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GI 3 Flashcards

1
Q

What are some systemic causes of a solitary oral ulcer?

A
  • Trauma - physical/chemical
  • Malignancy - oral squamous cell carcinoma
  • Infective - tuberculosis/syphilis
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2
Q

What are some causes of multiple ulcers?

A
  • Recurrent aphthous ulceration (RAU)
  • Bechets
  • Anaemia
  • Herpes -> primary herpetiform gingivo-stomatitis
  • Mucotaneous disorders
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3
Q

What is recurrent aphthous ulceration (RAU)?

A
  • Unknown aetiology
  • Most common cause of multiple ulcers
  • Patient usually otherwise well; stress related
  • 3 types: major/minor/herpetiform
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4
Q

What is Bechets?

A

Hereditary systemic vasculitis -> multisystem condition; other systemic features (genital ulceration, uveitis, erythema nodosum)

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5
Q

What are the oral symptoms of anaemia?

A
  • Mucosal pallor
  • Angular chelitis
  • Oral ulceration
  • Predisposal to candida (thrush)
  • Glossitis
  • Disturbed
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6
Q

What are some mucocutaneous disorders?

A
  • Lichen Planus
  • Lupus erythematosus
  • Vesiculobullous disease - pemphigus and pemphigoid
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7
Q

What is lichen planus?

A

Systemic rash; bilateral, asymptomatic, potentially malignant

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8
Q

What is lupus erythematosus?

A

Discoid or systemic; oral ulceration; red and white patches similar to lichen planus

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9
Q

What is pemphigus vesiculobullous disease (VBD)?

A
  • Intraepithelial bullae
  • Oral lesions first manifestations (50-80%)
  • Oral lesions precede skin lesions by 1 year
  • Painful extensive oral ulceration preceded by blisters which rupture easily
  • Nikolsky sign
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10
Q

What is pemphigoid vesiculobullous disease (VBD)?

A
  • Sub-epithelial bullae
  • Blisters more likely to be observed
  • Painful oral ulceration
  • Affects mucous membranes of other organs e.g. eyes
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11
Q

What are some GI diseases which produce oral manifestations?

A
  • Malabsorption -> hematinic deficiency
  • Crohn’s
  • Ulcerative colitis
  • Peutz Jeghers
  • Gardeners syndrome
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12
Q

What are the oral manifestations of Crohns disease?

A
  • Present in 0.5-20% of cases
  • May precede abdominal symptoms; do not correlate with intestinal activity
  • Cobble-stoning of mucosa
  • Localised mucogingivitis
  • Linear ulceration
  • Tissue tags/polyps
  • Diffuse swelling – commonly of the lips
  • Pyostomatitis vegetans
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13
Q

What are the oral manifestations in ulcerative colitis?

A
  • Reflects severity of disease - exacerbation and remission
  • Oral ulceration
  • Pyostomatitis vegetans
  • Angular stomatitis
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14
Q

What are the causes of oral white patches?

A
  • Those that wipe off -> usually pseudomembranous candidiasis/thrush
  • Those that don’t -> trauma, neoplasia, epithelial dysplasia, chronic mucocutaneous candidiasis
  • Consider underlying haematinic deficiency or immunosuppression
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15
Q

What are some causes of oral pigmentation?

A
  • Racial pigmentation
  • Melatonic macules
  • Smoking
  • Malignancy
  • Addison’s disease
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16
Q

What are some causes of xerostomia (dry mouth)?

A

1) Drugs
2) Sjogren’s syndrome
3) Radiation therapy

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17
Q

What is Sjogrens syndrome?

A
  • Dry eyes and mouth, most common in females
  • Primary/secondary (2nd associated with autoimmune)
  • Enlarged salivary glands
  • Xerostomia -> increased caries, depapillated/fissured tongue, red dry wrinkled mucosa, ↑ predisposition to candida
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18
Q

What are the oral manifestations that occur with leukaemia?

A
  • Gingival enlargement/bogginess
  • Petechiae
  • Mucosal bleeding
  • Ulceration
  • Infiltration by malignant cells
  • Immunocompromise -> candida, herpes, opportunistic infection
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19
Q

What are the oral manifestation that occur with lymphoma?

A
  • Palpable lymph nodes
  • Extra/intraoral diffuse swellings
  • Ulceration
  • Tooth migration/mobility
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20
Q

What are some oral manifestations that occur with HIV?

A
  • Ulceration
  • Kaposi’s sarcoma
  • HPV lesions
  • Salivary gland swelling
  • Increased risk of malignancy
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21
Q

What are the 3 types of inflammatory disorders of the oesophagus?

A

1) Acute oesophagitis
2) Chronic/reflux oesophagitis
3) Allergic (eosinophilic) oesophagitis

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22
Q

What is allergic (eosinophilic) oesophagitis?

A
  • Oesophageal inflammation due to personal/family history of allergy
  • Common in asthma, children, males
  • pH probe negative for reflux, increased eosinophils in blood
  • Corrugated or spotty oesophagus
  • Treatment w steroids/montelukast/chromoglycate
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23
Q

What is oesophageal squamous papilloma?

A
  • Benign oesophageal tumour
  • Rare, asymptomatic
  • HPV related
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24
Q

What are some causes of oesophageal squamous cell carcinoma?

A
  • Vitamin A/zinc deficiency
  • Tannic acid, strong tea, smoking/alcohol
  • HPV
  • Oesophagitis
  • Genetic factors
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25
Q

How do oral squamous cell carcinomas present?

A
  • White/red/speckled ulcer or lump
  • High risk sites: floor of mouth, lateral border/ventral tongue, soft palate, retromolar pad/tonsillar pillars
  • Rare on hard palate, dorm of tongue
  • 5 year survival 40-50%
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26
Q

What are the inflammatory disorders of the stomach?

A
  • Acute gastritis
  • Chronic gastritis
  • Rare = lymphocytic, eosinophilic, granulomatous
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27
Q

What are some causes of acute gastritis?

A
  • Severe burns
  • Shock
  • Severe trauma
  • Head injury
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28
Q

What are the different causes for chronic gastritis?

A
  • Bacterial (H Pylori)
  • Autoimmune
  • Chemical
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29
Q

What is H pylori associated chronic gastritis?

A
  • Most common chronic gastritis
  • Bacteria inhabits a niche between epithelial cell surface and mucous barrier
  • Gram negative curvilinear rod excites early acute inflammatory response
  • If not cleared -> chronic active inflammation
  • Increased risk of gastric+duodenal ulcers and gastric lymphoma and carcinoma
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30
Q

What is chemical gastritis?

A
  • Due to NSAIDs, alcohol and bile reflux
  • Direct injury to mucus layer by fat solvents
  • Marked epithelial regeneration, hyperplasia, congestion and little inflammation
  • May produce erosions or ulcers
31
Q

What is the definition of peptic ulceration?

A

A breach in the gastrointestinal mucosa as a result of acid and pepsin attack

32
Q

What are the causes of gastric adenocarcinomas?

A

1) H pylori infection
2) Pernicious anaemia
3) Partial gastrectomy
4) Lynch syndrome
5) Menetrier’s disease

33
Q

What are the two types of small bowel ischaemia?

A

1) Mesenteric arterial occlusion

2) Non-occlusive perfusion insufficiency

34
Q

What are the two causes of mesenteric arterial occlusion leading to small bowel ischaemia?

A

1) Mesenteric artery atherosclerosis

2) Thromboembolism from the heart

35
Q

What are the four causes of non-occlusive perfusion insufficiency leading to small bowel ischaemia?

A

1) Shock
2) Strangulation obstructing venous return (e.g. hernia, adhesion)
3) Drugs e.g. cocaine
4) Hyper-viscosity

36
Q

What are the outcomes of small bowel ischaemia?

A

1) Mucosal infarct -> regeneration
2) Mural infarct -> fibrous stricture
3) Transmural infarct -> gangrene

37
Q

What are the complications of small bowel ischaemia?

A
  • Fibrosis, stricture; fibrous stricture
  • Chronic ischaemia
  • Mesenteric angina
  • Obstruction
  • Gangrene
  • Perforation
  • Peritonitis
  • Sepsis
  • Death
38
Q

What is Meckel’s Diverticulum?

A
  • Result of incomplete regression of vitello-intestinal duct
  • May cause bleeding, perforation or diverticulitis which mimics appendicitis
  • Commonly assymptomatic, incidental finding
39
Q

What tumours are found in the small bowel?

A
  • Mostly secondary; primary very rare
  • Lymphomas
  • Carcinoid tumours
  • Carcinomas
40
Q

What are carcinoid tumours of the small bowel?

A
  • Rare, commonest site is the appendix
  • Small, yellow, slow-growing, locally invasive
  • Can cause intussusception, obstruction
  • Produce hormone like substances
  • Metastases to liver -> carcinoid syndrome (flushing, diarrhoea)
41
Q

What do carcinomas look like in the small bowel?

A
  • Very rare, associated with Crohn’s and Coeliac
  • Identical to colorectal carcinoma in appearance
  • Presents late
  • Metastases to lymph nodes and liver occur
42
Q

What are the causes of acute appendicitis?

A
  • Mostly unknown
  • Faecoliths (dehydration)
  • Lymphoid hyperplasia
  • Parasites
  • Tumours (rare)
43
Q

What is the pathology behind acute appendicitis?

A
  • Acute inflammation (neutrophils); must involve muscle coat
  • Mucosal ulceration
  • Serosal congestion, exudate
  • Pus in lumen
44
Q

What are the complications of appendicitis?

A

1) Peritonitis
2) Rupture
3) Abscess
4) Fistula
5) Sepsis and liver abscess

45
Q

What is Coeliac’s disease?

A

An abnormal reaction to a constituent of wheat flour, gluten, which damages enterocytes and reduces absorptive capacity

46
Q

What are the metabolic effects of Coeliac’s disease?

A
  • Malabsorption of sugars, fats, amino acids, water and electrolytes
  • Malabsorption of fats -> steatorrhea
  • Reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow (CCK) leading to gall stones
47
Q

What are the complication of Coeliac’s disease?

A
  • Malabsorption -> weight loss, anaemia, vitamin deficiencies, abdominal bloating, failure to thrive
  • T cell lymphomas of the GI tract
  • Increased risk of small bowel carcinoma
  • Gall stone
  • Ulcerative-jejunoilleitis
48
Q

What is dyspepsia?

A

Collection of symptoms causing epigastric discomfort

49
Q

What are the GI ALARM Signs?

A
  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset/progressive symptoms
  • Malaena/haematemesis
  • Swallowing difficulty
50
Q

What is the diagnostic criteria for functional dyspepsia?

A

Presence of one of these symptoms for last 3 months:

  • Bothersome postprandial fullness
  • Early satiation
  • Epigastric pain
  • Epigastric burning
51
Q

What are the risk factors for oral premalignancy?

A
  • Tobacco and alcohol
  • Diet and nutrition (low vitamin A, C and iron)
  • HPV, candida, syphilis
  • Dental factors
52
Q

Where is an oral malignancy likely to be found?

A

Soft, non-keratinising sites (e.g. ventral/lateral tongue, floor of mouth)

53
Q

What are the warning signs for oral cancer?

A
  • Red/white or red+white lesion
  • Ulcer (exclude trauma, drug, systemic etc)
  • Numb feeling (e.g. lip or face)
  • Unexplained pain in mouth or neck
  • Change in voice
  • Dysphagia
  • Double vision
  • Drooping eyelid or facial palsy
  • Blocked or bleeding nose
  • Facial swelling
54
Q

What sites does Crohn’s disease commonly affect?

A
  • 2/3 of patients -> small bowel only
  • 1/6 of patients -> colonic/anal disease only
  • 1/6 of patients -> both
  • Variable involvement of stomach, oesophagus and mouth
55
Q

What are the differences between Crohn’s disease and ulcerative colitis?

A

1) C - anywhere in GI tract; UC - colon and rectum
2) C - skip lesions; UC - no skip lesions
3) C - thickened bowel and stricture; UC - thin walls
4) C - transmural inflammation; UC - superficial
5) C - granulomas present; UC - no granulomas
6) C - fistulae common; UC - fistulae rare
7) C - cancer risk moderate; UC - cancer risk high
8) C - extra GI rare; UC - extra GI common

56
Q

What’s the difference between acute mesenteric ischaemia of the small and large bowel?

A
  • Small bowel -> dies

- Colon -> survives due to marginal artery

57
Q

What are the clinical signs of mesenteric ischaemia?

A
  • Pain out of proportion to the clinical findings
  • Acidosis on gases
  • Lactate elevated
  • CRP may be normal
  • WCC slightly elevates
58
Q

How is mesenteric ischaemia fixed?

A
  • Must be quick
  • If non-viable resect, re-anastamose, staple and planned return
  • If viable, can rarely preform SMA embolectomy
  • Sometimes may have an open and close surgery
59
Q

What are the different malabsorptive states?

A
  • Protein
  • Fat
  • Carbohydrate
  • Vitamins and minerals
60
Q

What is malabsorption?

A

Defective muscosal absorption caused by:

1) Defective luminal digestion
2) Mucosal disease
3) Structural disorders

61
Q

What are some common causes of malabsorption?

A
  • Coeliac disease
  • Crohn’s disease
  • Biliary obstruction
  • Cirrhosis
  • Post infectious
  • Rare: short bowel, drugs, bacterial overgrowth, parasites and pancreatic cancer
62
Q

What specific disease states cause malabsorption?

A
  • Coeliac disease
  • Whipple’s disease
  • Crohn’s disease
  • Parasitic infections
  • Small bowel bacterial overgrowth
63
Q

What is tropical sprue?

A

Colonisation of the intestine by an infectious agent or alterations in the intestinal bacterial flora induced by the exposure to another environmental agent

64
Q

What are the baseline investigations for malabsorption?

A
  • FBC
  • Coagulations
  • LFTs
  • Albumin
  • Calcium/magnesium
  • Stool culture
65
Q

What is malnutrition?

A

A state of nutrition in which a deficiency, excess or imbalance of energy, protein and other nutrients causes measurable adverse effects on tissue, body form (body shape, size and composition), function and clinical outcome

66
Q

What are the disease related causes of malnutrition?

A
  • Decreased intake
  • Impaired digestion and/or absorption
  • Increased nutritional requirements
  • Increased nutrient losses
67
Q

What are the effects of chronic malnutrition?

A
  • GI dysfunction
  • Increase in infection rate
  • Impaired immune response
  • Reduced muscle strength (+resp muscles) + fatigue
  • Decrease in wound healing
  • Physical weakness
  • Water and electrolytes disturbances
  • Impaired thermoregulation
  • Menstrual abnormalities/amenorrhea
  • Increase in LOS pressure
68
Q

What GI diseases can cause weight loss?

A

1) Impaired GI motility
2) Intra-abdominal infection
3) Crohn’s disease
4) Coeliac’s disease
5) Acute liver disease
6) Cancer

69
Q

How is nutrition support provided?

A
  • Food fortification & dietary counselling
  • Oral nutrition support
  • Enteral tube feeding
  • Parenteral nutrition (IV)
70
Q

Who needs nutritional support?

A
  • BMI <18.5
  • Unintentional weight loss >10% within the last 3–6 months
  • BMI <20 and unintentional weight loss >5% within the last 3–6 months
  • Have eaten or are likely to eat little or nothing for more than 5 days or longer
  • Poor absorptive capacity and/or high nutrient losses and/or increased nutritional needs from causes such as catabolism
71
Q

What are some features of refeeding syndrome?

A
  • Metabolic: hypo-kalaemia/phosphataemia/magnesiaemia, altered glucose metabolism, fluid overload
  • Physiological: arrhythmia, ↓GCS, seizure, respiratory failure, cardiovascular collapse, death
72
Q

What is intestinal failure?

A

The reduction in function below the minimum necessary for the absorption of macronutrients and/or water and electrolytes such that intravenous supplementation is required to maintain health and/or growth.

73
Q

What are the different types of intestinal failure?

A

1) Type 1 (acute, 2 wks) - self-limiting intestinal failure (surgical ileus, critical illness or GI problems)
2) Type 2 (acute, 4 wks) - significant & prolonged PN support (post surgery awaiting reconstruction)
3) Type 3 (chronic) - SBS, Crohn’s, radiation, dysmotility, malabsorption, inoperable obstruction

74
Q

What are some complications of parenteral nutrition?

A
  • SVC thrombosis
  • Sepsis
  • Line fracture/leakage/migration
  • Metabolic bone disease
  • Nutrient toxicity/insufficiency
  • Liver/metabolic disturbance
  • Psycho-social
  • Inappropriate usage

Gastrointestinal (8 decks)

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