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N&E > GI tract > Flashcards

GI tract Flashcards

1
Q

What are the functions of the GI tract?

A
  • secretion
  • digestion
  • absorption
  • motility
  • elimination
  • protection
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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
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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
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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)

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5
Q

What are changes in GI tract function triggered by:

A
  1. 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)
  2. signals from CNS i.e. anticipation of food, fear etc…
    - functions of GI tract not usually under voluntary control (SM/gland-controlled)
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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

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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
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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)
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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)

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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

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11
Q

In which 4 ways is blood flow controlled in the GI tract?

A
  1. haemodynamic factors (CO, BP, blood viscosity, volume)
  2. sympathetic activity + adrenaline levels (vasoconstriction)
  3. parasympathetic activity via indirect mechanisms of secretion of substances (vasodilation)
  4. activity of gut hormones e.g. gastrin, CCK
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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
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13
Q

What can go wrong with the GI tract blood supply?

A
  • emboli/thrombi
  • aortic aneurism
  • restriction
  • haemorrhage/circulatory shock and circulatory collapse
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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
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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
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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)
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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
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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
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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
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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
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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
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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
Q

What is a peptic ulcer, its contributing factors and aggressive factors?

A
  • 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
Q

What is the role of Helicobacter Pylori in causing peptic ulcers.

A
  • 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
Q

What are duodenal ulcers and where do they occur more often?

A
  • 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
Q

What are duodenal ulcers and where do they occur more often?

A
  • 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
Q

What are the symptoms of peptic and duodenal ulcers?

A

• 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
Q

How can peptic and duodenal ulcers be diagnosed?

A

• 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
Q

What is the urea breath test?

A
  • 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
Q

What is the treatment plan if a peptic or duodenal ulcer has been found?

A
  • triple therapy for 14 days

- proton pump inhibitor + clarithromycin + amoxicillin

33
Q

Which surgery can be used if a peptic or duodenal ulcer has been detected?

A
  • 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
Q

What are the figures for gastric cancer?

A
  • 13th most common cancer
  • more common in men than women
  • peak range = 40-60 years old
35
Q

What are the causes of gastric cancer?

A
  • 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
Q

What are the symptoms of gastric cancer?

A
  • abdominal pain
  • dyspepsia
  • anaemia
  • intestinal bleeding
  • advanced cancer
  • lymphatic spread
37
Q

How can gastric cancer be diagnosed?

A
  • X-ray examination

- endoscopy may reveal a gastric ulcer → non-healing ulcer = malignant

38
Q

How can gastric cancer be treated?

A

• 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
Q

What are the figures for colorectal cancer?

A
  • 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
Q

What are the symptoms of colorectal cancer?

A
  • blood in stools
  • unexplained change of bowel habits (prolonged diarrhoea)
  • weight loss
41
Q

What are the factors which increase the risk of colorectal cancer?

A
  • environmental factors such as western diet: high in fat + red meat, low in fibre predispose to CRC
  • smoking
  • chronic intestinal inflammation: ulcerative colitis
42
Q

How can colorectal cancer be diagnosed?

A
  • 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
Q

Which individuals is colorectal cancer screened for and how is it carried out?

A
  • 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
Q

How can colorectal cancer be treated and prevented?

A

• 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
Q

What is IBD and in which forms can it occur?

A
  • 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
Q

Describe the incidence of ulcerative colitis.

A
  • 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
Q

What are the symptoms of ulcerative colitis (subjective and objective)?

A
  • subjective: abdominal cramping, nausea, loss of appetite, irritability, anxiety + weakness
  • objective: bloody diarrhoea with pus/mucus, spastic rectum/anus, weight loss + vomiting
48
Q

How can ulcerative colitis be diagnosed and treated?

A

• 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
Q

What is the incidence and prevalence of Crohn’s disease?

A
  • 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
Q

What are the symptoms of Crohn’s disease and how can it be diagnosed?

A
  • 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
Q

How can Crohn’s disease be treated?

A

• 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
Q

What is IBS and how can it be treated?

A
  • 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
Q

What is coeliac disease?

A
  • 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
Q

What are the symptoms, management and complications associated with coeliac disease?

A
  • symptoms: dermatitis herpetiformis (associated itchy papular vesicular rash)
  • management: lifelong gluten-free diet (essentials on prescription)
  • complications:
    • anaemia
    • secondary lactose intolerance
    • osteoporosis

N&E (6 decks)

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