1)

A

In ileum

39
Q

Vit 12 deficiency - causes (3)

A

Dietary insufficiency
GI disease
Pernicious anaemia

40
Q

Pernicious anaemia features (4)

A
Auto-immune gastritis
Parietal cells damaged
Intrinsic factor – secreted by parietal cells
B12 not absorbed in small intestine
-achlorhydria 
-absent intrinsic factor
41
Q

Folate deficiency

  • folate absorption (1)
  • causes (4)
A

Absorbed in upper small intestine (100 -200 µg daily)

Dietary insufficiency
Malabsorption (especially coeliac disease)
Excessive use
Drugs – e.g. Anticonvulsants, suphasalazine

42
Q

Systemic features of iron deficiency anaemia (7)

A
Lethargy
Dyspnoea 
Skin and nail changes
Mucosal changes
Oesophageal webbing
Tachycardia/papitations
Cardiac failure/exacerbation of cardiac diseases
43
Q

Systemic features of megaloblastic anaemia (8)

A
Pallor
Jaundice 
Neurological changes
Neural tube defects
Gonadal dysfunction
Mucosal changes
Cardio-vascular disease
Risks with GA
44
Q

Oral manifestations of megaloblastic?? anaemia (1)

A
None 
Pallor  - Hb < 8g/dl
Oral ulceration and exacerbation of RAS
Mucosal atrophy /stomatitis / glossitis 
Depapillated, smooth tongue
Altered taste
Oral candidosis
Worsening of existing mucosal pathology
Burning mouth syndrome?
Dysphagia (oesophageal web). Look up Plummer-Vinson syndrome
45
Q

Leukemia (3)

A

Malignant diseases of blood forming cells in bone marrow
One type of WBC produced in excess at detriment of others
-Acute
–>lymphoblastic – children (85%) and late middle age
–>myeloid - older adults and children (15%)
-Chronic
–>lymphocytic - adults
–>myeloid - adults

46
Q

Acute leukaemia - symptoms due to bone marrow failure or organ infiltration (7)

A

Signs and symptoms of anaemia
Bacterial infections : mouth, throat, chest, skin, peri-anal
Delayed healing
Bruising and bleeding (including gingival)
Bone pain
Lymphadenopathy
Hepatosplenomegaly

47
Q

Clinical features of chronic leukaemia (7)

A
Anaemia 
Bleeding 
Infection 
Splenomegaly
Weight loss
Fatigue 
Sweating
48
Q

Oral manifestations of chronic leukaemia (3)

A

Gingival inflammation and swelling (and bleeding)
Ulceration (cytotoxic drugs/infection)
Increased susceptibility to oral infections

49
Q

Stem cell transplant / CVHD (3)

A

Chemotherapy or chemo-radiotherapy

Transplant of own or donor stem cells

May lead to GVHD

  • lichen planus
  • Sjögren’s like syndrome
50
Q

Describe multiple myeloma (8)

A

Tumour of monoclonal plasma cells (B cell origin)
Produce and secrete monoclonal protein (Ig)
Bence-Jones protein in urine (Ig light chain)
Bone pain, osteoporosis, osteolytic lesions
Recurrent infection
Anaemia
Renal failure
Amyloidosis

51
Q

What is amyloidosis caused by (2)

A

Fibrillar protein Ig light chain

52
Q

Leucopenia (3)

A

Reduction in white cell population
Primary: reduction in haemopoesis
Secondary: auto-immune disease, infection, drug therapy (e.g. carbamazepine), HIV

53
Q

Cyclical neutropenia features (6)

A
Rare
Unknown aetiology
Most common in childhood
Neutropenia 
Average cycles of 21 days
Infections
54
Q

Oral manifestations of cyclical neutropenia (4)

A

Ulceration
-irregular, any surface, may heal with scarring within 2/52
Gingivitis
Periodontitis
Susceptibility to infection e.g. candidosis

55
Q

Management of cyclical neutropenia (2)

A

Supportive

Self-limiting

56
Q

Angina bullosa haemorrhagica features and management (5)

A

Idiopathic

Can occur in thrombocytopenia

Diagnosis - history and clinical signs

FBC and clotting screen

Reassure

57
Q

Significance of angina bullosa haemorrhagica for dental care (5)

A
May observe signs suggestive of haematological disease
Appropriate referral
Risk of infection
Risk of bleeding
Importance of good quality care
58
Q

Typical exam questions - learn

A

What are the oral effects of Crohn’s disease?
What other conditions can share similar features?
Describe how you would manage the oral effects of anaemia