1
Q
What are the functions of the GI tract?
A
- secretion
- digestion
- absorption
- motility
- elimination
- protection
2
Q
Describe GI tract digestive organs?
A
- continuous, muscular digestive tube that extends through thorax and abdomen
- mechanical and chemical digestion of food into small molecules and absorption into blood
- organs/regions of alimentary canal (mouth, pharynx, esophagus, stomach, small and large intestine) separated by sphincters
- large intestine terminates in anal canal/anus
3
Q
Describe accessory digestive tract organs?
A
- teeth, tongue, gallbladder, several large digestive glands (salivary glands, liver and pancreas)
- teeth and tongue (oral cavity)
- digestive glands and gallbladder lie in abdomen (outside GI tract) and connect to it by ducts
- these organs produce variety of enzyme/fluid secretions, for breakdown of foods
4
Q
What are the layers/histology of the GI tract going inwards → outwards?
A
- mucousa → muscularus mucousa → submucousa → circular SM → longitudnal SM → serousa
- serosa has a “finished” edge of mesothelium - sample from near mesenteric attachment, much adipose tissue and fairly large blood vessels within
(muscularis externa = circular SM + longitudnal SM + serousa)
5
Q
What are changes in GI tract function triggered by:
A
- local stimuli i.e. distension/stretch of tract wall, osmolarity of solutes, pH of contents, conc. of specific nutrients like fats/peptides
- act on sensory receptors in mucosal layer of tract to initiate reflexes (act by muscles/glands) - signals from CNS i.e. anticipation of food, fear etc…
- functions of GI tract not usually under voluntary control (SM/gland-controlled)
6
Q
Describe extrinsic nervous GI tract control.
A
• extrinsic - outside GI tract via autonomic CNS nerves - long reflexes
• via parasympathetic (vagus) nerves
- stimulates blood flow, motility and secretion
- relaxes sphincters
• via SYMPATHETIC nerves
- inhibits blood flow, motility and secretion
- contracts sphincters
7
Q
Describe intrinsic nervous GI tract control.
A
• intrinsic; located inside GI tract via enteric nerves w/in plexus; short reflexes
- object in lumen
- activates sensory receptors of mucosa
- sensory nerves send impulses to
- submucous plexus → motor nerves to glands → secretion of fluid and mucus
- myenteric plexus → motor nerves to muscles → contraction of muscles to push object
8
Q
Describe hormonal GI tract control.
A
- largest endocrine organ → hormones secreted into bloodstream by specialised enterochromaffin cells in mucosal layer
- regulate functions of tract or accessory organs (+ communicate with CNS)
- hormones are peptides (20-40AAs long)
- at least 50 peptide hormones of GI tract identified i.e. gastrin, cholecystokinin, secretin, motilin, glucagon-like pepide 1
gastric inhibitory peptide/glucose dependent insulinotropic peptide (GIP)
9
Q
State the stages of secretin control of the GI tract.
A
- strongly acidic material enters duodenum as stomach empties
- causes release of secretin from duodenal mucousa into bloodstream
- secretin causes pancreas to secrete alkaline fluid into duodenum
- acid in duodenum nuetralised
(see notes for full table of hormone functions in detail)
10
Q
Describe the blood supply and drainage of the GI Tract via the splanchic circulation.
A
• largest regional circulation arising from aorta
• can receive 25% of cardiac output
- storage site for blood
- main branches:
→ coeliac arteries
→ superior mesenteric arteries
→ inferior mesenteric arteries
• smaller vessels support function (penetrate all layers of GI tract + accessory organs)
• mucosal blood flow is important
11
Q
In which 4 ways is blood flow controlled in the GI tract?
A
- haemodynamic factors (CO, BP, blood viscosity, volume)
- sympathetic activity + adrenaline levels (vasoconstriction)
- parasympathetic activity via indirect mechanisms of secretion of substances (vasodilation)
- activity of gut hormones e.g. gastrin, CCK
12
Q
Gastric mucosal blood flow is studied by injecting radio-labelled bases into blood secreted into gastric juice ionised and trapped in acidic stomach. Describe gastric mucosal blood flow.
A
- supports secretion of gastric mucosal cells (fluid, HCl, pepsins)
- main motor division for gut is parasympathetic (generally don’t involve blood vessels)
- controlled by indirect mechanisms controlled by increase in metabolic activity of secretory cells
- gastrin increases mucosal blood flow
13
Q
What can go wrong with the GI tract blood supply?
A
- emboli/thrombi
- aortic aneurism
- restriction
- haemorrhage/circulatory shock and circulatory collapse
14
Q
Describe haemorrhage/circulatory shock and circulatory collapse using the example of a congestive HF patient who goes into circulatory shock. Low BP and CO, develops abdominal pain, non-occlusive ischaemia of gut (often fatal)
A
- low CO = low perfusion of gut
- low flow rate = increased viscocity/development of microthrombi
- vasoconstriction so small vessels collapse
- ischaemia leads to necrosis of mucosa from tip of villi
- disruption of function + tissue by digestive enzymes
- intestinal permeability increases, toxic substances access body
- toxaemia + septicaemia occur (infection)
- blood and fluid lost via GI tract
15
Q
What happens to the gut when there are disturbances in the GI tract?
A
- acute ischaemia rare because of collaterals (extra vessels)
- if emergency perforation (hole in organs) occur, ischaemia is prolonged beyond a few hrs
- results from venous occlusion (obstruction) when gut twists/is trapped by hernia
- caused by back pressure into capillary beds by secondary obstruction of arterial blood flow
- the usual stages - damage to mucosa, initially reversible:
• bacteremia
• damage by enzymes
• perforation/strangulation
16
Q
Give an overview of diseases of the GI tract.
A
- peptic ulcer → gastric ulcer + duodenal ulcer
- gastric carcinoma
- colorectal carcinoma
- inflammatory bowel diseases (IBD) → ulcerative colitis + crohn’s disease
- irritable bowel syndrome (IBS)
17
Q
What are oral ulcers and what are their local causes?
A
- loss of the mucosal layer at a single site/diffuse
- idiopathic or as due to oropharyngeal/systemic problems
- shallow and round surrounded by reddened area and painful
- most often heal in few days unhealed for 3 weeks+ → concern
• local causes: - mechanical trauma most often: due to biting/scratching tongue or cheek or dentures along the gums
- chemical/thermal injury
18
Q
Describe aphthous mouth ulcers.
A
- most common oral ulcers
- usually resolve in 10-14 days
- affect 20% of population
- women more affected
- possible genetic factor predisposition
- mouthwashes and lozenges ease pain + speed up healing
19
Q
What is mucositis and how can it lead to ulcers?
A
- chemotherapy-associated inflammation of mucosa
- ulceration can be profound i.e. methotrexate and doxorubicin
- radiotherapy of head, neck, chest can also affect
20
Q
What are oral cancers and what is their incidence and occurrence?
A
- occur in the larynx, tonsils, tongue, parotids.
- incidence rates to rise by 33% in UK from 2014 to 2035
- head and neck cancer more common in deprived areas
- more common in white males than black and asian
- treat with surgery, radiotherapy, chemo depending on type
21
Q
What is GORD, its risks, symptoms, complications and indications for endoscopy?
A
- gastroesophageal reflux disease
- risks: smoking, drinking, obesity, pregnancy, hiatus hernia
- symptoms: heartburn, belching, acid regurgitation, nocturnal cough, morning sore throat
- complications: oesophagitis, ulcer, anaemia, Barrett’s Oesophagus
- indications for endoscopy: >55 years old, 4 weeks symptoms, dysphagia and persistence despite treatment usual pale pink darkens
22
Q
What is Barrett’s Oesophagus, why may it occur and how can it be treated?
A
- due to long-term acid reflux
- metaplasia: squamous columnar epithelium
- pre-malignant lesion
- annual endoscopy surveillance recommended + biopsy
- treatment: High dose Proton Pump Inhibitors (PPI), dietary/lifestyle advice, monitoring
23
Q
Describe squamous carcinoma (a form of oesophageal cancer) and its risk factors.
A
- more common in South Africa, Brazilian and Chinese
- develop from squamous epithelium → immature cells on histopathology
- risks: smoking, alcohol, nitrosamine in pickled/mouldy food, HPV infection
24
Q
Describe adenocarcinoma (a form of oesophageal cancer), its risk factors and treatment.
A
• incidence: rising in european men • risks: GORD and Barrett’s - both usually start as ulcer + spread - can become constricting and cause dysphagia • treatment: - oesophagostomy (cut + reconstruct) - radiotherapy > chemotherapy - palliative (poor prognosis usually)
25
What is a peptic ulcer, its contributing factors and aggressive factors?
- a mucosal break that is 3mm or greater
- contributing factors: Helicobacter pylori, NSAIDs, acid and pepsin
- aggressive factors: smoking, alcohol, bile acids, steroids, genetics and stress
26
What is the role of Helicobacter Pylori in causing peptic ulcers.
- gram-VE, spiral bacteria in the stomach
- damages mucous coating protecting stomach + duodenum
- allows powerful stomach acid to get through to sensitive lining beneath
• up to 80% of population infected → 15% get peptic ulcer
• others may develop: gastritis, gastric cancer + gastric lymphoma
- eradicating Helicobacter pylori infection permanently cures peptic ulcer
27
What are duodenal ulcers and where do they occur more often?
- 4x as common as gastric sites
- most common in middle-aged
- M:F = 4:1
- genetic link: 3x more common in 1st degree relatives
- more common in patients with blood group O
- Helicobacter pylori infection common (95%)
28
What are duodenal ulcers and where do they occur more often?
- common in late middle age - M:F = 2:1
- more common in patients with blood group A
- use of NSAIDs associated with 3 to 4-fold increase in risk
- less-related to Helicobacter pylori (80%)
- 10-20% patients with gastric ulcer have concomitant duodenal ulcer
29
What are the symptoms of peptic and duodenal ulcers?
• epigastric pain
- DU: occurs 1-3 hours after a meal. Pain is relieved by food, antacids or vomiting
- GU: food may exacerbate the pain while vomiting relieves it
- nausea, vomiting, dyspepsia, bloating, chest discomfort, anorexia and haematemesis may occur
- nausea, vomiting + weight loss more common with gastric GU
30
How can peptic and duodenal ulcers be diagnosed?
• upper GI endoscopy
• barium contrast X-rays
• Helicobacter pylori can be diagnosed by:
- blood tests which identify H. pylori antibodies
- stool antigen assays testing for H. pylori antigen
- rapid urease test on a biopsy sample
- urea breath test
31
What is the urea breath test?
- patient swallows a capsule containing urea made from a C isotope
- if H. pylori present in stomach, urea is broken up and turned into CO₂
- CO₂ absorbed across the lining of stomach and excreted in breath
- if isotope detected → H. pylori is present in stomach
32
What is the treatment plan if a peptic or duodenal ulcer has been found?
- triple therapy for 14 days
| - proton pump inhibitor + clarithromycin + amoxicillin
33
Which surgery can be used if a peptic or duodenal ulcer has been detected?
- vagotomy: cutting the vagus nerve to reduce acid secretion
- antrectomy/partial gastrectomy: remove part of gastrin producing G-cell rich antrum
- pyloroplasty: opening into pylorus isenlarged, enabling contents to pass more freely
34
What are the figures for gastric cancer?
- 13th most common cancer
- more common in men than women
- peak range = 40-60 years old
35
What are the causes of gastric cancer?
- Helicobacter pylori present in stomach
- 1 in 5 gastric cancers are caused by smoking
- high intake of salt increases risk
- fruit and vegetable have a protective effect
36
What are the symptoms of gastric cancer?
- abdominal pain
- dyspepsia
- anaemia
- intestinal bleeding
- advanced cancer
- lymphatic spread
37
How can gastric cancer be diagnosed?
- X-ray examination
| - endoscopy may reveal a gastric ulcer → non-healing ulcer = malignant
38
How can gastric cancer be treated?
• surgery
- most effective treatment
- cure rate = 30%
• chemotherapy
- sometimes combined with radiotherapy
- highly effective against some forms of stomach cancer
- help convert an inoperable tumour → operable one
39
What are the figures for colorectal cancer?
- 2nd most common death-causing cancer
- 4th most common type of cancer
- 3rd most common cancer in males
- 2nd most common cancer in females
- 80% of cases develop in people who are 60 or over
- 2/3 develop in colon with remaining 1/3 developing in rectum
40
What are the symptoms of colorectal cancer?
- blood in stools
- unexplained change of bowel habits (prolonged diarrhoea)
- weight loss
41
What are the factors which increase the risk of colorectal cancer?
- environmental factors such as western diet: high in fat + red meat, low in fibre predispose to CRC
- smoking
- chronic intestinal inflammation: ulcerative colitis
42
How can colorectal cancer be diagnosed?
- barium enema and colonoscopy
- histology of colonic polyp biopsies demonstrate dysplasia and neoplasia
- faecal occult blood testing
- blood tests may show iron deficiency or anaemia
43
Which individuals is colorectal cancer screened for and how is it carried out?
- individuals between the ages of 60-74 screened every 2 years
- carried out by taking a small stool sample + testing for presence of blood
44
How can colorectal cancer be treated and prevented?
• treatment:
- surgery: removed surgically together with a margin of normal tissue to ensure total resection
- chemotherapy: may increase survival after surgery
- radiotherapy: used to reduce tumour bulk
• prevention: a diet low in fat/red meat and high in carbohydrate/fibre is recommended
45
What is IBD and in which forms can it occur?
- inflammatory bowel disease
- inflammation and ulceration of intestine lining
- ulcerative colitis only affects large intestine
- crohn’s disease affects any part of the intestinal tract, although 3 patterns predominate: terminal ileal inflammation, colitis and anorectal inflammation
46
Describe the incidence of ulcerative colitis.
- uncommon condition
- appears in ages 15-30
- more common in white people of European descent
- much rarer in people of asian background
- both sexes equally affected
47
What are the symptoms of ulcerative colitis (subjective and objective)?
- subjective: abdominal cramping, nausea, loss of appetite, irritability, anxiety + weakness
- objective: bloody diarrhoea with pus/mucus, spastic rectum/anus, weight loss + vomiting
48
How can ulcerative colitis be diagnosed and treated?
• diagnosis:
- stool exam, sigmoidoscopy, colonoscopy, barium enema and lab studies
• treatment:
- medical treatment: steroids to treat acute exacerbations, immunosuppressants for frequent relapses, antidiarrheal meds, antibiotics aminosalicyclates for local anti-inflammatory action, iron and vit B12, low roughage diet and no milk
- surgery: total colectomy with ileostomy is cure → not until nothing else works
49
What is the incidence and prevalence of Crohn's disease?
- rare condition
- appears in ages 16-30
- affects slightly more women than men
- more common in white people than black or asian
- most prevalent among Jewish people
50
What are the symptoms of Crohn's disease and how can it be diagnosed?
- both subjective and objective symptoms are relatively identical to ulcerative colitis
- assessments are identical
• diagnostic tests the same except:
- string sign: segments of structure separated by normal bowel
- colonoscopy: patchy area of inflammations
- need biopsy for definitive diagnosis
51
How can Crohn's disease be treated?
• Medications
- sulfasalazine for anti-inflammatory effects
- steroids
- antibiotics
- anticholinergics
• dietary changes
- low-fat diet to reduce fatty acids
- restricted fibre diet with no raw fruit or vegetable and no nuts or whole grains
• surgery: may need surgery for partial removal of diseased portion of bowel
52
What is IBS and how can it be treated?
- common, long-term, non-dangerous condition
- no obvious abnormality of bowel and no serious threat to health
- sensitises nerves which cause peristalsis and partially digested food propels through gut
- muscular inner wall overreacts to mild stimuli (i.e. milk products) and goes into spasm
- no cure but symptoms can be relieved by:
- dietary changes: identify and avoid foods/drinks that trigger symptoms
- lifestyle changes: exercise and managing stress levels
- medication: antispasmodic, laxatives and antidepressant
53
What is coeliac disease?
- T-cell mediated autoimmune disease
- affects small bowel
- reaction to prolamins (gluten proteins) resistant to proteases in gut
- somehow gluten proteins get into submucosa from lumen
- Here TTG (tissue transglutaminase) de-amidates gluten so it can bind to coeliac-associated HLA peptides (HLA DQ2 and HLA DQ8/HLA B8)
- stimulates T-Helper cells to attack gut resulting in villous atrophy (losing villi)
54
What are the symptoms, management and complications associated with coeliac disease?
- symptoms: dermatitis herpetiformis (associated itchy papular vesicular rash)
- management: lifelong gluten-free diet (essentials on prescription)
- complications:
• anaemia
• secondary lactose intolerance
• osteoporosis
N&E
flashcards
Decks in class (6)
# Cards
