Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

4th Year Medicine 2 > Gastroenterology (Luminal) > Flashcards

Gastroenterology (Luminal) Flashcards

1
Q

Explain the features of crohns disease?

A
  • Inflammatory bowel disease that can affect any part of the GI tract from mouth to anus but most commonly affects the terminal ileum and colon
  • Inflammation is discontinuous and occurs in skip lesions
  • Inflammation is transmural meaning it extends down to the serosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Who gets crohns disease?

A
  • Crohn’s disease is thought to be an immune-mediated condition caused by environmental triggering events in genetically susceptible people
  • Risk factors include a family history of inflammatory bowel disease, smoking, previous infectious gastroenteritis, and drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presentation of crohns disease?

A
  • Depends on what part of the GI tract is affected
  • Persistent diarrhoea with potential blood or mucus in the stool
  • Abdominal pain and/ or discomfort
  • Weight loss and failure to thrive in children
  • Fatigue, malaise, anorexia or fever
  • On examination may have abdo tenderness, perianal pain or tenderness as well as perianal skin tags, abscesses, fissures or fistulas
  • May also see extra-intestinal manifestations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigations for crohns disease?

A
  • If suspected need referred to secondary care
  • Initial investigations include FBC, CRP, ESR, U and Es, LFTs, coeliac serology, stool culture and microscopy (inflammatory markers likely to be raised)
  • Check serum ferritin, vitamin B12, folate and vitamin D as there may be nutritional deficiencies
  • Check thyroid function to exclude hyperthyroidism
  • Faecal calprotectin and lactoferrin are usually raised in active inflammatory intestinal disease
  • Diagnosis generally needs biopsy from colonoscopy and/ or endoscopy
  • May be ASCA positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Management of crohns disease?

A
  • Give steroids to induce remission and manage flares
  • Azathioprine or mercaptopurine can be used to maintain remission
  • Anti-TNF e.g. infliximab and adalimumab are used in severe cases
  • Surgery for Crohns can be done but is not curative and need to minimise the amount of bowel removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Extra-intestinal manifestations of crohns and ulcerative colitis?

A
  • Enteropathic arthritis
  • Skin rashes – erythema nodosum, pyoderma gangrenosum, anal skin tags, enterocutaneous fistulas, anal fissures
  • Osteoporosis and osteomalacia (partially due to disease and also use of steroids)
  • Uveitis and episcleritis
  • Primary sclerosing cholangitis, gallstones, hepatitis, fatty liver disease
  • Anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Complications of crohns disease?

A
  • Abscesses
  • Strictures
  • Fistulas
  • Malnutrition and altered growth in children
  • Cancer of the small and large intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is ulcerative colitis and some features?

A
  • Inflammatory bowel disease confined to the colon and rectum, inflammation is continuous and moves from the rectum upwards
  • Can occur in the form of a proctitis (inflammation involving only the rectum), a left sided colitis (up to the splenic flexure), or as a pancolitis (the whole colon)
  • Inflammation only extends to the submucosa and there are no granulomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Who gets ulcerative colitis?

A
  • Thought to be autoimmune disease with environmental triggers in susceptibly genetic individuals
  • Smoking has actually been shown to be protective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Presentation of ulcerative colitis?

A
  • Bloody diarrhoea
  • Rectal bleeding
  • Faecal urgency or incontinence
  • Nocturnal defaecation
  • Tenesmus (feeling that you need to pass stools even though bowels are already empty)
  • Abdominal pain
  • Fatigue, weight loss, anorexia or fever
  • On examinations may find pallor, clubbing, abdominal distension, tenderness or mass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Investigations for ulcerative colitis?

A
  • May be PANCA positive
  • Initial investigations include FBC, CRP, ESR, U and Es, LFTs, coeliac serology, stool culture and microscopy (inflammatory markers likely to be raised)
  • Check serum ferritin, vitamin B12, folate and vitamin D as there may be nutritional deficiencies
  • Check thyroid function to exclude hyperthyroidism
  • Faecal calprotectin and lactoferrin are raised in active intestinal disease
  • Colonoscopy is usually done for diagnosis and biopsy taken
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Management of ulcerative colitis?

A
  • Aminosalicylates are first line for UC to induce and maintain remission e.g. mesalazine, delzicol, asacol HD, pentasa (can be topical first if not extensive disease then may convert to oral if not enough)
  • If remission still not achieved use steroid
  • Biologics and immunosuppressants can be used for severely active disease
  • Surgery can be done in severe disease and in UC this is curative and also eliminates the risk of colorectal cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Complications of ulcerative colitis?

A
  • Toxic megacolon
  • Increased risk of primary sclerosing cholangitis and developing cholangiocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

8 differences between crohns and UC?

A

Crohns
- disease anywhere mouth to anus
- occurs in skip lesions
- is transmural
- anal disease common
- granulomatous
-smoking aggravates
- surgery curative
- less increased risk of colorectal cancer

UC
- disease only in rectum and colon
-continuous inflammation from rectum up
- inflammation only to submucosa
- smoking is protective
- surgery is curative
- no granulomas
- PSC and cholangiocarcinoma as complication
- increased risk of colorectal cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is IBS?

A
  • Functional GI disorder
  • Characterised by abdominal discomfort, bloating or pain associated with defaecation or a change in bowel habit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Risk factors for IBS?

A
  • It is not fully understood but thought to be some motor/ sensory dysfunction in the GI tract or changes in gut reactivity
  • IBS is more common in middle aged women and is thought to be associated with emotional stimuli such as stress or abuse and is also linked to trauma
  • Sometimes has initial trigger of gastroenteritis
  • Related to other functional disorders e.g. fibromyalgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Presentation of IBS?

A
  • Abdominal pain and cramping
  • Generally pain is relieved by defaecating
  • Diarrhoea
  • Constipation
  • Food intolerance
  • Can be classified as IBS with diarrhoea, IBS with constipation or mixed IBS
  • Might get worse with stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diagnosis of IBS?

A

Need to exclude red flag symptoms for cancer:
* https://www.cancerreferral.scot.nhs.uk/lower-gastrointestinal-cancer/
* Bleeding – repeated rectal bleeding without an obvious anal cause or any blood mixed with stool
* Bowel habit – persistent (more than 4 weeks) change in bowel habit especially to looser stools (not so interested in constipation)
* Pain – abdominal pain with weight loss
* Iron deficiency anaemia – unexplained iron deficiency anaemia

Then need to exclude inflammatory bowel disease:

Tests:
* QFit to check for blood in stool (sign of IBD or cancer)
* FBC (checking for anaemia and signs of a systemic disease)
* ESR AND CRP (for IBD) and faecal calprotectin and lactoferrin
* TTG (for coeliacs)

If all these tests come back negative can diagnose IBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management of IBS?

A
  • Education and information on lifestyle, physical activity, diet and relaxation
  • Diet and nutritional advice – general advice such as reducing caffeine and sugary drinks, reducing high fibre foods and resistant starch (recooked foods have this), if going to recommend the FODMAP diet should refer to a dietician
  • Antispasmodic agents e.g. mebeverine hydrochloride, alverine citrate and peppermint oil
  • Laxatives can be used and titrated to effect for those with constipation
  • Loperamide can be used for acute diarrhoea
  • Tricyclics and SSRIs can be used for pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of antibody for coeliac disease?

A

IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is coeliac disease?

A
  • Condition in which there is inflammation of the mucosa of the small bowel (mainly duodenum) that improves when gluten is removed from the diet and relapses when gluten is reintroduced
  • Life long condition, not an allergy, it is T cell mediated, it is not antibody mediated
  • In the small bowel when consuming gluten there is inflammation resulting in villous atrophy, the villi become flat and surface area is lost meaning there is impaired absorption of nutrients
22
Q

Who gets coeliac disease?

A
  • Genetically predisposed people, triggered by exposure to gluten
  • Coeliac disease can develop at any age, cause is not fully understand but HLA-DQ2 and HLA-DQ8 are thought to be associated, does tend to run in families
  • Also more common in people with other autoimmune diseases e.g. type 1 diabetes, Addisons, autoimmune hepatitis, pernicious anaemia etc.
23
Q

List some foods that have gluten in them?

A
  • Gluten is in wheat, rye and barley
  • Bread
  • Cake
  • Pies
  • Cereal
  • Pasta and noodles
24
Q

List some foods that are gluten free?

A
  • Rice
  • Potato
  • Polenta
  • Quinoa
25
Q

Presentation of coeliac disease?

A
  • Diarrhoea
  • can be asymptomatic and picked up incidentally by testing
  • Steatorrhoea (increase in fat secretion in stools due to malabsorption of fat – stools are looser and paler)
  • Abdominal pain
  • Weight loss
  • In children may present with failure to thrive
  • Skin manifestation: dermatitis herpetiformis which is an itchy blistering rash which usually arises on the elbows and extensor surfaces (IgA mediated)
26
Q

Investigations for coeliac disease?

A
  • Duodenal biopsy would show villus atrophy and crypt hyperplasia
  • Biopsy was previously considered gold standard for diagnosis but seem to be moving to serological testing as accuracy is increasing
  • Main serological test is tissue transglutaminase IgA, only issue with this test is that person still has to be eating gluten for it to be accurate, other antibody is anti-EMA
27
Q

Management of coeliac disease?

A
  • Only effective treatment is long term adherence to gluten free diet
  • Selection of gluten free products can be prescribed on the NHS
28
Q

Complications of coeliac disease?

A
  • Vitamin deficiencies
  • Anaemia
  • Increased risk of T cell lymphomas and small bowel carcinomas
  • Risk of these is reduced if patient adheres to a gluten free diet
29
Q

What is important to note about tests for coeliacs?

A

they will only give a positive result if the person is still consuming gluten when they have them done

30
Q

Skin manifestation of coeliacs?

A

dermatitis herpetiformes - IgA mediated rash

31
Q

Biopsy for coeliacs would show?

A

villus atrophy and crypt hyperplasia

32
Q

What is GORD?

A
  • Most people have a degree of reflux but if acidic stomach contacts stay in contact with oesophagus for longer than normal, people may complain of symptoms of GORD
  • GORD is caused by combination of incompetent LOS, poor oesophageal clearance and visceral sensitivity (someone may be very sensitive to reflux and complain of severe symptoms but actually very little oesophagitis present)
33
Q

Risk factors/ who gets GORD?

A
  • Increased intra-abdominal pressure e.g. obesity or pregnancy
  • High fat diet
  • Caffeine
  • Alcohol
  • Smoking (nicotine relaxes sphincter)
  • Certain drugs can cause reflux such as antihistamines, steroid, CCBs, benzodiazepines and antidepressants
  • Some medical conditions increase risk: hiatal hernia (part of stomach has squeezed up into diaphragm), scleroderma, Zollinger-ellison syndrome (gastrin secreting tumours cause your stomach to secrete too much acid))
34
Q

Presentation of GORD?

A
  • Main symptom is heartburn (burning pain behind sternum), may also complain of regurgitation and odynophagia (due to oesophagitis)
  • If there is severe oesophagitis there can be scarring of the oesophagus which causes oesophageal stenosis and then patient may complain of dysphagia
  • If reflux is severe, it can cause chronic coughing and hoarseness
35
Q

Diagnosis of GORD?

A
  • Clinical diagnosis can be made without investigation but if red flag symptoms or uncertainty can do endoscopy
  • 24hr pH monitoring can be helpful to confirm diagnosis if not responding to treatment
  • Therapeutic trial – try PPIs – if they work it’s GORD
36
Q

Management of GORD?

A
  • PPIs (omeprazole) are best drug treatment as they both eliminate symptoms and heal oesophagitis
  • Take for 8 weeks, see if symptoms come back or if settles, if symptoms come back can start taking again
  • Patients should also be encouraged to make lifestyle changes e.g., lose weight and diet changes
  • Antacids and H2 antagonists can provide symptomatic relief
  • Those who are young and suitable can have surgery to help with GORD (Nissen fundoplication – wrap part of the gastric fundus around the LOS)
37
Q

Explain what Barretts oesophagus is and management?

A
  • Barretts is a complication of GORD where there is intestinal metaplasia- change from the normal squamous epithelium to columnar epithelium
  • Barretts increases risk of adenocarcinoma so those with it on endoscopy need lifelong PPI treatment and regular surveillance (made on case by case basis how much surveillance etc)
  • If Barretts appears dysplastic on endoscopic surveillance then may ablate it
38
Q

What is a peptic ulcer?

A
  • Peptic ulcer is a break in the mucosa of the stomach or duodenum
  • Gastric ulcers tend to occur on the lesser curvature of the stomach and duodenal ulcers tend to occur in the duodenal cap
39
Q

Who gets a peptic ulcer?

A
  • Majority are caused by H. pylori infection
  • H pylori is a gram negative bacillus, spread by faeco-oral route, infection usually occurs in infancy, majority of those infected have no pathology, small number develop peptic ulcers, an even smaller number go on to develop gastric cancer
  • NSAID induced peptic ulcers occur due to long term NSAID use as NSAIDs increase stomach acid secretion and inhibit prostaglandins which usually stimulate mucus production
40
Q

Presentation of peptic ulcer?

A
  • Patients usually present with burning epigastric pain that may get worse at night or when the patient is hungry
  • Classically gastric ulcers are worse when eating but those with duodenal ulcers experience less pain when eating
  • This is because as food passes into the stomach it will irritate an ulcer that is the stomach, however if the ulcer is in the duodenum eating is helpful because food has mopped up stomach acid meaning less acid passes to the duodenum
  • Iron deficiency anaemia due to chronic small amounts of bleeding
  • Could present acutely with life threatening haemorrhage or perforation
41
Q

Investigations for peptic ulcers?

A
  • Peptic ulcers need confirmed by endoscopy and biopsy
  • Patients then need tested for H. pylori using carbon-13 urea breath test or stool antigen test (test is not accurate if patient has been on antibiotics or PPIs)
42
Q

Management of peptic ulcers?

A
  • Everyone should get general advice e.g. avoid alcohol, caffeine and smoking
  • If positive for H. pylori and on NSAIDs, start off by stopping NSAIDs and going on a PPI for 2 months then give H. pylori eradication therapy
  • If not on PPI go straight onto H. pylori eradication therapy
  • Antibiotic therapy for H. pylori involves amoxicillin with either clarithromycin or metronidazole
43
Q

Complications of peptic ulcer?

A
  • GI bleed if ulcer erodes through an artery
  • Perforation if ulcer erodes whole way through causing peritonitis and sepsis
  • Gastric outlet obstruction if chronic and there is oedema or scarring
44
Q

Management of a peptic ulcer bleed?

A
  • If bleeding peptic ulcer usually do dual therapy with endoscopic injection of adrenaline to cause vasoconstriction and heater probe therapy, IV omeprazole reduces risk of re-bleeding, if can’t get bleeding under control may need open surgery
45
Q

4 causes of a upper GI bleed?

A

ruptured oesophageal varices, mallory-weiss tear, ulcers of stomach or duodenum, cancers of stomach or duodenum

46
Q

Presentation of upper GI bleed?

A
  • Presents with haematemesis (vomiting blood), coffee ground vomit (vomiting digested blood), melaena (tar like, black, greasy and offensive stool caused by digested blood), haemodynamic instability
  • Symptoms and signs relating to underlying pathology e.g. epigastric pain and dyspepsia (suggests ulcers or cancers), jaundice or ascites (if liver disease and varices)
47
Q

2 scoring systems for upper GI bleed?

A
  • Glasgow Blatchford score is a scoring system in suspected upper GI bleed – establishes risk that they have a bleed and allows a plan to be made
  • Rockall score is for patients that have had an endoscopy to calculate risk of rebleed
48
Q

Management of upper GI bleed?

A
  • ABATED – ABCDE, bloods, access (ideally 2 large bore cannulas), transfuse, endoscopy (arrange urgent within 24 hours), drugs (stop anticoagulants and NSAIDs)
  • Bloods that should be sent = FBC, U and Es, coagulation, LFTs and 2 units crossmatch
  • If oesophageal varices are suspected give terlipressin and prophylactic antibiotics
49
Q

What may be raised in upper GI bleed and why?

A

urea as breakdown product of blood in GI tract

50
Q

What is the most common site affected by crohns disease?

A

ileum

4th Year Medicine 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions