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Sem 2 Year 2 > GI tract disorders > Flashcards

GI tract disorders Flashcards

1
Q

How does the oesophagus normally function (and what is the diagram that represents this)?

A

The upper oesophageal sphincter relaxes
Food enters and a peristaltic wave is triggered in the striated muscle
Lower oesophageal sphincter relaxes as swallow is initiated and food enters stomach
Seen below:

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2
Q

What are common oesophageal disorders?

A

Gastro-oesophageal reflux disease
Oesophageal motility disorders
Eosinophilic oesophagitis
Oesophageal cancer

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3
Q

What are different manifestations of GORD (gastro-oesophageal reflux disease)?

A

Oesophagitis
Barett’s oesophagus
Benign oesophageal stricture

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4
Q

What are symptoms of oesophageal disease?

A

COMMON
Dysphagia and odynophagia (difficulty and pain swallowing)
Heartburn
Acid regurgitation
Waterbrash
LESS COMMON
Chest pain
Food regurgitation
Food bolus obstruction
Cough
Altered voice- dysphonia
Globus (sensation of food being stuck but swallowing not affected)

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5
Q

Why can cough and altered voice in oesophageal disease?

A

Cough= when acid gets into respiratory system
Altered voice= irritated vocal chords

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6
Q

What are the different types of dysphagia?

A
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7
Q

What are the two main types of GORD (gastro-oesophageal reflux disease) and how are they different?

A

Transient lower relaxations= Usually acid is immediately cleared so no inflammation
Lower sphincter pressure decrease= inflammation due to chronic acid

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8
Q

What are the typical symptoms of GORD (gastro-oesophageal reflux disease)?

A

HEARTBURN= burning discomfort behind the breast bone spreading upwards
ACID REGURGITATION= often meal related or postural
WATERBRASH= hypersalivation secondary to gastro-oesophageal reflux

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9
Q

What are different investiagtions that can be done in oesophageal disease?

A

Endoscopy and biopsy
Barium swallow= x-ray after barium is swallowed.
Oesophageal function tests (Manometry, pH and Impedence monitoring)
CT, CT-PET scans or endoscopic ultrasound for tumours

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10
Q

What is a manometry test?

A

The manometry test senses the pressure and constriction of muscles in the esophagus as you swallow. It can detect patterns of muscle activity throughout the length of the esophagus, including contractions that are too weak or too powerful

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11
Q

What is impedence monitoring?

A

Esophageal 24-hour pH/impedance reflux monitoring measures the amount of reflux (both acidic and non-acidic) in your esophagus during a 24-hour period, and assesses whether your symptoms are correlated with the reflux.

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12
Q

What is oesopahgitis?

A

Inflammation of the oesophagus
Secondary to acid reflux
Can cause stricture

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13
Q

What is oesophageal stricture?

A

An esophageal stricture refers to the abnormal narrowing of the esophageal lumen; it often presents as dysphagia

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14
Q

What is Barrett’s oesophagus?

A

The squamous (oesophagus) is replaced by columnar (stomach) epithelium
Way for oesophagus to defend against large amounts of acid in chronic acid reflux
Often asymptomatic and commenest in obese men >50
If untreated can lead to adenocarcinomas

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15
Q

What is the treatment for Barrett’s oesophagus?

A

Barrets can be ablated (removed) so it does not become malignant. PPI are given long term (omeprazole ect)

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16
Q

What is the general treatment of gastro-intestinal reflux disease?

A

Lifestyle= smoking, alcohol, diet, weight
Mechanical= posture, elevate head in bed
Antacids
Acid supression= PPIs e.g. omeprazol, H2RA e.g. randitidine
Surgical- fundoplication (stomach wrapped around lower oesophagus)

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17
Q

What is an example of a oesophageal motility disorder?

A

Achalasia

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18
Q

What is achalasia and what does it present with?

A

Failure of the LOS relaxation together with absence of peristalsis
Degenerative lesion of oesophageal innervation
Typically presents in younger people with dysphagia to liquids and solids, weight loss, chest pain

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19
Q

What is the treatment for achalasia?

A

BoTox (paralyses LOS)
Endoscopic Dilatation
Surgical myotomy (surgeon cuts LOS)
POEM (Peroral endoscopic myotomy- cut without incision through skin)

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20
Q

What does achalasia look like on a barium swallow scan?

A

Dilated oesophagus, tight sphincter, ‘rat tail’

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21
Q

What is eosinophilic oesophagitis?

A

Eosinophilic esophagitis
is a chronic, immune/antigen-mediated esophageal inflammatory disease associated with esophageal dysfunction resulting from severe inflammation

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22
Q

What does eosinophilic oesoiphagitis present with?

A

Common presentation with Food bolus obstruction, dysphagia
Younger age, M>F, prevalence 50/100,000
History of atopy (asthma, hay fever)

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23
Q

What does an endoscopy of eosinophilic oesophagitis look like?

A

Endoscopy - furrows (lumps), rings, exudates, strictures

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24
Q

How is eosinophilic oesophagitis diagnosed?

A

Biopsy required for diagnosis

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25
Q

What is the treatment for eosinophilic oesophagitis?

A

Diet changes (eliminate egg, wheat, milk, nuts, soya, fish)
Drugs – PPI, topical sterois ( budesonide fluticazone known as jorvesa)
Dilatation – for strictures

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26
Q

What can cause oesophageal stricture?

A

GORD
Barett’s
Extrinsic compression (lung tumour)
Corrosive (ingestion)
Oesophageal cancer
Post-radiotherapy

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27
Q

What is the treatment for oesophageal stricture?

A

Proton pump inhibitors if it is caused by inflammation
Treatment of cancer
Push and balloon dilators

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28
Q

What are the different types of oesophageal cancer?

A

Adenocarcinoma- lower 1/3
Squamous cell carcinoma- mid and upper oesophagus

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29
Q

What is the staging of oesophageal cancer?

A

Use TNM classification ( T=tumour N=Nodes M= metastases)

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30
Q

What is the treatment of oesophageal cancer?

A

Sugery
Chemotherapy
Radiotherapy
Targed therapy/ immunotherapy
Palliation- symptom management

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31
Q

What is pharyngeal pouch?

A

PP= pouch just before the cricopharynheous, patients eats, the pouch fills and the patient experiances dysphasia then the pouch is emptied and food from previous days brought up

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32
Q

What is the first thoughts of younger and older patients presenting woith dysphagia?

A

In the elderly think of neurological causes particularly if intermittent / long standing or sinister causes (oesophageal Ca) if new, progressive with regurgitation and weight loss.
Oesophageal Ca presents with progressive dysphagia for solids first then liquids.
In the younger think of dysmotility (achalasia, or 2ndary to acid reflux,).
In dysmotility syndromes dysphagia for liquids is as bad as for solids.
Young patients with food bolus obstruction: think of eosinophilic oesophagitis.

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33
Q

What does tarry black stool indicate?

A

Chronic blood loss in the GI tract

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34
Q

What drugs can cause bad stomach ulcers?

A

Aspirin or NSAIDs

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35
Q

What is Helicobacter Pylori?

A

Bacterium that resides in stomach
Interferes with acid secretion and alters the lining of stomach. End result is ulceration
Helicobacter utilises UREA and interacts with it. Splits it into bicarb and ammonia, bicarb neutralises acid- how is survives

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36
Q

What is the diagnosis of H. pylori?

A

Breath test
Antibody test- only IgG so cannot tell if currently have infection
Stool antigen test
Culture
Histology
CLO test

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37
Q

What is a CLO test?

A

CLO test= petri dish containing ammonia where a biopsy is placed. If H. pylori is present it will split the urea and petri dish will become alkaline and can be tested with pH paper

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38
Q

What is the breath test in diagnosis of H. pylori?

A

Radiolabeled urea can also be drank (C13), splits urea and this will be exhaled as radiolabeled CO2 and if there is any radioactivity this will be proportional to Hp in stomach

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39
Q

What is maldigestion and malabsorption?

A

Maldigestion= Impaired breakdown of nutrients in the lumenal phase
Malabsorption= defective mucosal uptake and transport of adequately digested nutrients

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40
Q

What is the term for diseases that cause both maldigestion and malabsoption?

A

Malassimilation

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41
Q

Where are the 3 areas that malabsorption can occur?

A

Luminal phase of absorption
Mucosal phase of absorption
‘Post mucosal’ phase of absorption

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42
Q

What can cause enzyme problems that leads to malabsoption?

A

Enzyme deficiency: pancreatic insufficiency
Enzyme inactivation: ZE syndrome
Inadequacy of mixing: rapid transit, surgical resection (remove part of GI)

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43
Q

What bile salt problems can cause malabsorption?

A

Decreased bile salts: cholestasis, cirrhosis
Bile salt deconjugation: bacterial overgrowth
Bile salt loss: ileal disease or resection

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44
Q

What problems can occur in the luminal stage of digestion that causes malabsorption?

A

Enzyme problems
Bile salt problems
Bacterial overgrowth- competes for food
B12 deficiency

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45
Q

What problems can occur in the mucosal stage of digestion that causes malabsorption?

A

Brush border hydrolysis: lactase deficiency (post gastroenteritis, alcohol, radiation)

Epithelial transport:
Reduced absorptive surface - resection
Damaged absorptive surface – coeliac disease, tropical sprue, Crohn’s disease, ischaemia
Infections – Giardia, SIBO
Infiltration – lymphoma, amyloid

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46
Q

What problems can occur in the post- mucosal stage of digestion that causes malabsorption?

A

Lymphatic obstruction (lymphangectasia, neoplastic, TB) that prevents transport of fat through lympthatics

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47
Q

What are the clinical features of malabsoption in general?

A

Diarrhoea and weight loss despite adequate intake
Bloating, distension, cramps and borborygmi (excess noise)
Lethary or malaise
Symptoms often mild and non specific

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48
Q

What are the symptoms of malabsorption syndrome?

A

Steatorrhoea (pale, oily stools that float), distention, weight loss, oedema
RARE presentation

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49
Q

What is intestinal ‘angina’?

A

After a meal get abdominal pain

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50
Q

What clues on examination will you get of someone who is malabsorbed?

A

Evidence of malnutrition
Cracking of skin around mouth (angular cheilitis) inflammation of tongue (glossitis), oedma, rash, psychosis, dementia, ataxia and neuropathy

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51
Q

What neurological symptoms will you see in someone who is B12 deficient?

A

Peripheral neuropathy
Ataxia- balance, coordination, speech
Psychosis, dementia

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52
Q

What is the rash called often seen in coeliac disease?

A

Dermatitis herpetiformis

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53
Q

What can happen to red blood cells in malabsorption?

A

Microcytosis- iron deficiency (coeliac)
Macrocytosis- B12 and folate deficiency but also in coeliac and alcohol

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54
Q

What are the 3 main causes of malabsorption?

A

Coeliac disease
Pancreatic insufficiency
Small bowel bacterial overgrowth (SIBO)

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55
Q

What main test is used to diagnose coeliac disease?

A

Tissue transglutaminase (TTG) antibody test
Or a small intestinal biopsy if antibody levels not high enough

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56
Q

What main test is used to diagnose pancreatic insufficiency?

A

Faecal elastase - Enzyme measure in stool

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57
Q

What main test is used to diagnose SIBO?

A

Quantitative culture of jejunal fluid is the gold standard (> 105/mL is abnormal)
Glucose/Hydrogen breath test more practical
Small bowel radiology to look for anatomical abnormalities

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58
Q

What are the 3 main features of coeliac disease?

A
  • Mucosal inflammation
  • Villous atrophy
  • Crypt hyperplasia
    Which occur upon exposure to dietary gluten and which demonstrate improvement after withdrawal of gluten from the diet.
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59
Q

What causes coeliac disease?

A

Gentic predisposition- need specific HLA
Exposure to gluten as well as triggering event (immunological challenge e.g. illness, pregnancy)
This results in gliaden reactive T lymphocytes and an autoimmune attack on the intestine

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60
Q

What changes in a microscopic view of villi in coeliac disease?

A

Villi lost, crypts are longer and epithelium lining full of inflammatory cells

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61
Q

What are the symptoms of coeliac disease?

A

Diarrhoea
Anaemia
Dyspepsia (indigestion)
Abdominal pain and bloating
Weight loss
Mouth ulcers
Fatigue
Children- short stature, delayed puberty
Osteomalacia

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62
Q

What clues on investigation would link to coeliac disease?

A

Anaemia
Iron and folate deficiency
Low calcium and elevated alkaline phosphatase (metastatic bone disease)

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63
Q

What diseases does coeliac disease cause?

A

Osteoporosis
Infertility
Dermatitis herpetiformins (rash)
Lymphoma
Ulcerative jejunitis

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64
Q

What is the treatment for coeliac disease?

A

Gluten free diet (life long)
Nutritional supplements
Screen for complications (e.g. bone disease
Very rarely is immunosupressant medication

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65
Q

What is pancreatic exocrine insufficiency and what are the symptoms of it?

A

Any disease of exocrine pancreas in theory can lead to this- lack of production of bicarbonate and enzyme-rich fluid
Symptoms do not occur until disease has progressed (90%) of function lost
Steatorrhoea, weight loss, vitamin deficiency (A,D,E,K)

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66
Q

What are the main causes of pancreatic exocrine insufficiency?

A

Chronic pancreatitis (alcohol)
Pancreatic cancer
Cystic fibrosis
Haemochromatosis
Pancreatic or gastric resection

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67
Q

What is haemochromatosis?

A

Abnormal Fe deposits in liver/pancreas

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68
Q

What can cause chronic pancreatitis?

A

Alcohol
Duct obstruction – tumours, stones
Cystic fibrosis, other genetic causes
Systemic disease eg lupus
Autoimmune pancreatitis
All can lead to pancreatic exocrine insuffiency

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69
Q

How is pancreatic endocrine insufficiency diagnosed?

A

Symptoms
Pancreatic imaging (CT, MRI)
Tests- faecal elastase, secretin stimulation tests

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70
Q

What is the treatment for PEI?

A

Pancreatic enzyme replacement- taken with meals and snacks
Gastric acid suppression and vitamin supplements

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71
Q

What is small intestinal bacterial overgrowth?

A

Bacteria from colon moves up and grows the in the small intestine. Competes with you for food and ferments food higher in the GI tract
Loss of balance between gram - and +

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72
Q

What are the causes of bacterial overgrowth?

A

STASIS
- strictures- Crohn’s disease or TB
- hypomolitity- old age, opiates, diabetes
BLIND LOOPS
- surgery

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73
Q

What are blind loops?

A

Seen in patients with surgical change of GI
The part of loop where food not passing through= stagnant overgrowth

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74
Q

What are the consequences of small bowel bacterial overgrowth?

A

Vit B12 malabsorption (bacteria competes for it)
Bile acid deconjugation
Intraluminal protein utilisation
Brush border damage
Ulceration of mucosa
Bowel dysmotility

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75
Q

What is the glucose/ H2 breath test?

A

Human cells do not produce hydrogen therefore any H2 in breath is coming from bacteria. Drink glucose drink and if there is abnormal numbers of bacteria in small intestine H2 will rise

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76
Q

What is the treatment of SIBO?

A

Treatment with 2 weeks of antibiotics e.g. tetracycline, ciprofloxacin, rifaximin

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77
Q

What can impair bile acid reabsorption?

A

Ileal disease or resection
Post-cholecystectomy
Rapid transit
Coeliac, SIBO, chronic pancreatitis

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78
Q

What is giardia lamblia?

A

Non-invasive pathogen
Causes malabsorption- brush border damage and bile acid utilisation

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79
Q

What is Whipple’s disease?

A

Uncommon bacterial infection
Presents with diarrhoea, arthritis, fever, cough, headache, muscle weakness
Antibiotic therapy for months to years.

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80
Q

What is the screening test done for colorectal cancer?

A

The Quantitative Faecal ImmunochemicalTest(qFIT) is atestto detect hidden or ‘occult’ blood in stool samples. qFIT testuses antibodies and can quantify the level of blood in stools

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81
Q

What is a polyp?

A

A polyp is a projecting growth of tissue from a surface in the body, usually a mucous membrane. Polyps can develop in the: colon and rectum.
Polypoid lesion on a stalk, projecting into the lumen of the colon

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82
Q

What medications pre-dispose a polyp to bleeding?

A

Blood thining medication e.g. aspirin

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83
Q

What are the different features of this polyp?

A

A= dysplastic (abnormal) glands forming tubular and villous structures- adenoma
B= Abnormal gland that is invading the wall of the colon and the glandular appearance a lot more disorganised- started becoming malignant- adenocarcinoma

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84
Q

What histological features of a polyp would indicate an adenocarcimona?

A

High nucleus: cytoplasm ratio (for proliferatiuon)
Hyperchromasia= increased staining, production of nuclear material
Pleomorphism= differences in size and shape between cells

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85
Q

What are the red and blue parts of this polyp?

A

Adenoma circled in blue; adenocarcinoma circled in red

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86
Q

What are the different types of colonic polyp and do they have malignant potential?

A

Adenomas have the highest progression potential to adenocarcinoma
Hyperplastic ( metaplastic) polyps don’t have malignant potential. These are small lumps that are essentially projections of normal lining
A special type of hyperplastic polyp called serrated polyp has some malignant potential. These are flat and difficult to remove

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87
Q

What is the adenoma-carcinoma sequence?

A

Theadenoma-carcinoma sequencerefers to a stepwise pattern of mutational activation of oncogenes (e.g.K-ras) and inactivation oftumour suppressor genes(e.g.p53) that results in cancer.
Anoncogeneis a gene that has the potential to cause cancer. In tumour cells, these are often mutated or expressed at high levels.
A tumour suppressor gene is a gene that is involved in dampening the cell cycle or promotion of apoptosis or both. Examples include inactivation ofp53.
Deletion of the APC gene (suppressor) predisposes to cancer.

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88
Q

What is the timeframe for normal epithelium to progress into cancer?

A

Takes many decades for early adenomas to occur
Once these are present it can take 4-10 years to develop into a cancer

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89
Q

What are alarm features that suggest colorectal cancer?

A

Rectal bleeding
Anaemia or thrombocytosis (high platelet count)
Persistant diarrhoea with frequent noctural symptoms
Weigh loss
New onset on symptoma > 50 years
Family history of bowel cancer or past medical history of IBD

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90
Q

What is the difference between grading and staging of cancer?

A

GRADE The grade of a cancer is based on how the patterns of cancer cells look under a microscope: normal (or differentiated) or abnormal. Higher grade tumors tend to grow and spread faster than lower grade tumors. SHOWS POTENTIAL FOR GROWTH

STAGE The stage of colorectal cancer is a standard way for doctors to sum up how far the cancer has spread. SHOWS EXTEND OF GROWTH

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91
Q

What is the TNM staging system for cancer?

A

T refers to how far the primary tumor has grown into the wall of the nearby organs.
N refers to cancer spread to nearby lymph nodes.
M indicates whether the cancer has metastasized (spread to distant organs).

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92
Q

What constitutes a T1-4 stage for cancer?

A

1= mucosa, 2= muscle, 3= serosa and 4= nearby organs

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93
Q

What are risk factors for colorectal cancer?

A

A diet high in redmeatsand processedmeats and low in fibre
Cookingmeatsat very high temperatures (frying, broiling, or grilling)
Obesity, physical inactivity, smoking, alcohol excess
Older age
Family history of colorectal cancer/ polyps
History of IBD

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94
Q

Where are the most common sites of colorectal cancer?

A

50% occurin rectum and sigmoid colon
Caecum and ascending colon also important

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95
Q

Who is screened for colorectal cancer?

A

Population > 50 years every 2 years via a stool sample taken at home
If at risk- colonoscopy every 5 years from the age of 45

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96
Q

What is a functional gastrointestinal disorder?

A

Functional gastrointestinal disorders (FGID) are a group of disorders characterised by chronic gastrointestinal (GI) symptoms (eg abdominal pain, dysphagia, dyspepsia, diarrhoea, constipation and bloating) in the absence of demonstrable pathology on conventional testing.
Associated with the motility of the gut. There is significant brain-gut interaction that leads to the symptoms

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97
Q

What is the basic structure of the enteric nervous system?

A

Myenteric plexus= controls longitudional muscle
Submucosal plexus= controls circular muscle
These need to be coordinated together
Controlled via the parasympathetic and sympathetic nervous system

98
Q

What neurotransmitters are involved in the enteric nervous system?

A

Sympathetic= adrenergic
Parasympathetic= cholinergic
Enteric= 5HT (serotonin)

99
Q

What investigations should be done in someone presenting with diahorrea?

A

TTG test for coeliac
Stool tests for bacteria
Faecal calprotectin (inflammation)
Abdominal ultrasound
Colonoscopy
Small bowel MRI scan
Blood tests in general, e.g. thyroid function and full blood count

100
Q

What is the Rome IV criteria for diagnosing irritable bowel syndrome?

A

Abdominal pain
AND 2 of:
- related to defaecation
- change in stool frequency
- change in stool form

101
Q

What is some of the suggested pathophysiology in IBS?

A

Misbalance of neurotransmitters e.g. serotonin
Immune activation
Microbiota
CNS pain processing (visceral hypersensitivity)
HPA stress response
Genetics
Abnormal motor functioning

102
Q

What is visceral hypersensitivity?

A

When the brain misinterprets normal signals from gut as pain

103
Q

What are the rates of psychological disease in IBS patients, IBS non-patients and normal patients?

A

IBS non patients- had symptoms but never went to the doctor

104
Q

What are the different IBS subtypes?

A

C= constipated, D= diahorrea, M= mixed and U= unsubtyped

105
Q

What are the symptoms of IBS?

A

Onset of symptoms following gastroenteritis
Post-prandial urgency
Alternating diarhoea and constipation
Passing mucus
Sensation of incomplete evacuation
Abdominal bloating and distention

106
Q

What symptoms mean it is unlikely to be IBS?

A

Nocturnal diahorrea
Rectal bleeding

107
Q

What is the management advice of IBS?

A

Dietary advice- individualised, lactose or wheat restriction? Or low FODMAP (low short chain carbs)
Psychological therapy- CBT, relaxation or hypotherapy
Drug therapy based on predominant symptoms

108
Q

What drugs might be recommended to those with IBS?

A

FOR PAIN/BLOATING= antispasmodic, peppermint oil, tricyclics
FOR DIARRHOEA= loperamide, ondanestron
FOR CONSTIPATION= ispaghula, macrogol

109
Q

What is dyspepsia?

A

Indigestion

110
Q

What are the 4 categories of functional gastrointestinal disorders?

A

Functional dyspepsia= recurring symptoms of an upset stomach that have no obvious cause.
Belching disorders
Chronic nausea and vomiting disorders
Rumination syndrome= patient repeatedly and unintentionally spits up undigested or partially digested food from the stomach,

111
Q

What is the rome IV criteria for functional dyspepsia?

A

Need at least 3 months of one or more of the following
(a) bothersome postpradial fullness
(b) bothersome early satiety
(c) bothersome epigastric pain
(d) bothersome epigastric burning
AND no evidence of structural disease

112
Q

What are the different types of functional dyspepsia?

A

Post-prandial distress syndrome= falla and satiety but no pain. Gastric dysmotility or abnormal accomadation (keeping food longer in stomach)
Epigastric pain syndrome= pain and burning, visceral hypersensitivity

113
Q

What is the pathophysiology of functional dyspepsia?

A

Gastroduodenal motor and sensory dysfunction as well as immune activation, inflammation, visceral hypersensitivty, delayed gastric emptying and increased reflux
May be triggered by the environment- infection, or genetics or psychosical factors

114
Q

What is the treatment of functional dyspepsia?

A

Address the specific symptoms accordingly
- Proton pump inhibitors for reflux
- Tricyclics for hypersensitvity
- Cyclizine for delayed gastric emptying
- Acid reflux control= help control acid reflux

115
Q

What drugs are a potential cause of stomach ulceration and GI ulceration?

A

NSAIDs, antibiotics and steroids

116
Q

What are some causes of mucosal injury?

A
  • GI tract secretions- acid, pepsin, biliary and pancreatic secretions
  • Ischaemia
  • Drugs
  • Immunological causes such as coeliac disease
  • Infections
  • Ideopathic such as ulcerative colitis and Crohn’s disease
117
Q

What are some manifestations of mucosal injury?

A
  • Inflammation
  • Apoptosis or necrosis
  • Erosion/ulceration
  • Hypoplasia (reduced cell turnover) and hyperplasia
  • Metaplasia (change from one fully differentiated cell to another another)
  • Dysplasia (abnormal cell types)
118
Q

What does apoptosis of mucosal cells suggest?

A

Suggests HIV, graft vs host disease (bone marrow graft attacks host) and reaction to some drugs e.g. mycophenolate

119
Q

What is the sydney system?

A

Sydney system is an attempt to reach a standardised nomenclature. Splits gastritis into three broad groups= acute, chronic and special forms of chronic
Uses a combination of endoscopic features, histology and aetiology to classify gastritis

120
Q

What are causes of acute gastritis?

A
  • Acute erosive or haemorrhagic gastritis
  • Acute H. pylori infection
121
Q

What are the causes of chronic gastritis?

A
  • Non atrophic and atrophic H. pylori infections
  • Autoimmune gastritis
122
Q

What is autoimmune gastritis?

A

Autoimmune gastritis is a chronic inflammatory disease with destruction of parietal cells of the corpus and fundus of the stomach. The known consequence is vitamin B12 deficiency and, consequently, pernicious anemia

123
Q

What are the special forms of chronic gastritis?

A
  • chemical, e.g. bile reflux, NSAIDs
  • radiation gastritis
  • Eosinophillic gastritis (food allergies)
  • Lymphocytic gastritis
  • Non-infectious granulomatous gastritis
  • Other infections that are non H. pylori
124
Q

What does acute gastritis look like in histology?

A
125
Q

What does chronic H. pylori gastritis look like?

A

Pattern of acute and chronic gastritis often seen in H. pylori infection

126
Q

Can diagnosis of H pylori be made from a biopsy?

A

Yes

127
Q

What causes chemical gastritis and what does it look like in histology?

A

Bile reflux or NSAIDs
Often shows very little actual inflammation

128
Q

What has occured in this biopsy, and what might it lead to?

A

Circular cell= goblet cells. Metaplasia has occurred. Can develop to neoplasia

129
Q

What does having coeliac disease increase the risk of?

A

30 x increased risk of small bowel adenocarcinoma
20 x increased risk of enteropathy associated T-cell lymphoma (EATL)

130
Q

What are the histiological features of coeliac disease?

A
  • Variable villous atrophy
  • Chronic inflammation
  • Increased CD8+ T lymphocytes in epithelium
  • Epithelial damage
  • Crypt hyperplasia
131
Q

What does healthy villi look like in a histological image?

A
132
Q

What is pseudomembranous colitis?

A

Pseudomembranous colitis refers to swelling or inflammation of the large intestine (colon) due to an overgrowth of Clostridioides difficile (C difficile) bacteria

133
Q

What are the two main types of inflammatory bowel disease?

A

Ulcerative colitis
Crohn’s disease

134
Q

What are the ideas on the aetiology of IBD?

A
  • infection
  • loss of tolerance to commensal bacteria
  • genetics
  • environmental factors e.g. food antigens
135
Q

What is ulcerative colitis and where does it affect?

A

Chronic relapsing and remitting condition typically presenting with recurrent episodes of rectal bleeding

Typically involves rectum +/- left colon

Inflammation confined to mucosa unless severe

136
Q

What age are the highest incidences of ulcerative colitis?

A

Highest incidence 15-25 years, with smaller peak at 60-70 years. No gender difference

137
Q

What is the difference between polyps and pseudopolyps?

A

Polyp projects out from surface
Pseudopolyp= not actually projecting but in an ulcer and everything around it has been destroyed

138
Q

What are the common patterns of colonic inflammation in ulcerative colitis?

A
139
Q

What does the histological image of ulcerative colitis?

A
140
Q

What is Crohn’s disease and what does it affect?

A

Chronic, multifocal, relapsing condition that can affect any part of the GI tract
Variety of presentations depending on part of GI tract involved e.g. abdominal pain, diarrhoea, weight loss, strictures and obstruction, fistulae
Transmural inflammation that is often patchy and discontinuous (“skip lesions”)

141
Q

What is the peak incidence of Crohn’s disease?

A

Peak incidence 20-30 years with smaller peak 60-70 years. No gender difference

142
Q

Where are the most common cases of Crohn’s disease located?

A
143
Q

In what inflammatory condition can you develop granulomas?

A

Crohns disease- present in up to 70% of cases
Fewer after 2 years of disease
Commoner in children

144
Q

Are the following present in ulcerative colitis and crohns disease?

A
145
Q

What is the increased risk of neoplasia in IBD?

A

Most commonly colorectal carcinomas but also increased risk of small bowel carcinomas and other malignancies
Risk increases with severity, extend and duration of disease

146
Q

Are fistulae common in IBD?

A

Ulcerative colitis= no
Crohns disease= yes

147
Q

Are (pseudo)polyps common in IBD?

A

Ulcerative colitis= yes
Crohns= fewer in number but larger

148
Q

What are causes of colonic strictures?

A
  • Crohn’s disease
  • Ischaemic colitis
  • NSAIDs
  • neoplasia
  • divertciular disease
149
Q

What is Diverticular disease?

A

Diverticular disease is caused by small bulges in the large intestine (diverticula) developing and becoming inflam

150
Q

What is microscopic colitis?

A

Microscopic colitis is an inflammation of the large intestine (colon) that causes persistent watery diarrhea. The disorder gets its name from the fact that it’s necessary to examine colon tissue under a microscope to identify it, since the tissue may appear normal with a colonoscopy or flexible sigmoidoscopy
Cause often not identified
Treated with steroids

151
Q

What is important to know in IBD about treatment when looking at a biopsy?

A

It is important to know whether or not the patient is receiving medical therapy (e.g. steroids) as this can alter the pattern and distribution of inflammation.

152
Q

What happens if diagnosis between ulcerative colitis and Crohn’s disease cannot be differentiated?

A

In some cases the distinction between UC and CD may be very difficult. In this scenario, a label of “IBD-U” (IBD unclassified) is sometimes used.

153
Q

What is the information in this table for ulcerative colitis and Crohn’s disease?

A
154
Q

What innervates the oesophagus?

A

The oesophageal plexus which is formed by nerve fibers from two sources, branches of the vagus nerve, and visceral branches of the sympathetic trunk

155
Q

Where are the different oesophageal constrictions?

A
  1. Level of cricoid cartilage in the junction with the pharynx
  2. When it is crossed by the aortic arch
  3. When the left main bronchus crosses it
  4. The diaphragmatic sphincter
156
Q

What are the different layers of the oesophageal wall seen on the histology?

A

Mucosa- split into epithelium, lamina propia, and muscularis mucosae
Submucosa
Muscularis externa- split into circular muscle, connective tissue and longitutional muscle
Adventitia

157
Q

Whaqt is the TNM system?

A

Stages cancer
T= tumour
N= lymph nodes
M= metastases

158
Q

In oesophageal cancer, what do T1-4 mean when staging it?

A

T1- invaded mucosa and submucosa
T2- invaded muscularis propia
T3- invaved adventitia
T4- nearby organs

159
Q

What are the 5 layers seen on a oesophagus endoscope ultrasound?

A

1) Mucosal interface
2) Mucosa
3) Submucosa
4)Muscularis propria
5) Adventitia

160
Q

Where are common locations for metastases of oesphageal cancer?

A

Nodes between bifurcation of the trachea, also near aortic arch and the pulmonary artery area and up or down the oesophagus

161
Q

What is wrong with this barium swallow?

A

The area without any barium= a tumour is present

162
Q

Why can a patient with oesophageal cancer develop a hoarse voice?

A

L recurrent laryngeal nerve is related to movement of vocal chords. If that nerve gets infiltrated the patient will develop hoarse voice. Tumour invaded the nerve

163
Q

What 5 main vessels jpoin to make the portal vein?

A

Superior mesenteric (from small and R large bowel)
Inferior mesenteric (from L large bowel)
Splenic vein
Also important to remember:
L gastric vein from lesser curve of stomach
Coronary vein- from oesophageal plexus

164
Q

What occurs in portal hypertension after cirrhosis?

A
  • First thing that happens is reversal of flow and blood goes into the oesophageal plexus and oesophageal varices occur
  • Collateral circulation forms- then blood drains into azygous and hemiazygous systems and into the superior vena cava, bypassing the liver. Important anastomoses
  • If pressure is very high, reversal of blood in splenic vein which causes gastric varies- also connect to aygous and hemiazygous systems
165
Q

What happens to the blood when the portal vein gets obstructed (portal vein thrombosis)

A

Same as in hypertension, oesophgeal and gastric varices

166
Q

What is the treatment of oesophgeal and gastric varices?

A

Oesophageal= placing bands over varices with an endoscope and stopping the blood flow.
Gastric= = inject a thrombotic agent e.g. thrombin into the varice and thrombosis occurs

167
Q

What are the different regions of the stomach?

A

-Cardiac
-Fundus
-Body/corpus
-Pyloric; antrum, canal and sphincter

168
Q

Where in the stomach do gastric varices occur?

A

The fundus

169
Q

What are the different layers of the stomach?

A
170
Q

What is different between the layers of stomach and oesophagus?

A

Outer layer of stomach= serosa whilst the oesophagus= adventitia

171
Q

What are the important branches off the celiac trunk?

A
  • Common hepatic -> gives off hepatic proper (to L,R and middle), gastroduodenal, supraduodenal and right gastric
  • Left gastric
  • Splenic
172
Q

What is the arterial supply to the foregut, midgut and hindgut?

A

Celiac trunk= fore
superior mesenteric= mid
Inferior= hind

173
Q

What is anaemia?

A

Where serum haemoglobin levels are 2 standard deviations below the normal

174
Q

What is iron deficiency?

A

When the total body iron is low as a result of absorption not matching demand

175
Q

What are the causes of iron deficiency anaemia?

A
  • poor dietary intake
  • reduced absorption e.g. coeliac or post surgical
  • increased iron/blood loss e.g. menstruation or cancer
  • increased demand e.g. pregnant or adolescence
176
Q

What are the signs and symptoms of iron deficiency anaemia?

A

Often asymptomatic
Common symptoms- tiredness, dyspnoea and headaches
Common signs- pallor, atrophic glossitis (papillae projections on tongue are worn away- smooth tongue)

177
Q

What foods are a good source of iron?

A

Meat espeically liver
Spinach, leafy greens, chickpeas, lentils
Cereals and bread are fortified with iron in the UK

178
Q

What are the two different types of iron from the diet?

A

Ferous (Fe2+) found in red meat and seafood- readily uptaken by body.
Little amount of ferric iron absorbed but most needs to be converted to ferrous iron in order to be absorbed. Exists in plants

179
Q

What are iron absorption enhancers?

A

Vit C
Fructose
Sorbitol
Alcohol

180
Q

What is haemochromatosis?

A

Genetic haemochromatosis (GH) is a genetic disorder causing the body to absorb an excessive amount of iron from the diet.
Absorb 2-4 x the usual amount- iron builds up

181
Q

What is iron stored and transported within the body as?

A

Iron is stored in the body as ferritin (in the liver, spleen, muscle tissue, and bone marrow) and is delivered throughout the body by transferrin

182
Q

What is anemia of chronic disease?

A

Occurs when there is ongoing inflammatory stimulus in chronic disease
This inflammation activates monocytes and T cells which in turn:
- inhibits erythropoiten release
- inhibits erythroid proliferation
- increases synthesis of hepacytin (inhibits release of iron)
- auguments hemophagocytosis

183
Q

How can you tell the difference between iron deficiency anaemia and anaemia of chronic disease?

A

serum iron unhelpful
- Look at ferratin and also transferrin to tell the difference
- if the body is low in iron it will make more transferratin
- IAD= high transferratin, low ferratin
- ACD= low transferratin, high ferratin

184
Q

What is iron deficiency anaemia defined as?

A

​Iron deficiency anaemia is defined as a low haemoglobin in the presence of either
Low ferritin (best diagnostic marker)
Low serum iron in the presence of transferrin >3.0

185
Q

If a menstruating women has iron deficient anaemia, what investigations neeed to be done? (no family history or symptoms)

A

Coeliac testing only

186
Q

What is the gold standard investigation for a non-menstruating patient presenting with iron deficiency anaemia?

A

Endoscopy and colonscopy

187
Q

What is a standard endoscopy?

A

Camera down throat, gag reflex is numbed- to duodenum and stomach
Two ways- topic spray lidocaine so patient is awake, or topical lidocaine and sedation- midazolam or fentanyl in addition. Patient is conscious but it is hazy

188
Q

What is transnasal endoscopy and what are the positives and negatives of it?

A

Can go through nose instead- ultra thin wire
POSITIVES- better tolerated, only need local anaethesia
NEGATIVES- unable to perform most therapeutic procedures with it

189
Q

What are the positives and negatives of colonoscopies?

A

POSITIVES= Able to take biopsies and perform polypectomy (remove a polyp)
NEGATIVES= invasive, uncomfortable, need to take prep, can still miss lesions and posibility of complications such as bleeding

190
Q

What cancers are most commonly missed in colonoscopies?

A

Right colon and caecum

191
Q

What is CT colonoscopy?

A

CT colonography, also known as virtual colonoscopy, uses low dose radiation CT scanning to obtain an interior view of the colon
During the exam, the doctor inserts a small tube a short distance into the rectum. The doctor uses gas or air to inflate the colon and the rectum and takes pictures.

192
Q

What is capsule endoscopy?

A

Done on few patients- capsule looks at small bowel
Camera on a pill and takes photos of the small bowel- still have to take prep. One use only, gets flushed down toilet

193
Q

What investigation should be done in patients with iron deficient anaemia and in what order?

A

Investigate and image upper GI and colon
Check blood for urine
No further investigations needed- lack of dietary intake assumed
Only investigate small bowel if recurrent IDA

194
Q

What are the side effects of oral iron supplementation?

A

Main side effects are constipation, GI upset and dark stools

195
Q

How long should iron supplements be given for in iron deficient anaemia?

A

Oral iron supplementation for 3 months after iron deficiency corrected

196
Q

What is hyperplasia?

A

Tissue growth due to an increase in cell number (rather than size= hypertrophy)

197
Q

What is metaplasia?

A

A change from one fully differentiated cell type to another fully differentiated one

198
Q

What is neoplasia?

A

The development of a neoplasm, i.e. an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissue

199
Q

What is dysplasia?

A

This is a descriptive term used by pathologists to indicate a pattern of disordered growth, architecture and maturation within a tissue
Describes an appearance seen down the microscope
Does not mean the cells are neoplastic however

200
Q

What are the 5 main features of dysplasia?

A

Increased cell proliferation- abnormal mitotic figures
Cell crowding
Loss of orientation
Nuclear pleomorphism- variation in nuclear shape and size
Hyperchromatism- dark staining of nuclei reflecting an increase in DNA content

201
Q

What are the different types of cancer that can arrise?

A
202
Q

What are the mechanisms in neoplasia that allow tumours to grow?

A

Direct or indirect damage to DNA
Reduced ability to repair DNA damage
Increased stimuli to proliferate
Reduced ability to inhibit growth
Defects in apoptosis

203
Q

What are the differences between benign and malignant tumours?

A
204
Q

What are some of the negative effects of bnign tumours?

A

Bleeding – erosion and ulceration
Space occupying lesions within skull
Compression of adjacent structures
Obstruction of lumina
Hormonal effects

205
Q

What is Intussusception

A

Intussusception is a condition where part of the intestine slides into an adjacent part of the intestine. This telescoping action often blocks food or fluid from passing through
Can be caused by a polyp:

206
Q

What are the two main types of borderline tumours?

A

Tumours that show extensive local invasion but almost never metastasise. These are prone to local recurrence if incompletely excised.

Tumours that appear entirely benign at the time of diagnosis, but which can develop distant metastases, often presenting many years after the initial diagnosis. (must have metestasised before the surgery to remove them)

207
Q

Are high grade cancers poorly differentiated or well differentiated?

A

POORLY

208
Q

What are the symptoms of GI malignancy?

A

Tiredness (anaemia)
Bleeding
Anorexia and vomiting
Weight loss
Pain caused by obstruction
Dysphagia
Alteration in bowel habit

209
Q

What type of cancer is associated with Barrett’s oesophagus?

A

Adenocarcinoma

210
Q

What type of cancer is shown here?

A
211
Q

In what cells does metaplasia occur in oesophageal adenocarcinomas?

A

Metaplasia represents a phenotypic shift in the stem cells present at the base of the epithelium (not a change in differentiation of mature cells).

212
Q

How is GI cancer staged?

A

Based on the TNM system
The T stage relates to the depth of tumour invasion through the anatomical layers of the GI tract wall
The N stage is based on the number of involved lymph nodes
The M stage is based on the presence of distant metastases (and site)

213
Q

What are the two common histological patterns observed in gastric adenocarcinoma and what do they look like?

A
  • Intestinal- resembles what is seen in the intestine
  • Diffuse, may show a leather bottle stomach (thickening and deformation of stomach wall)
214
Q

Are gastric polyps always neoplastic?

A

No- can get fundic gland polyps or regenerative polyps

215
Q

Why might neoplasia of the small intestine be uncommon?

A

Diet passes through SI quickly so carcinogenic foods not staying there long or gut bacteria composition but mainly unknown

216
Q

What is a neuroendocrine tumour?

A

Epithelial tumours associated with the synthesis of hormone or neurotransmitter-like substances
Range from well-differentiated benign tumours through to aggressive and poorly differentiated malignancies such as small cell carcinoma
Appendiceal tumours are the most common most likely, but they are usually benign

217
Q

Where do neuroendocrine tumours tend to be based?

A

The submucosa rather than the mucosa

218
Q

What are gastrointestinal stromal tumours?

A

Soft tissue tumour that can arise anywhere in the GI tract- stomach is commonest site

219
Q

What are the different types of polyp in the colorectal area?

A

Inflammatory
Hamartomatous (benign hapazard cells)
Hyperplastic
Lesions in the submucosa causing it to bulge into lumen and presenting as a polyp
Also neoplastic- adenomas and adenocarcinomas

220
Q

What do Tubular, Tubulovillous and Villous ademona polyps look like?

A
221
Q

What dietary risk factors can lead to colorectal cancer?

A

Excessive calories relative to requirement
Low fibre
High intake of refined carbohydrates
High intake of red meat
Low intake of protective micronutrients e.g. vitamins A, C, D and E

222
Q

What gene is inactivated in about 80% of colorectal carcinomas and what condition is this the genetic basis of?

A

Inactivation of APC (Adenomatous Polyposis Coli) tumour suppressor gene
Basis of FAP- familial adenomatous polyposis

223
Q

What is the old and new colorectal cancer screening test?

A

Uses faecal occult blood test (FOBt) or faecal immunochemical test (qFIT),

224
Q

What is the causes of hereditory non-polyposis colorectal carcinoma syndrome (HNPCC)

A

the microsatellite instability pathway- Inactivation of DNA mismatch repair genes

225
Q

What are the two main causes of familial colorectal carcinomas?

A

FAP and HNPCC

226
Q

What are the main causes of upper GI bleed?

A

Peptic ulcer disease and varices

227
Q

What is injected into gastric varices?

A

Histoaryl (superglue- sterile) or thrombin

228
Q

What do PPIs block?

A

Block parietal cell H+/K+ pumps

229
Q

What do gastrin and cholecystokinin cellls secrete?

A

gastrin tells parietal cells to produce acid. Cholecystokinin signals to gallbladder to contract so bile is released into duodenum

230
Q

What is the difference between gastric erosins and ulcers?

A

Erosion= superficial, just mucosa
Ulcer is much deeper. Beyond the mucosa- meets the vessels and causes bleeding.

231
Q

What is a perforated ulcer?

A

Surgical emergency
When a deep ulcer meets blood vessels and opens a hole in the serosa and there is free communication with the peritoneum

232
Q

What are the most common causes of peptic ulcer disease?

A

H.Pylori

NSAID’s (Non-Selective NSAIDs deplete mucosal defense)

233
Q

What is the mechanism of injury in H. pylori?

A

Hypergastrinemia
Negative feedback for gastrin is blocked – resulted in uncontrolled excess gastrin and thus hyperacidity

Direct mucosal Injury
Cytotoxins cause increased production of ammonia Ammonia is toxin to epithelial cells

Inflammatory response
Mediated by macrophages, neutrophils, T-cell.

234
Q

What are the possible outcomes of a H pylori infection?

A
235
Q

What is peritonitis?

A

When stomach ulcers are so deep it splits a hole in the stomach wall and bacteria infects the lining of the peritoneum
Presents with sudden severe pain and shock and shoulder tip pain

236
Q

What are the main symptoms of GI bleeding?

A

Melaena= black stool
Haematemesis- vomiting blood

237
Q

What arteries most commonly get eroded in duodenal ulcers?

A

Supraduodenal and gastroduodenal arteries

238
Q

What are the two main causes of acute pancreatitis?

A

Gallstones, and gallstones stuck in ampulla

239
Q

What happens to amylase if there us an abstruction in the ampulla?

A

Secreted by the pancreas, if it can not pass into the GI tract then will spill over into the blood and also start digesting pancreas

240
Q

What happens if the superior mesenteric, inferior mesenteric or coeliac trunk gets blocked?

A

If these arteries get blocked, people can present with ischaemic bowel which is life threatening
Can lose your colon but cannot live without a small bowel. Can lose part of it but not all of it otherwise you are not absorbing nutrients, minerals and vitamins

Sem 2 Year 2 (16 decks)

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