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1st year GI > diseases of the mouth, oesophagus, stomach and small bowel > Flashcards

diseases of the mouth, oesophagus, stomach and small bowel Flashcards

1
Q

what is jaundice

A

the yellowing of the sclera (white of eyes) and the skin. It is caused by an increase in the blood levels of bilirubin

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2
Q

what is bilirubin

A

The normal byproduct of breakdown of RBCs and it travels through your liver, gallbladder, and digestive tract before being excreted.

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3
Q

what vessels are in the interlobular portal triad

A
  • Biliary duct
  • Branch of hepatic artery
  • Branch of hepatic portal vein
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4
Q

what do the left and right hepatic ducts unite to form

A

common hepatic duct

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5
Q

what is formed when the common hepatic duct joins with the cystic duct

A

Bile duct

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6
Q

what is formed when the bile duct descends posteriorly to the 1st superior part of the duodenum and then joins with the main pancreatic duct

A

Ampulla of Vater

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7
Q

where does the Ampulla of Vater drain through and into

A

it drains through the major duodenal papilla into the second part of the duodenum

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8
Q

what are the sphincters in the area of the bile duct

A
  • Bile duct sphincter - at distil end of bile duct
  • Pancreatic duct sphincter - at the distal end of the pancreatic duct
  • Sphincter of Oddi - surrounds the end portion of the common bile duct and pancreatic duct
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9
Q

what investigation is used to study the biliary tree and the pancreas

A

ERCP - endoscopic retrograde cholangiopancreatography

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10
Q

how can jaundice form

A

Obstruction of the biliary tree by gallstones if carcinoma at the head of the pancreas causing the bile to flow back up to the liver instead of being created into the duodenum. These extra hepatic obstructive causes of jaundice

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11
Q

What are the anatomical relationships of the pancreas to the:

1) stomach
2) duodenum
3) splenic vessels

A

1) anteriorly lies the stomach
2) the duodenum surrounds the head of the pancreas
3) superoposteriorly

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12
Q

what are functions of the exocrine and endocrine pancreas

A
  • Exocrine - acinar cells - pancreatic digestive enzymes into the main pancreatic duct
  • Endocrine - islets of Langerhans - insulin and glucagon into the blood stream
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13
Q

what vessel does blood travel to the pancreas

A

Mainly branches of the splenic artery. The head is additionally supplied by the superior and inferior pancreaticoduodenal arteries which are branches of the gastroduodenal and superior mesenteric arteries, respectively.

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14
Q

what is a cause of pancreatitis

A

blockage if the ampulla by the gallstone

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15
Q

where will pain be felt in regards to the pancreas

A

Pain in the epigastric region and or umbilical region. It can also radiate through to the patients back

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16
Q

what part of the duodenum is intraperitaneal and which is retroperitoneal

A
  • intraoeriteneal = superior

- retroperitoneal = descending, horizontal and ascending

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17
Q

where does the duodenum start

A

the pyloric sphincter

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18
Q

what does the duodenum secrete

A

peptide hormones into the blood

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19
Q

what area of the duodenum does the superior pancreaticoduodenal (gasproduodenal artery) supply

A

supplies proximal parts 1 and 2 (foregut)

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20
Q

what area of the duodenum does the inferior pancreaticoduodenal ( superior mesenteric artery) supply

A

supplies distal parts 3 and 4

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21
Q

what are plaice circulares

A

The lining of the small intestine consists of a series of permanent spiral or circular folds, termed the plicae circulares, which amplify the organ’s surface area, promoting efficient nutrient absorption.

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22
Q

for the jejunum an ileum where does the arterial blood come from and where does the venous drainage from

A
  • arterial blood from superior mesenteric artery via the jejunal and ill arteries
  • venous drainage from the jejunal and ill veins to the superior mesenteric vein at hepatic portal vein
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23
Q

what are the main groups of lymph nodes draining abdominal organs

A
  • celiac = foregut organs
  • superior mesenteric = midgut organs
  • inferior mesenteric = hingut organs
  • lumbar = kidneys, posterior abdominal wall, pelvis and lower limbs
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24
Q

aetiology of oral pre-malignancy and cancer

A
  • tobacco
  • alcohol
  • HPV
  • diet and nutrition
  • Candida
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25
Q

what is the uk recommended units of alcohol for men in a week

A

14

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26
Q

why does alcohol cause oral cancer

A

Ethanol (procarcinogens) is converted to Acetaldehyde (AA carcinogen, mutagen) using Alcohol dehydrogenase which exists in the mouth. Acetaldehyde is the converted to Acetate using aldehyde dehydrogenase

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27
Q

what effects does diet and nutrition have on oral cancer

A

Low in vitamin A, C, iron increase the risk of oral cancer.

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28
Q

What are some characteristics of asymptomatic invasive oral cancers

A
  • Surface texture: granular (48%) or smooth (33%)
  • Elevation: 1mm max in 20% of cases
  • No ulceration in 85% and no bleeding in 98%
  • Not indurated in 90%
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29
Q

what are high risk sites of oral cancers

A

90% occurs in the lining of the mouth

10% occurs in salivary glands or bones

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30
Q

what is Erythroplakia

A

red patch

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31
Q

what is Erythroleukoplakia

A

red and white patch

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32
Q

what is leukoplakia

A

white patch

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33
Q

what are warning signs for oral cancer

A
  • Red/ white/ red and white lesion
  • Ulcer (exclude trauma, drug, systemic)
  • Numb feeling eg lip, face
  • Unexplained pain in mouth or neck
  • Change in voice
  • Dysphagia
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34
Q

what are some orofacial manifestations of cancer

A
  • Drooping eye lid or facial palsy
  • Fracture of mandible
  • Double vision
  • Blocked or bleeding nose
  • Facial swelling
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35
Q

what are key questions you should ask for checking for oral cancer

A
  • How long has the pain been present - mouth heals 7-10 days. If there for 3 weeks look at with suspicion
  • Is it painful? - pain is usually a late manifestation of oral cancer but would be expected to be a benign ulcer
  • Does patient smoke or drink
  • What colour is the lesion
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36
Q

what cells line the oesophagus

A

stratifies squamous epithelium

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37
Q

what is oesophagitis

A

inflammation that may damage tissues of the oesophagus

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38
Q

what is reflux oesophagitis and what may cause it

A

inflammation of the oesophagus due to refluxed low pH gastric contents
it may be caused by defective sphincter mechanism +/- Hiatus hernia (where part of the stomach pushes up into. the lower chest through a weakness in the diaphragm)

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39
Q

what is seen under a microscope for reflux oesophagitis

A
  • Basal zone epithelial expansion (basal cell hyperplasia)

- Intraepithelial neutrophils, lymphocytes and eosinophils

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40
Q

what are some complications of reflux oesophagitis

A
  • Ulceration (bleeding)
  • Stricture - abnormal narrowing of a bodily passage
  • Barretts oesophagus = replacement of stratified squamous epithelium by columnar epithelium
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41
Q

what causes Barretts oesophagus

A
  • Persistent reflux of acid or bile
  • May be due to expansion of columnar epithelium from gastric glands or from submucosal glands
  • May be due to differentiation from oesophageal stem cells
  • Protective response, faster regeneration
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42
Q

what is allergic oesophagitis or ‘eosinophilic oesophagitis’

A

When eosinophils deposit in the lining of the oesophagus . This can be the result of an allergic reaction to food or the environment

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43
Q

how do you treat eosinophilic oesophagitis

A

treatment may include steroids/ chromoglycate / montelukast

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44
Q

what are squamous papilloma

A

small benign (non cancerous) growth that begins in squamous cells - rare tumour in the oesophagus

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45
Q

what are leiomyomas

A

“fibroids”. Benign smooth muscle tumour that’s a very rare oesophageal tumour

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46
Q

what are lipomas

A

fatty tumours below skin (not cancer)

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47
Q

what are fibrovascular polyps

A

intraluminal, submucosal tumour like lesions that usually remain asymptomatic

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48
Q

what are granular cell tumours

A

mesenchymal soft tissue tumours

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49
Q

what are some common malignant oesophageal tumours

A
  • squamous cell carcinoma

- adenocarcinoma

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50
Q

squamous cell carcinoma aetiology

A
  • Vitamin A, zinc deficiency
  • Tannic acid/ strong tea
  • Smoking, alcohol
  • HPV
  • oesophagus
  • genetic
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51
Q

explain the pathogenesis of squamous small cell carcinoma

A

A stepwise progression occurs: Normal –> severe dysplasia –> carcinoma

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52
Q

what does squamous cell carcinoma in the oesophagus cause

A

obstruction and dysphagia

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53
Q

what is Barretts oesophagus

A

replacement of stratified squamous epithelium by columnar epithelium with interstitial metaplasia

  • Increased risk of developing dysplasia than adenocarcinoma of the oesophagus
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54
Q

what is the pathogenesis of an adenocarcinoma of the oesophagus

A

genetic factors, reflux disease, others –> chronic reflux, oesophagitis –>Barretts oesophagitis (interstitial metaplasia) –> Low grade dysplasia –> high grade dysplasia –> Adenocarcinoma

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55
Q

what are some mechanisms of metastases for carcinoma of the oesophagus

A
  • Direct invasion
  • Lymphatic permeation
  • Vascular invasion
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56
Q

what are some clinical presentations of carcinoma of the oesophagus

A
  • Dysphagia (due to tumour obstruction)

- General symptoms of malignancy (anaemia, weight loss, loss of energy)

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57
Q

what are some histopathology features relating to prognosis of small cell carcinoma

A
  • Tumour diameter
  • Depth of invasion
  • Pattern of invasion - cohesive vs non-cohesive
  • Lymphovascular invasion
  • Neutral invasion by tumour
  • Involvement of surgical margins
  • Metastatic disease
  • Extracapsular spread of lymph node metastases
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58
Q

what are some common types of chronic gastritis

A
  • Autoimmune
  • Bacterial H.pylori
  • Chemical
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59
Q

what is autoimmune chronic gastritis

A

Autoimmune atrophic gastritis is a chronic inflammatory disease in which the immune system mistakenly destroys a special type of cell (parietal cells) in the stomach. Parietal cells make stomach acid (gastric acid) and a substance our body needs to help absorb vitamin B12 (called intrinsic factor)

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60
Q

what is SACDC (subacute combined degeneration of the cord

A

when myelin sheath withers away due to lack of vitamin B12

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61
Q

How does H pylori cause gastritis

A

Both the acid and bacteria irritate the lining and cause an ulcer to form. If left untreated, a H. pylori infection can cause gastritis

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62
Q

how does chemical gastritis occur

A
  • Due to NSAIDs, alcohol, bile reflux
  • Direct injury to mucous layer by fat solvents
  • Marked epithelial regeneration, hyperplasia, congestion and little inflammation
  • May produce erosions or ulcers
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63
Q

what is peptic ulceration

A

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

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64
Q

where can chronic peptic ulcers form

A
  • Duodenum
  • Stomach
  • Oesophago-gastric junction
  • Stomal ulcers
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65
Q

how are chronic peptic ulcers formed

A

excess acid in the duodenum produces gastric metaplasia and leads to H.Pylori infection, inflammation, epithelial damage and ulceration

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66
Q

microscopically what are some features of peptic ulcers

A
  • Layered appearance
  • Floor of necrotic fibrinopurulent debris
  • Base of inflamed granulation tissue
  • Deepest layer is fibrotic scar tissue
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67
Q

what are some complications of peptic ulcers

A
  • Perforation
  • Penetration
  • Haemorrhage
  • Stenosis
  • Intractable pain
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68
Q

what are some benign gastric tumours

A
  • hyperplastic polyps

- cystic funds gland polyps

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69
Q

what are some malignant gastric tumours

A
  • carcinomas
  • lymphoma - cancer that begins in infection fighting cells of the immune system (lymphocytes)
  • gastrointestinal stromal tumours - abnormal cells in the GI tract
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70
Q

what is the pathogenesis of gastric adenocarcinoma

A

H.Pylori infection –> chronic gastritis –> intestinal metaplasia/ atrophy –> dysplasia –> carcinoma

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71
Q

what is pernicious anaemia

A

vitamin B12 deficiency

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72
Q

what is partial gastrectomy

A

surgical removal of a portion of the stomach

73
Q

what is HNPCC/ Lynch syndrome

A

autosomal dominant genetic condition associated with a high risk of colon cancer

74
Q

what is Menetriers disease

A

Rare disorder characterised by massive outgrowths of mucous cells in the mucus membrane lining the stomach, resulting in large gastric folds

75
Q

what are the subtypes of gastric adenocarcinoma

A
  • Intestinal type - exophytic/polypoid mass

- Diffuse type - expands/ infiltrates stomach wall

76
Q

what is intestinal type of gastric adenocarcinoma

A

The intestinal-type is the end-result of an inflammatory process that progresses from chronic gastritis to atrophic gastritis and finally to intestinal metaplasia and dysplasia

77
Q

what is diffuse type of adenocarcinoma

A

Diffuse gastric cancer is a specific type of stomach cancer, sometimes also called “signet ring cell gastric cancer” or “linitis plastic.” The word “diffuse” is used because this cancer tends to affect much of the stomach, rather than staying in 1 area of the stomac

78
Q

where can gastric adrenocarcinoma spread to

A
  • Local - directly into other organs
  • Lymph nodes - omental
  • Haematogenous - to the liver and beyond
  • Tanscoelomic - Into peritoneal cavity and ovaries
79
Q

what is maltoma

A

MALT lymphoma (MALToma) is a form of lymphoma involving the mucosa-associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be afflicted. It is a cancer originating from B cells in the marginal zone of the MALT, and is also called extranodal marginal zone B cell lymphoma.

80
Q

what is GIST ( gastrointestinal stromal tumour)

A

Very rare gastric tumour which are stromal in nature, producing spindle cell masses driven by mutations in the KIT oncogene

81
Q

what is dyspepsia

A

Epigastric pain or burning (epigastric pain syndrome), postprandial fullness (postprandrial distress syndrome). Early satiety (postprandial distress syndrome)

82
Q

what are the foregut structures

A
  • oesophagus
  • stomach
  • duodenum
  • pancreas
  • gallbladder
83
Q

what are organic causes of dyspepsia

A
  • peptic ulcer disease
  • drugs (esp NSAIDs, COX2 inhibitors)
  • gastric cancer
84
Q

what is functional dypepsia

A

Functional dyspepsia is a term for recurring signs and symptoms of indigestion that have no obvious cause.

85
Q

what are causes of peptic ulcer disease

A
  • H pylori
  • NSAIDs
  • gastric dysmotility
86
Q

what is H.pylori

A

Gram -ve microaerophilic flagellated bacillus. Acquired in infancy but consequences not until later in life

87
Q

what are the consequences for H.pylori

A
  • no pathology
  • peptic ulcer disease
  • gastric cancer (almost all non cardia gastric adenocarcinoma)
88
Q

what is the homeostasis mechanism of gastric acid secretion

A
  • G cells in the distal part of the stomach are stimulated by acid.
  • G cells stimulate the production of Gastrin that then enters the blood stream and stimulates the parietal cells to produce acid
89
Q

how do we diagnose a H.pylori infection

A
  • gastric biopsy can gain tissue to be used to get info on a urease test (if helicofactor is present), histology, culture/sensitivity
  • urease breath test
  • FAT (faecal antigen test)
  • Serology (IgA anitbodies) - not accurate with increasing patient age
90
Q

what is urease

A

Urease, an enzyme that catalyzes the hydrolysis of urea

91
Q

how do you treat peptic ulcer disease

A
  • all people should get :
    > antisecretory therapy ie proton pump inhibitors
    > tested for presence of H.pylori
  • H.pylori +ve the eradicate and confirm
  • H.pylori -ve then antisecretory therapy
  • withdraw NSAIDs
  • lifestyle (difficult)
  • non-HP/ non-NSAID ulcers - nutrition and optimise comorbidites
  • no firm dietary recommendations
92
Q

what is eradication therapy for H.pylori

A
  • “tripple therapy” for 1 week =
    PPI+ amoxycillin 1g bd + clarithromycin 250mg bd

PPI + metronidazole 400mg bd + clarithromycin 250mg bd

  • 2 week regimens
    > higher eradication rates
    > poorer compliance
  • dual therapy = PPI + 1 antibiotic not recommended
  • quadrouple therapy + culture directed therapy
93
Q

what are complications of peptic ulcer disease

A
  • anaemia
  • bleeding
  • perforation
  • gastric outlet/ duodenal obstruction - fibrotic scar
94
Q

what are causes of GORD

A
  • incompetent closing of lower oesophageal sphincter
  • poor oesophageal clearance
  • barrier function/ visceral sensitivity
95
Q

what are symptoms of GORD

A
  • heartburn
  • acid reflux
  • waterbrash
  • dysphagia
  • odynophagia
  • weight loss
  • chest pain
  • hoarseness
  • coughing
96
Q

what are some investigations for GORD

A
  • endoscopy
  • Ba swallow
  • oesophageal manometry and pH studies
97
Q

what are alarm symptoms

A
  • dysphagia
  • weight loss
  • anaemia
  • vomiting
  • F/H UGI cancer
  • Barretts
  • Pernicious anaemia
  • PUD surgery > 20 years
98
Q

what are complications of GORD

A
  • oesophagitis
  • schatzki’s ring
  • adenocarcinoma of the oesophagus
99
Q

what is the pathogenesis of adenocarcinoma

A

normal –> ongoing erosive damage for years –> oesophagitis (reversible) –> more errosive damage for years –> Barretts oesophagus (irreversible) –> adenocarcinoma (too late)

100
Q

what is the management of GORD

A
  • symptom relief
  • healing oesophagitis
  • prevent complications
  • lifestyle modifications (stop smoking, loose weight is obese, prop up the bead head, avoid provoking factors)
101
Q

what are the dug managment of GORD

A
  • Antacids - symptomatic relief, no benefit in healing or preventing complications
  • proton pump inhibitors - block the acid pumping mechanism and prevent ongoing acid production in the stomach eg Ranitidine, Omeprazole

they help heal all grades of oesophagitis

102
Q

what are some features of Barretts oesophagus

A
  • 10% of GORD patients
  • Intestinal metaplasia
  • Irreversible
  • increased risk of adenocarcinoma
  • PPI +/- surveillance
103
Q

what is low grade dysplasia management

A
  • surveillance more frequently every 3 month s

- optimise their PPI dose 40mg twice daily

104
Q

what is high grade or persistent low grade dysplasia management

A
  • remove with endoscopic mucosal resection
105
Q

what is Hiatus hernia

A
  • sliding hiatus hernia

- paraesophageal hiatus hernia

106
Q

what is gastroparesis

A

condition where there is poor emptying of the stomach without a physical blockage in the pyloris

107
Q

what are symptoms of gastroparesis

A
  • feeling of fullness
  • nausea
  • vomiting
  • weight loss
  • upper abdominal pain
108
Q

what are causes of gastroparesis

A
  • idiopathic
  • diabetes mellitus
  • cannabis
  • medication eg opiates, anticholinergenics
  • systemic diseases eg systemic sclerosis
109
Q

what is the management of gastroparesis

A
  • removal of precipitating factors eg drugs
  • liquid/sloppy diet
  • eat little and often
  • promotility agents
  • gastric pacemaker
110
Q

what is achalasia

A

Motility disorder of the lower oesophageal sphincter failing to relax. it is almost in spasm all of the time. Reduced peristalsis in the body of the oesophagus. Due to obstruction at the LOS –> the oesophagus becomes dilated

111
Q

what is the management of achalasia

A
  • balloon dilation

- surgical - cardiomyopathy

112
Q

what are the 2 types of oesophageal cancer

A
  • squamous cell carcinoma

- adenocarcinoma

113
Q

what is progressive dysphagia

A

difficulty swallowing initially for red meat etc and eventially not being able to swallow saliva

114
Q

what are the steps of fat digestion and absorption

A
  • lipolysis
  • micellar solubilisation with bile acid
  • absorption
  • digestion
115
Q

what is malabsorption

A

Malabsorption is a disorder that occurs when people are unable to absorb nutrients from their diets, such as carbohydrates, fats, minerals, proteins, or vitamins

116
Q

what is coeliac disease

A

Caused by an abnormal reaction to a constituent of wheat flour, gluten, which damages enterocytes and reduces absorbtive capacity

117
Q

what is lactose malabsorption

A

deficiency of lactase giving a history of diarrhoea, abdominal discomfort, and flatulance following the indigestion of dairy products

118
Q

what is tropical sprue

A

colonisation of the small intestine by a infectious agent or alterations in the intestinal bacterial folora

119
Q

what is whipples disease

A

Whipple disease is a rare bacterial infection that most often affects your joints and digestive system. Whipple disease interferes with normal digestion by impairing the breakdown of foods, and hampering your body’s ability to absorb nutrients, such as fats and carbohydrates

120
Q

what is Crohns disease

A

patients with extensive ill involvement, extensive intestinal resections, enterocoelic fistulas, and strictures leading to small intestinal bacterial overgrowth may develop significant and occasionally devastating malabsorption

121
Q

what is small bowel bacterial overgrowth

A

small intestinal bacterial overgrowth (SIBO) occurs when there is an abnormal increase in the overall bacterial population in the small intestine — particularly types of bacteria not commonly found in that part of the digestive tract. This condition is sometimes called blind loop syndrome.

122
Q

what history should you look at of a patient for malabsorption

A
  • GI symptoms
  • Past medical history
  • Travel history
  • Social history
  • Drug history
  • Dietary history
123
Q

what are GI stool symptoms

A
  • Diarrhoea ( duration, fat gobbles, floating, hard to flush away)
124
Q

what are baseline investigations of the malabsorption

A
  • FBC
  • coagulation
  • LFT’s
  • albumin
  • calcium/magnesium
  • stool culture
125
Q

what are the basic steps of management of malabsorption

A
  • treat the underlying causes
  • replace the deficiency
  • support nutritionally
126
Q

what supplies blood to the small bowel

A

Superior mesenteric artery

127
Q

what can cause ischaemia of the small bowel

A
  • mesenteric arterial occlusion ie mesenteric artery atherosclerosis or thromboembolism from heart
  • non occlusive perfusion insufficiency ie shock, strangulation obstructing venous return, drugs, hyper viscosity
128
Q

what is the most metabolically active part of the bowel wall

A

the mucosa is the most metabolically active part of the bowel wall and therefore the most sensitive to the effects of hypoxia

129
Q

what are the degrees of infarction in acute ischeamia of the gut

A
  • mucosal infarct = early ischaemia affecting mucosa
  • mural infarct = mucosa and submucosa
  • transmural infarct = late ischeamia involving all the layers of the gut
130
Q

what are some complications of ischaemia of the small bowel

A

fibrosis, stricture, chronic ischaemia, gangrene, perforation, sepsis and death

131
Q

what is Meckels diverticulum

A

Result of incomplete regression of Vitelli-intestinal duct. Its a tubular structure, 2 inches longs, 2 foot above IC valve in 2% of people. It may contain heterotrophic gastric mucosa. It may cause bleeding, perforation or diverticulitis which mimic appendicitis

132
Q

Are primary or secondary tumours more common in the small bowel

A

secondary tumours are much more common

133
Q

what primary tumours are in the small bowel

A
  • lymphomas
  • neuroendocrine (carcinoid) tumours
  • carcinomas
134
Q

what are lymphomas

A

malignant tumours of the lymphoid cells

135
Q

what are neuroendocrine tumours of the small bowel

A

Small, yellow, slow growing tumours that are locally invasive.

136
Q

what is a carcinoid tumour

A

Carcinoid tumors are a type of slow-growing cancer that can arise in several places throughout your body. Carcinoid tumors, which are one subset of tumors called neuroendocrine tumors, usually begin in the digestive tract (stomach, appendix, small intestine, colon, rectum) or in the lungs

137
Q

what diseases are primary carcinomas associated with

A

Crohns disease and Coelaic disease

138
Q

what is appendicitis

A

Appendicitis is inflammation of the appendix, a small pouch connected to your large intestine. Causes vomiting, abdominal pain, RIF tenderness and increased white cell count

139
Q

what are causes of acute appendicitis

A
  • unknown
  • faecoliths (dehydration)
  • lymphoid hyperplasia
  • parasites
  • tumours (rare)
140
Q

what I the pathology of acute appendicitis

A
  • acute inflammation (neutrophils)
  • mucosal ulceration
  • serial congestion, exudate
  • pus in lumen
  • Acute inflammation must involve the muscle coat
141
Q

what may be seen for acute appendicitis

A
  • yellow surface exudate is seen
  • wall thickened ready to perforate, containing pus
  • mucosal ulceration and mural inflammation
  • pus in the lumen
  • neutrophils invade the appendix wall
142
Q

what can be complications of appendicitis

A
  • peritonitis
  • rupture
  • abscess
  • fistula
  • sepsis and liver abscess
143
Q

what is the aetiology of coeliac disease

A
  • Gliadin a component of gluten is the suspected toxic agent
  • But tissue injury may be a bystander effect of abnormal immune reaction to Gliadin
  • Mediated by T cell lymphocytes which exist within the small intestinal epithelium ‘intraepithelial lymphocytes’
144
Q

what happens in coeliac disease when there is an increasing loss of enterocytes due to IEL mediated damage

A

this leads to loss of villous structure, loss of surface area, a reduction In absorption and a flat duodenal mucosa

145
Q

what is the clinical appearance of coeliac disease

A
  • mucosa may be endoscopically normal or appear attenuated/flat
  • lesion worse in proximal bowel so duodenal biopsy is very sensitive
146
Q

what is the serology of coeliac disease

A
  • antibodies are seen (anti-TTG, anti-endomesial, anti-gliadin)
147
Q

what are the metabolic effects of coeliac disease

A
  • malabsorption of sugars, fats, amino acids, water and electrolytes
  • malabsorption of fats leads to steatorrhea
  • reduced intestinal hormone production leads to a reduced pancreatic secretion and bile flow (CCK) leading to gallstones
148
Q

what are effects of malabsorption

A
  • loss of weight
  • anaemia (Fe, Vit B12, folate)
  • abdominal bloating
  • failure to thrive
  • vitamin deficiencies
149
Q

what are other complications of coeliac disease

A
  • T cell lymphomas of GI tract
  • increased risk of small bowel carcinoma
  • gall stones
  • ulcerative-jejenoilleitis
150
Q

what vessel supplies blood to the appendix

A

appendicular artery

151
Q

what is the aetiology of appendicitis

A
  • no unifying hyposthesis
  • obstruction of the lumen with faecolith
  • bacterial
  • viral (clustering of cases)
  • parasites
152
Q

what is the pathology of appendicitis

A
  • huge variation in macroscopic disease
  • lumen may or may not be occluded
  • mucosal inflammation
  • lymphoid hyperplasia
  • obstruction
  • build up of mucus and exudate
  • venous obstruction
  • ischaemia… bacterial invasion through wall
  • perforation
153
Q

what are classic clinical symptoms of appendicitis

A
  • central pain that migrates to the RIF
  • anorexia
  • nausea
  • one or two vomits
  • may not have moved bowels
  • pelvic: vaguer pain localisation: rectal tenderness
  • elderly
154
Q

what are signs of appendicitis

A
  • mild pyrexia (never high temp initially)
  • mild tachycardia
  • localised pain in RIF (right iliac fossa)
  • guarding
  • rebound
155
Q

what are specific signs of appendicitis

A
  • Rosvings = pressing on the left causes pain on the right
  • Psoas = patient keeps the right hip flexed as this lifts an inflammed appendix off the psoas
  • Obturator = appendix is touching obturator internus, flexing the hip and internally rotating will cause pain
  • pointing = where did it start and where is it now?
156
Q

what investigations to carry out for appendicitis

A
  • clinical diagnoses
  • USS useful in women with kids
  • AXR to exclude other causes
  • bloods (important CRP, WCC)
  • Urinalysis
157
Q

what is management of appendicitis

A
  • Analgesia
  • Antipyretics
  • Theatre
  • Antibiotics
  • Appendicectomy = laparascopic (best) , convert to open sometimes (not first line)
  • laparotomy sometimes
158
Q

how to treat an appendix mass

A
  • antibiotics first line
  • can operate or not
  • theatre if fails or complicated (tachycardia, worsening pain, increase in size, vomiting or copious NG aspirates (ileus))
159
Q

how to treat an appendix absess

A
  • not an appendix mass
  • usually delayed
  • usually has liquidised
  • radiologically drains
160
Q

what can go wrong with a small bowel

A
  • obstruction
161
Q

what happens with small bowel obstruction

A
  • colicky central pain
  • absolute constipation
  • vomiting
  • burping
  • abdominal distension
162
Q

what is the definition of malnutrition

A

is a major clinical and public health issue within the United Kingdom with the wider determinants of health including poverty, social isolation and deprivation all exacerbating its incidence (Elia,2003)

163
Q

what are the effects of starvation

A
  • Metabolic rate decreases.
  • Weight will decrease, slow loss almost all from fat stores.
  • Decrease in nitrogen losses
  • Early small increases in catecholamines, cortisol, GH, then slow fall. Insulin decreased.
  • Water is initially lossed then late retention
164
Q

what are the effects of injury

A
  • Increased metabolic rate …
165
Q

what is enteral tube feeding

A
  • delivery of a nutritionally complete feed via a tube into the stomach, duodenum or jejunum
166
Q

what are indications for ETF

A
  • Inadequate or unsafe oral intake, and a functional, accessible GI tract
  • ‘If the gut works, use it’ - unconscious patients, neuromusculat swallowing disorder, upper GI obstruction, GI dysfunction
167
Q

contradictions for ETF

A
  • Lower GI obstruction
  • Prolonged intestinal ileus
  • Severe diarrhoea and vomiting
  • High entercutaneous fistula
  • Intestinal ischaemia
168
Q

what is refeeding syndrome

A

Refeeding syndrome is a serious and potentially fatal complication of nutritional rehabilitation in patients with severe anorexia nervosa. It occurs in significantly malnourished patients when a diet of increasing calories is initiated orally, by nasogastric (NG) tube and/or delivered intravenously.

169
Q

what are metabolic features of refeeding syndrome

A 
Hypokalaemia
Hypophosphataemia
Hypomagnesaemia
Altered glucose metabolism
Fluid overload
170
Q

what are physiological features of refeeding syndrome

A 
Arrhythmias
Altered level of consciousness
Seizure
Respiratory failure
Cardiovascular collapse
Death
171
Q

how do you screen for malnutrition risk

A

‘MUST’

172
Q

what are the main sections for resuscitation of a patients who has GI bleeding

A
  • Airway
  • Breathing
  • Circulation
  • Airway protection
  • Oxygen
  • IV access
  • Fluids
173
Q

what bore access is needed for a patient with GI bleeding

A

large bore IV access is mandatory

174
Q

what are the signs of the ‘100 rule’: poor prognosis group

A 
systolic BP < 100mmHg
pulse > 100/min
Hb < 100 g/l
age > 60
comorbid disease
postural drop in blood pressure
175
Q

what are the main takeaways for an endoscopy for a GI bleed

A
  • Identify cause
  • Therapeutic manoeuvres
  • Assess risk of rebleeding
176
Q

what is stigmata of recent haemorrhage

A
  • active bleeding/oozing
  • overlying clot
  • ‘visible vessel’
177
Q

what are treatments for bleeding peptic ulcers

A
  1. endoscopic treatment (high risk ulcers)
  2. acid suppression (?infusions)
  3. interventional radiology
  4. surgery
  5. H.pylori eradication - secondary prevention
178
Q

what are some endoscopic treatment of peptic ulcers

A
  1. injection
  2. heater probe coagulation
  3. combinations
  4. clips
  5. haemospray

1st year GI (16 decks)

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