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Osha 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is considered to be an upper GI bleed?

A
  • Bleeding above the duodenum
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2
Q

What are the causes of upper GI bleeds?

A
  • oesophageal varices
  • Mallory-Weiss tear (tear of oesophageal mucous membrane)
  • ulcers or cancers of stomach and duodenum
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3
Q

What are the 1st and 2nd line drugs for oesophageal varices?

A
  • IV terlipressin
  • IV somatostatin (CI due to IHD)
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4
Q

What is the presentation of GI bleeds?

A
  • haematemesis
  • coffee ground vomit
  • melaenea
  • haemodynamic instability occurs in large blood loss and leads to low BP
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5
Q

How can you tell (from their bloods) if a patient is bleeding?

A
  • low Hb and high urea from breakdown products
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6
Q

How are upper GI bleeds investigated?

A
  • Bloods: Hb, urea, coagulation (INR, FBC), LFTs and crossmatch
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7
Q

How are upper GI bleeds managed (ABATEDO)?

A
  • ABCDE approach
  • Bloods
  • Access
  • Transfuse: blood, platelets, clotting factors, prothrombin
  • Endoscopy
  • Drugs
  • OGD to cauterise bleeds
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8
Q

What are some causes of intraluminal obstruction?

A
  • tumour: carcinoma or lymphoma
  • diaphragm disease
  • meconium ileus
  • gallstone ileus
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9
Q

What are some causes of intramural obstruction?

A
  • inflammatory: Crohn’s disease, diverticulitis
  • tumours
  • neural: Hirschsprung’s disease
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10
Q

What are the causes of extraluminal obstruction?

A
  • adhesions
  • volvulus: occurs in sigmoid colon as it’s not fixed
  • tumour
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11
Q

What is small bowel obstruction?

A
  • a mechanical blockage of the bowel
  • from within or outside the lumen
  • form of intestinal failure
  • inability of gut to absorb necessary water, macronutrients and electrolytes
  • requires IV supplementation or replacement
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12
Q

What is the aetiology of small bowel obstruction?

A
  • adhesions
  • hernia (bulges)
  • cancer
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13
Q

How do adhesions cause obstruction?

A
  • fibrous bands of scar tissue
  • cause kinking or squeezing of bowel
  • occurs due to surgery, peritonitis, infection or endometriosis
  • occurs in small bowel more than large
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14
Q

How do cancers cause obstruction?

A
  • primary tumours can be surgically removed
  • secondary difficult to remove and can encase bowel
  • local tumour or tumour spread
  • single or multilevel
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15
Q

How does bowel obstruction present?

A
  • green bilious vomiting
  • abdo distention
  • tinkling bowel sounds
  • constipation and lack of flatulence
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16
Q

How can you tell the difference between small and large bowel obstruction?

A
  • small presents with vomiting early on, before constipation
  • large presents with constipation and late onset vomiting
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17
Q

How do you take a history for small bowel obstruction?

A
  • colic
  • bloating/distention
  • sudden vs gradual onset
  • bilious vomiting
  • ask about previous surgery, last eat and drink
  • medical comorbidities
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18
Q

Which investigations are used for small bowel obstruction?

A
  • FBC: shows anaemia if cancer
  • U&E
  • Lactate raised - bowel ischaemia
  • X-ray: distended loops of bowel
  • metabolic alkalosis
  • CT: gold
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19
Q

Why is contrast CT useful for small bowel obstruction?

A
  • localises site of obstruction
  • indicates the cause
  • tells you if bowel is ischaemic and if intervention is required immediately
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20
Q

How is small bowel obstruction treated?

A
  • IV analgesia for pain
  • antiemetics
  • nutrition: may need parenteral feed
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21
Q

What is the most common complication of small bowel obstruction?

A
  • renal failure
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22
Q

What is the epithelium lining the oesophagus and the stomach?

A
  • oesophagus: squamous
  • stomach: columnar with glands covered with mucus
  • acid refluxed up into oesophagus kills squamous cells leading to gap at junction
  • leads to Barrett’s oesophagus
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23
Q

What is Gastro-oesophageal reflux disease?

A
  • dysfunction of the lower oesophageal sphincter
  • allows acid reflux
  • irritates sensitive squamous lining of oesophagus
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24
Q

How does GORD present?

A
  • heartburn: related to meals, lying down, strain
  • nocturnal asthma
  • acid/bile regurgitation
  • bloating
  • odynophagia (painful swallowing)
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25
Q

How is GORD investigated and what are the criteria?

A
  • endoscopy
  • over 55
  • symptoms lasting 4+ weeks
  • dysphagia
  • weight loss
  • indigestion despite treatment
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26
Q

What are the possible causes of GORD?

A
  • smoking
  • alcohol
  • hiatus hernia
  • pregnancy
  • obesity
  • big meals
  • tricyclics/anticholinergics/nitrates
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27
Q

What is the lifestyle advice given for GORD?

A
  • weight loss
  • small regular meals
  • avoid alcohol, hot drinks, eating before bed
  • stay upright after meals
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28
Q

How is GORD managed (drugs and surgery)?

A
  • antacids
  • alginates (Gaviscon)
  • PPIs: omeprazole, lansoprazole
  • surgery: laparoscopic fundoplication
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29
Q
  • Barrett’s oesophagus:
  • what is it
  • what is it a risk factor for
  • how is it treated?
A
  • metaplasia from squamous to columnar epithelium
  • premalignant RF for adenocarcinoma, monitored by endoscopy
  • treated by PPIs
  • ablation treatment (laser, cryotherapy) prevents progression to cancer
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30
Q

What are the typical characteristics of Crohn’s (NESTS)

A
  • No blood or mucus
  • Entire GI tract (mainly ileum)
  • Skip lesions: unaffected areas between active disease
  • Terminal ileum (and proximal colon) most affected with transmural inflammation
  • Smoking is a risk factor
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31
Q

What are the characteristics of ulcerative colitis (CLOSE)?

A
  • continuous inflammation
  • limited to colon and rectum
  • only superficial mucosa affected
  • smoking is protective
  • excreted blood and mucus
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32
Q

What is the pathophysiology of IBD?

A
  • develops as a result of environmental trigger in genetically susceptible individual
  • bacteria or dietary antigens taken up by M cells, pass through gap between cells
  • picked up by antigen presenting cells causing secretion of pro-inflammatory cytokines
  • activates T cells leading to inflammation
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33
Q

How does IBD present?

A
  • diarrhoea
  • abdominal pain
  • passing blood
  • weight loss
  • clubbing
  • erythema nodosum
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34
Q

What are some specific features of the presentation of ulcerative colitis?

A
  • blood and mucus with gradual onset of diarrhoea
  • bowel frequency related to severity of disease
  • crampy abdominal discomfort
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35
Q

How is IBD investigated?

A
  • bloods: anaemia, FBC, U&Es, cultures
  • CRP: inflammation and active disease
  • faecal calprotectin
  • endoscopy
  • imaging for complications
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36
Q

How is ulcerative colitis managed?

A

inducing remission:
- 1st line: aminosalocylate (mesalazine)
- 2nd line: corticosteroids: prednisolone
- hydrocortisone ± cyclosporin if severe
- maintaining remission: sulfasalazine, mesalazine
- surgery: can remove colon > ileostomy pouch

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37
Q

How is Crohn’s managed?

A
  • inducing remission: steroids: prednisolone
  • hydrocortisone if severe
  • maintaining remission: azathioprine, methotrexate
  • surgery: can resect distal ileum, strictures and fistulas
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38
Q

What is irritable bowel syndrome?

A
  • functional bowel disorder
  • symptoms resulting from abnormal functioning of bowel
  • due to disorders of gut motility or brain-gut axis
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39
Q

What are the symptoms of IBS?

A
  • fluctuating bowel habit: alternating constipation and diarrhoea
  • abdominal pain relieved by defecation
  • bloating
  • chronic and exacerbated by stress
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40
Q

How is IBS diagnosed?

A
  • exclusion: bloods, faecal calprotectin (IBD), anti-TTG (coeliac), colonoscopy
  • abdo pain + 2 symptoms
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41
Q

How is IBS managed?

A
  • try exclusion diets
  • reduced processed food, caffeine and alcohol
  • regular small meals and fluid
  • loperamide for diarrhoea
  • laxatives for constipation
  • tricyclic antidepressants, SSRIs
42
Q

What is the pathophysiology behind coeliac disease?

A
  • T-cell mediated: auto-antibodies created in response to gluten exposure, targeting epithelial cells
  • anti-tissue transglutaminase and anti-endomysial (IgA)
  • affects small bowel, particularly jejunum, causing villus atrophy and malabsorption
43
Q

How does coeliac disease present?

A
  • fatigue
  • diarrhoea
  • weigh loss
  • anaemia secondary to iron, B12, folate deficiency
  • dermatitis herpetiformis
  • failure to thrive (children)
44
Q

How is coeliac disease diagnosed and managed?

A
  • check IgA levels
  • raised anti-TTG or anti-endomysial
  • endoscopy: crypt hypertrophy and villous atrophy
  • management: lifelong gluten-free diet
45
Q

Which conditions is coeliac disease associated with?

A
  • T1DM
  • thyroid disease
  • autoimmune hepatitis
  • primary biliary cirrhosis, primary sclerosing cholangitis
  • HLA-DQ2 gene
46
Q

What is gastritis and what are the causes?

A
  • gastric mucosal inflammation
  • caused by H. pylori, NSAIDs, alcohol use, bile reflex, stress
47
Q

What are the symptoms of gastritis?

A
  • nausea, vomiting
  • loss of appetite
  • dyspepsia/epigastric discomfort
48
Q

How is gastritis investigated?

A
  • H. pylori urea breath test
  • H. pylori faecal antigen test
  • FBC
  • endoscopy
49
Q

What is the anatomy of the appendix and epidemiology of appendicitis?

A
  • small, thin tube arising from caecum, leads to dead end
  • located where 3 teniae coli meet
  • patients aged 10-20
50
Q

What is the pathophysiology behind appendicitis?

A
  • pathogens trapped due to obstruction where the appendix meets the bowel
  • trapped pathogens > infection + inflammation
  • can lead to gangrene and rupture > faeces and infectious material released into peritoneum
  • leads to peritonitis
51
Q

What is the presentation of appendicitis?

A
  • central abdo pain > R iliac fossa
  • tenderness at McBurney’s point on palpation
  • loss of appetite
  • guarding
  • rebound and percussion tenderness
52
Q

How is appendicitis diagnosed?

A
  • clinical presentation
  • raised inflammatory markers
  • CT/ultrasound
  • potential diagnostic laparoscopy
53
Q

What are the key differential diagnoses of appendicitis?

A
  • ovarian cysts
  • Meckel’s diverticulum
  • ectopic pregnancy (hCG to exclude)
54
Q

How is appendicitis managed?

A
  • appendectomy
  • laparoscopic surgery is ideal over open
55
Q

What is the pathophysiology behind peptic ulcers?

A
  • occurs from breakdown of protective mucosal layer or inc in stomach acid
  • broken down by medications, H, pylori
  • stomach acid inc by: stress, alcohol, caffeine, smoking, spicy food
  • duodenal more common than gastric
56
Q

How do peptic ulcers present?

A
  • epigastric discomfort/pain
  • nausea and vomiting
  • dyspepsia
  • coffee ground vomiting and melaena
  • iron deficiency anaemia
57
Q

How are peptic ulcers diagnosed and managed?

A
  • endoscopy and biopsy to exclude cancer
  • high dose PPIs
58
Q

What are the complications of peptic ulcers?

A
  • bleeding
  • perforation
  • scarring and strictures leading to pyloric stenosis
59
Q

What are the diverticula?

A
  • pouch or pocket in the bowel wall ranging between 0.5-1cm
  • diverticulosis: presence of diverticula without inflammation/infection
60
Q

What is the difference between diverticulosis, diverticular disease and diverticulitis?

A
  • diverticulosis: presence of diverticula without inflammation/infection
  • diverticular disease: when patients experience symptoms
  • diverticulitis: inflammation and infection of diverticula
61
Q

What is the pathophysiology behind diverticular disease?

A
  • small intestine contains circular muscle which is weaker in areas where it is penetrated by blood vessles
  • inc pressure in lumen over time causes gaps allowing mucosa to herniate and diverticula formation
  • diverticula don’t form in rectum due to teniae coli
  • lack of dietary fibre inc risk
62
Q

Describe diverticulosis (definition, causes)

A
  • wear and tear of bowel
  • mostly affects sigmoid colon
  • common with inc age, low fibre diet, obesity, NSAIDs
63
Q

How is diverticulosis diagnosed and managed?

A
  • colonoscopy or CT
  • advice: high fibre diet and weight loss
  • bulk forming laxatives, surgery if serious
  • avoid stimulant laxatives
64
Q

How does acute diverticulitis present?

A
  • pain in left iliac fossa
  • fever
  • diarrhoea, nausea, vomiting
  • rectal bleeding
  • raised inflammatory markers and WBC
65
Q

How is acute diverticulitis treated?

A
  • oral co-amoxiclav
  • analgesia
  • only clear liquids until symptoms improve
  • may need surgery
66
Q

What are the types of oesophageal cancer?

A
  • Adenocarcinoma: lower 1/3 of oesophagus, is associated with Barret’s oesophagus
  • squamous cell carcinoma: smoking, alcohol, hot fluids, upper 2/3 of oesophagus
67
Q

How does oesophageal cancer present?

A
  • lymphadenopathy
  • vocal cord paralysis
  • melaena
  • dysphagia, regurgitation, heartburn, hoarseness
68
Q

How is oesophageal cancer investigated and managed?

A
  • OGD and biopsy
  • chemotherapy/radiotherapy, surgery
69
Q

What are the types and causes of gastric carcinomas?

A
  • mostly adenocarcinomas
  • H. pylori
  • smoking
  • CDH-1 mutation
  • pernicious anaemia
70
Q

What is chronic mesenteric ischaemia?

A
  • caused by a lack of blood flow due to atherosclerosis through the mesenteric vessels resulting in ischaemia
71
Q

How does mesenteric ischaemia present?

A
  • central, colicky abdo pain after eating
  • weight loss due to food avoidance
  • abdo bruit on auscultation
72
Q

How is mesenteric ischaemia diagnosed and managed?

A
  • CT angiography
  • reduce modifiable risk factors
  • 2º prevention: statins, antiplatelets
  • revascularisation: endovascular procedure
73
Q

What is the pathophysiology behind acute mesenteric ischaemia?

A
  • rapid blockage in blood flow through superior mesenteric artery
  • caused by thrombus blocking blood flow
  • AF causes clot to travel LA > aorta > SMA
74
Q

How is acute mesenteric ischaemia diagnosed?

A
  • presentation with acute, non-specific abdo pain
  • contrast CT
  • metabolic acidosis and raised lactate levels
75
Q

What is ischaemic colitis?

A
  • most common ischaemic bowel disease
  • lack of blood flow to colon
  • splenic flexure most commonly affected
  • rectum is resistant due to dual supply from IMA and int iliac.
76
Q

What is the pathophysiology behind pancreatic cancer?

A
  • majority adenocarcinomas
  • mostly occur in head of pancreas
  • leads to obstructive jaundice
  • also presents with new onset or worsening T2DM
77
Q

What is the Whipple procedure?

A
  • pancreaticoduocenectomy
  • removal of: head of pancreas, pylorus of stomach, duodenum, gallbladder, bile duct, relevant lymph nodes
78
Q

What investigations can be done in pancreatic cancer?

A
  • staging CT (CT TAP)
  • CA 19-9: tumour marker: may be raised in pancreatic cancer
  • MCRP or ERCP
79
Q

What are the features of an abdominal wall hernia?

A
  • soft lump protruding from abdo wall
  • may be reducible or protrude on coughing
  • aching, pulling or dragging sensation
80
Q

What is a hiatus hernia?

A
  • herniation of stomach up through the diaphragm
  • contents of stomach reflux into oesophagus
81
Q

What are the symptoms of hiatus hernias?

A
  • heartburn
  • acid or food reflux
  • burping and bloating
  • halitosis
82
Q

How are hernias investigated?

A
  • CXR
  • CT
  • endoscopy
  • barium swallow
83
Q

What are the complications of hernias?

A
  1. incarceration: irreducible into proper position
  2. obstruction: causes blockage of passage of faeces through bowel
  3. strangulation: non-deductible and causes ischaemia of bowel
84
Q

What is the general management of hernias?

A
  • conservative management
  • tension-free repair: placing a mesh over the defect
  • tension repair: suturing muscle and tissue
85
Q

What is gastroenteritis?

A
  • inflammation from the stomach through to the intestines presenting with nausea, vomiting and diarrhoea
86
Q

What is an indirect inguinal hernia?

A
  • bowel herniates through inguinal canal
  • IIHs remain reduced when pressure is applied to the deep inguinal ring
87
Q

What is a direct inguinal hernia?

A
  • occurs due to weakness at Hesselbach’s triangle
  • boundaries: rectus abdominus (medial), inferior epigastric vessels (superior/lateral border), Poupart’s ligament
88
Q

What are the most common causes of viral gastroenteritis?

A
  • rotavirus
  • norovirus
  • adenovirus
89
Q

Which bacteria commonly causes gastroenteritis?

A
  • E. coli
  • campylobacter jejuni
  • shigella
  • bacillus cereus
90
Q

How does E. coli spread?

A
  • through infected faeces, unwashed salad, water
91
Q

What toxin does E. coli produce and what symptoms does this lead to?

A
  • shiga toxin
  • abdo cramps, bloody diarrhoea and vomiting
  • destroys blood cells > haemolytic uraemia syndrome
92
Q

What type of bacteria is campylobacter jejuni and how is it spread?

A
  • causes travellers diarrhoea
  • gram negative curved/spiral bacteria
  • raw/improperly cooked poultry, untreated water, unpasteurised milk
93
Q

What are the symptoms and treatment of campylobacter jejuni infection?

A
  • abdo cramps, bloody diarrhoea, vomiting, fever
  • azithromycin and ciprofloxacin
94
Q

How does shigella spread and what are the symptoms?

A
  • faeces contaminating drinking water, pools and food
  • abdo cramps, bloody diarrhoea, fever
  • shiga toxin > haemolytic uraemia syndrome
95
Q

How is salmonella spread and what are the symptoms?

A
  • raw eggs and poultry
  • water diarrhoea with mucus/blood, abdo pain and vomiting
96
Q

What type of bacteria is bacillus cereus and on what food is it produced?

A
  • gram positive rod
  • inadequately cooked food/food not immediately refrigerated
  • fried rice
97
Q

What toxin does bacillus cereus produce and what symptoms does it cause?

A
  • cereulide
  • abdo cramping, vomiting and water diarrhoea
98
Q

What is giardiasis, what are the symptoms and how is it treated?

A
  • Giardia lamblia is a microscopic parasite spread by faeco-oral transmission
  • can be asymptomatic or cause chronic diarrhoea
  • treated with metronidazole
99
Q

How is gastroenteritis managed?

A
  • isolation, barrier nursing, infection control
  • microscopy, culture and sensitivities
  • fluid challenge and rehydration
100
Q

What is the presentation of malabsorption?

A
  • diarrhoea
  • weight loss
  • lethargy
  • steatorrhoea
101
Q

What are the investigations for malabsorption?

A
  • FBC
  • dec Ca, Fe, B12, folate
  • Sudan for fat globules
102
Q

What is Meckel’s diverticulum?

A
  • congenital outpouching of small bowel
  • GI bleeding, obstructive symptoms
  • leads to volvulus and intussusception

Osha 2a (15 decks)

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