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MY PHASE 2A MEDICINE > GI > Flashcards

GI Flashcards

1
Q

Describe the distribution of inflammation seen in Crohn’s disease.

A

Patchy, granulomatous, transmural inflammation (can affect just the mucosa or go through the bowel wall).

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2
Q

Describe the distribution of inflammation seen in ulcerative colitis.

A

Continuous inflammation affecting only the mucosa.

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3
Q

Histologically, what part of the bowel wall is affected in ulcerative colitis?

A

Just the mucosa.

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4
Q

Histologically, what part of the bowel wall is affected in crohn’s disease?

A

Can affect just the mucosa or can go all the way through to the bowel wall -> transmural inflammation.

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5
Q

What is the treatment for UC?

A

5-Aminosalicylic acid (mesalazine) - Drug of choice for remission and relapse prevention. Surgical resection.

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6
Q

What is the treatment for crohn’s?

A

Stop smoking. Corticosteroids induce remission (but don’t prevent relapse). Thiopurines maintain remission (but have side effects) Azathioprine

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7
Q

State one histological feature that will be seen in ulcerative colitis.

A
  1. Crypt abscess.

2. Increase in plasma cells in the lamina propria.

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8
Q

Name 5 things that can break down the mucin layer in the stomach and cause gastritis.

A
  1. Not enough blood - mucosal ischaemia.
  2. H.pylori.
  3. Aspirin, NSAIDS.
  4. Increased acid - stress.
  5. Bile reflux - direct irritant.
  6. Alcohol.
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9
Q

What part of the bowel is commonly affected by Crohn’s disease?

A

Can affect anywhere from the mouth to anus.

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10
Q

What part of the bowel is commonly affected by ulcerative colitis?

A

It only affects the rectum. It spreads proximally but only affects the colon.

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11
Q

Give 5 complications of Crohn’s disease.

A
  1. Malabsorption.
  2. Fistula.
  3. Obstruction.
  4. Perforation.
  5. Anal fissures.
  6. Neoplasia.
  7. Amyloidosis (rare).
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12
Q

Give 5 complications of ulcerative colitis.

A
  1. Colon: blood loss and colorectal cancer.
  2. Arthritis.
  3. Iritis and episcleritis.
  4. Fatty liver and primary sclerosing cholangitis.
  5. Erythema nodosum.
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13
Q

Give 5 causes of diarrhoeal infection.

A
  1. Traveller’s diarrhoea.
  2. Viral e.g. rotavirus, norovirus.
  3. Bacterial e.g. E.coli.
  4. Parasites e.g. helminths.
  5. Nosocomial e.g. c.diff.
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14
Q

Give 3 causes of traveller’s diarrhoea.

A
  1. Enterotoxigenic e.coli (ETEC).
  2. Campylobacter.
  3. Norovirus.
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15
Q

Give 2 infective causes of non-bloody diarrhoea.

A
  1. Rotavirus.

2. Norovirus.

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16
Q

Give 3 ways in which diarrhoea can be prevented.

A
  1. Access to clean water.
  2. Good sanitation.
  3. Hand hygiene.
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17
Q

Name 5 antibiotics prone to causing c.diff infection.

A
  1. Ciprofloxacin.
  2. Co-amoxiclav.
  3. Clindamycin.
  4. Cephlasporins.
  5. Carbapenems.

RULE OF C’s!

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18
Q

Describe the treatment for c.diff infection.

A

Metronidazole and vancomyocin (PO).

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19
Q

Give 5 causes of non-diarrhoeal infection.

A
  1. Gastritis/peptic ulcer disease e.g. h.pylori.
  2. Acute cholecystitis.
  3. Peritonitis.
  4. Typhoid/paratyphoid.
  5. Amoebic liver disease.
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20
Q

What is the leading cause of diarrhoeal illness in young children?

A

Rotavirus.

There is a vaccine - rotarix.

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21
Q

Name a helminth responsible for causing diarrhoeal infection.

A

Schistosomiasis.

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22
Q

Why is c.diff highly infectious?

A

It is a spore forming bacteria.

Gram positive

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23
Q

What symptoms would Norovirus present with?

A

‘Winter vomiting’ -> VOMITING

- also diarrhoea, nausea, cramps headache, fever, chills, myalgia

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24
Q

How long does norovirus last for?

A

1-3 days

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25
Q

Where does norovirus occur?

A
  • schools
  • care homes
  • cruise ships
  • families
  • hospitals
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26
Q

Give 5 risk factors for c.diff infection.

A
  1. Increasing age.
  2. Co-morbidities.
  3. Antibiotic use.
  4. PPI.
  5. Long hospital stays.
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27
Q

What can helicobacter pylori infection cause?

A

H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation.
This can cause GASTRITIS; peptic ulcer disease and gastric cancer.

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28
Q

Describe h.pylori.

A

A gram negative bacilli with a flagellum.

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29
Q

Describe the treatment for H.pylori infection.

A

Triple therapy: 2 antibiotics and 1 PPI e.g.

Omeprazole, Clarithromyocin and Amoxicillin.

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30
Q

What is gastritis?

A

Inflammation of the gastric mucosa, can be acute or chronic

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31
Q

What symptoms are associated with gastritis?

A

Mostly asymptomatic but can present with functional dyspepsia

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32
Q

How would you detect the presence of H Pylori?

A
  • endoscopy see peptic ulcers
  • urea breath test
  • serology
  • stool antigen test
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33
Q

What are risk factors for infective diarrhoea?

A

Foreign travel
poor hygiene
overcrowding
new or different foods

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34
Q

What are the common causes of infective diarrhoea?

A
  1. Usually viral: rotavirus (children), norovirus, adenovirus
  2. Sometimes bacterial: Campylobacter jejuni, E.coli, Salmonella, Shigella
  3. Occasionally parasitic: Giardia lamblia, cryptosporidium
  4. Abx Associated (C diff): clindamycin, ciprofloxacin, coamoxiclav, cephalosporins
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35
Q

What are the common presentations of infective diarrhoea?

A
  • Blood suggests bacteria

- May also experience vomiting, fever, fatigue, headache and muscle pains

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36
Q

Describe the chain of infection

A

Reservoir -> agent -> transmission -> host -> person to person spread.

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37
Q

Give 4 groups at risk of diarrhoeal infection.

A
  1. Food handlers.
  2. Health care workers.
  3. Children who attend nursery.
  4. Persons of doubtful personal hygiene.
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38
Q

Give 3 causes of peptic ulcer

A
  1. Prolonged NSAID use -> decreased mucin production.
  2. H.pylori infection.
  3. Hyper-acidity.
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39
Q

Give 3 symptoms of peptic ulcers.

A

Often acute onset of symptoms:

  1. Pain.
  2. Bleeding.
  3. Perforation.
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40
Q

What investigations might you do in someone who you suspect to have peptic ulcers?

A
  1. H.pylori test e.g. urease breath test and faecal antigen test.
  2. Gastroscopy.
  3. Barium meal.
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41
Q

Give 3 treatments for peptic ulcers.

A
  1. Stop NSAIDS.
  2. PPI’s e.g. omeprazole.
  3. H.pylori eradication.
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42
Q

What is dysentry?

A
  1. Intestinal inflammation, primarily of the colon.
  2. It can lead to mild or severe stomach cramps
  3. Severe diarrhoea with mucus or blood in the faeces
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43
Q

Name the 3 broad categories that describe the causes of intestinal obstruction.

A
  1. Blockage.
  2. Contraction.
  3. Pressure.
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44
Q

Intestinal obstruction: give 3 causes of blockage.

A
  1. Tumour.
  2. Diaphragm disease.
  3. Gallstones in ileum (rare).
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45
Q

Intestinal obstruction: what is thought to cause diaphragm disease?

A

NSAIDS.

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46
Q

Intestinal obstruction: give 3 causes of contraction.

A
  1. Inflammation.
  2. Intramural tumours.
  3. Hirschprung’s disease.
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47
Q

Describe how Crohn’s disease can cause intestinal obstruction.

A

Crohn’s disease -> fibrosis -> contraction -> obstruction.

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48
Q

Describe how Diverticular disease can cause intestinal obstruction.

A

Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction.

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49
Q

What is Hirschprung’s disease?

A

A congenital condition where there is a lack of nerves in the bowel and so motility is affected. This leads to obstruction and gross dilatation of the bowel.

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50
Q

Intestinal obstruction: give 3 causes of pressure.

A
  1. Adhesions.
  2. Volvulus.
  3. Peritoneal tumour.
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51
Q

Intestinal obstruction: what are adhesions?

A

Adhesions often form secondary to abdominal surgery. Loops of bowel stick together and the bowel is pulled and distorted. 40% of intestinal obstructions are due to adhesions.

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52
Q

Intestinal obstruction: what causes adhesions?

A

Adhesions often form secondary to abdominal surgery.

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53
Q

Intestinal obstruction: what is volvulus?

A

Volvulus is a twist/rotation in the bowel; closed loop obstruction. There is a risk of necrosis.

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54
Q

Intestinal obstruction: which areas of the bowel are most likely to be affected by volvulus?

A

Volvulus occurs in free floating areas of the bowel e.g. bowel with mesentery. The sigmoid colon has a long mesentery and so can twist on itself.

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55
Q

Give 4 common causes of small bowel obstruction in adults.

A
  1. Adhesions.
  2. Hernias.
  3. Crohn’s disease.
  4. Malignancy.
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56
Q

Which is more common: small bowel obstruction or large bowel obstruction?

A

Small bowel obstruction is more common; it makes up 75% of intestinal obstruction.

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57
Q

Give 3 common causes of small bowel obstruction in children.

A
  1. Appendicitis.
  2. Volvulus.
  3. Intussusception.
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58
Q

Intestinal obstruction: what is intussusception?

A

Intussusception is when part of the intestine invaginates into another section of the intestine -> telescoping. It is caused by force in-balances.

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59
Q

What are the four cardinal symptoms of bowel obstruction?

A
  1. Nausea/ Vomiting
  2. Absolute constipation
  3. Abdominal Distention
  4. Abdominal Pain (colociky/constant).
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60
Q

What would you hear on auscultation with a patient with intestinal obstruction?

A

Tinkling bowel sounds

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61
Q

If the obstruction is in the
a) small bowel
b) large bowel
what is it most likely to be due to?

A

a) small bowel - adhesions (75%)

b) large bowel - malignancies (60%)

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62
Q

Give 5 symptoms of small bowel obstruction

A
  1. Vomiting.
  2. Pain.
  3. Constipation.
  4. Distension.
  5. Tenderness.
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63
Q

Would dilatation, distension and increased secretions be seen proximal or distal to an intestinal obstruction?

A

Proximal.

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64
Q

Give 4 signs of small bowel obstruction.

A
  1. Vital signs e.g. increased HR, hypotension, raised temperature.
  2. Tenderness and swelling.
  3. Resonance.
  4. Bowel sounds.
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65
Q

What investigations might you do in someone who you suspect to have a small bowel obstruction?

A
  1. Take a good history - ask about previous surgery (adhesions)!
  2. FBC, U+E, lactate.
  3. X-ray.
  4. CT, ultrasound, MRI.
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66
Q

What is the management/treatment for small bowel obstruction?

A
  1. Fluid resuscitation.
  2. Bowel decompression.
  3. Analgesia and anti-emetics.
  4. Antibiotics.
  5. Surgery e.g. laparotomy, bypass segment, resection.
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67
Q

Give 2 common causes of large bowel obstruction.

A
  1. Colorectal malignancy.

2. Volvulus (especially in the developing world).

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68
Q

Give 5 symptoms of large bowel obstruction.

A
  1. Tenesmus.
  2. Constipation.
  3. Abdominal discomfort.
  4. Bloating.
  5. Vomiting.
  6. Weight loss.
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69
Q

What investigations might you do in someone who you suspect to have a large bowel obstruction?

A
  1. Digital rectal examination.
  2. Sigmoidoscopy.
  3. Plain X-ray.
  4. CT scan.
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70
Q

Describe the management for a large bowel obstruction.

A
  1. Fast the patient.
  2. Supplement O2.
  3. IV fluids to replace losses and correct electrolyte imbalance.
  4. Urinary catheterisation to monitor urine output.
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71
Q

Give 3 consequences of untreated intestinal obstructions.

A
  1. Ischaemia.
  2. Necrosis.
  3. Perforation.
72
Q

Give 2 indications for the need of immediate surgical intervention in someone with a small bowel obstruction.

A
  1. Signs of perforation (peritonitis).

2. Signs of strangulation.

73
Q

Describe the pathophysiology of coeliac disease.

A
  1. Gliadin binds to secretory IgA in the mucosal membrane
  2. The gliadin-IgA is transcytosed to the lamina propia
    Gliadin binds to tissue TransGlutamase and is deaminated
  3. Deaminated gliadin is taken up by macrophages and expressed on MHC2
  4. T helper cells release inflammatory cytokines and stimulate B cells
  5. This causes gut damage.
74
Q

What is alpha gliadin?

A

The toxic portion of gluten

75
Q

What is coeliac disease?

A

An immune-mediated, inflammatory systemic disorder provoked by gluten which can lead to malabsorption of nutrients

76
Q

What are the clincial features of coeliac disease?

A
  1. Weight Loss
  2. Chronic Diarrhoea
  3. Malabsorption
  4. Abdo Pain
  5. Steatorrhoea
  6. Dermatitis Herpetiformes
77
Q

What investigations might you do in someone who you suspect to have coeliac disease?

A
  1. Serology - look for auto-antibodies - TTG and EMA.

2. Gastroscopy - duodenal biopsies.

78
Q

Name the break down product of gluten that can trigger coeliac disease

A

Gliadin

79
Q

What part of the small intestine is mainly affected by coeliac disease?

A

Duodenum

80
Q

What disorders might be associated with coeliac disease?

A

Other autoimmune disorders:

  1. T1 diabetes.
  2. Thyroxoicosis.
  3. Hypothyroidism.
  4. Addisons disease.

Osteoporosis is also commonly seen in people with coeliac disease.

81
Q

What is the prevalence of coeliac disease?

A

1%

82
Q

What 3 histological features are needed in order to make a diagnosis of coeliac disease?

A
  1. Raised intraepithelial lymphocytes.
  2. Crypt hyperplasia.
  3. Villous atrophy.
83
Q

In someone with coeliac disease, what are they most likely to be deficient in - iron, folate, or B12?

A

Iron.

Coeliac disease mainly affects the duodenum and iron is absorbed in the duodenum. Folate is absorbed in the jejunum and B12 in the terminal ileum.

84
Q

Give 5 broad causes of malabsorption

A
  1. Defective intra-luminal digestion.
  2. Insufficient absorptive area.
  3. Lack of digestive enzymes.
  4. Defective epithelial transport.
  5. Lymphatic obstruction.
85
Q

Malabsorption: what can cause defective intra-luminal digestion?

A
  1. Pancreatic insufficiency due to pancreatitis, CF. There is a lack of digestive enzymes.
  2. Defective bile secretion due to biliary obstruction or ileal resection.
  3. Bacterial overgrowth.
86
Q

Why can pancreatitis cause malabsorption?

A

Pancreatitis results in pancreatic insufficiency and so a lack of pancreatic digestive enzymes. There is defective intra-luminal digestion which leads to malabsorption.

87
Q

Malabsorption: what can cause insufficient absorptive area?

A
  1. Coeliac disease.
  2. Crohn’s disease.
  3. Extensive parasitisation.
  4. Small intestine resection
88
Q

Malabsorption: give an example of when there is a lack of digestive enzymes.

A

Lactose intolerance - disaccharide enzyme deficiency.

89
Q

Malabsorption: what can cause lymphatic obstruction?

A
  1. Lymphoma.

2. TB.

90
Q

Describe the progression from normal epithelium to colorectal cancer.

A
  1. Normal epithelium.
  2. Adenoma.
  3. Colorectal adenocarcinoma.
  4. Metastatic colorectal adenocarcinoma.
91
Q

Define adenocarcinoma.

A

A malignant tumour of glandular epithelium.

92
Q

What is familial adenomatous polyposis?

A

Auto dominant condition where you develop thousands of polyps in your teens

93
Q

Describe the pathophysiology of Hereditary nonpolyposis colorectal cancer (HNPCC)

A

There are no DNA repair proteins meaning there is a risk of colon cancer and endometrial cancers.

94
Q

How can adenoma formation be prevented?

A

NSAIDS are believed to prevent adenoma formation.

95
Q

What is the Amsterdam criteria?

A

Used to identify which families have HNPCC
3:2:1 RULE
3 first degree relatives over
2 or more generations with
1 under 50 years of age
affecred with COLORECTAL/ENDOMETRIAL cancer

96
Q

How is FAP managed?

A

Prophylactic resection offered

97
Q

Give 5 risk factors for colorectal cancer.

A
  1. Low fibre diet.
  2. Diet high in red meat.
  3. Alcohol.
  4. Smoking.
  5. A PMH of adenoma or ulcerative colitis.
  6. A family history of colorectal cancer; FAP or HNPCC.
98
Q

What can affect the clinical presentation of a colorectal cancer?

A

How close the cancer is to the rectum affects its clinical presentation.

99
Q

Give 3 reasons why bowel cancer survival has increased over recent years.

A
  1. Introduction of the bowel cancer screening programme.
  2. Colonoscopic techniques.
  3. Improvements in treatment options.
100
Q

Give 5 symptoms of bowel cancer

A
  1. Diarrhoea
  2. Constipation
  3. Alternating bowel habit
  4. blood PR
  5. A mass
101
Q

Give 5 signs of bowel cancer

A
  1. Anaemia
  2. a mass
  3. Weight loss.
  4. Jaundice + Hepatomegaly (Mets)
  5. DVT
  6. Signs of shock if perf.
102
Q

What investigations would you carry out on a Pt with suspected CA bowel?

A

Colonoscopy, biopsy and histology are gold standard.
CT used in staging (DUKES/TNM).

Grading is 1-3. 1= Well differentiated. 3=Poorly differentiated

103
Q

What cells normally line the oesophagus?

A

Stratified squamous non-keratinising cells.

104
Q

What is Barrett’s oesophagus?

A

When squamous cells undergo metaplastic changes and become columnar cells.

105
Q

What can cause Barrett’s oesophagus?

A
  1. GORD.

2. Obesity.

106
Q

Give a potential consequence of Barrett’s oesophagus.

A

Adenocarcinoma.

107
Q

Describe how Barrett’s oesophagus can lead to oesophageal adenocarcinoma.

A
  1. GORD damages normal oesophageal squamous cells.
  2. Glandular columnar epithelial cells replace squamous cells (metaplasia).
  3. Continuing reflux leads to dysplastic oesophageal glandular epithelium.
  4. Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
108
Q

Give 3 causes of squamous cell carcinoma.

A
  1. Smoking.
  2. Alcohol.
  3. Poor diet.
109
Q

What can cause oesophageal adenocarcinoma?

A

Barrett’s oesophagus.

110
Q

Give 3 causes of gastric cancer.

A
  1. Smoked foods.
  2. Pickles.
  3. H.pylori infection.
  4. Pernicious anaemia.
111
Q

Describe how gastric cancer can develop from normal gastric mucosa.

A
  1. Smoked/pickled food diet leads to intestinal metaplasia of the normal gastric mucosa.
  2. Several genetic changes lead to dysplasia and then eventually intra-mucosal and invasive carcinoma.
112
Q

Give 3 causes of oesophageal carcinoma.

A
  1. GORD -> Barrett’s.
  2. Smoking.
  3. Alcohol.
113
Q

What investigations might you do in someone who you suspect to have oesophageal carcinoma?

A
  1. Barium swallow.

2. Endoscopy.

114
Q

Describe the 2 treatment options for oesophageal cancer.

A
  1. Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery.
  2. Medically unfit and metastases = palliative care. Stents can help with dysphagia.
115
Q

Give 3 signs of gastric cancer.

A
  1. Weight loss.
  2. Anaemia.
  3. Vomiting blood.
  4. Melaena.
  5. Dyspepsia.
116
Q

A mutation in what gene can cause familial diffuse gastric cancer?

A

CDH1 - 80% chance of gastric cancer.

Prophylactic gastrectomy is done in these patients.

117
Q

What investigations might you do in someone who you suspect has gastric cancer?

A
  1. Endoscopy.
  2. CT.
  3. Laparoscopy.
118
Q

What is the advantage of doing a laparoscopy in someone with gastric cancer?

A

It can detect metastatic disease that may not be detected on ultrasound/endoscopy.

119
Q

What is the treatment for proximal gastric cancers that have no spread?

A
  1. 3 cycles of chemo
  2. Full gastrectomy.
  3. Lymph node removal
120
Q

What is the treatment for distal gastric cancers that have no spread?

A
  1. 3 cycles of chemo
  2. Partial gastrectomy if the tumour is causing stenosis or bleeding.
  3. Lymph node removal
121
Q

What vitamin supplement will a patient need following gastrectomy?

A

They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia.

122
Q

What S and S would receive a 2 week wait referral for upper GI cancer?

A
  1. Dysphagia or
  2. Age >55 with weight loss and any of:
    • Upper abdo pain
    • Reflux
    • Dyspepsia
123
Q

Upper GI cancer: What S&S would require a non-urgent endoscopy?

A
  1. Haematemesis
  2. > 55 with any of:
    • Treatment-resistant Dyspepsia
    • Upper abdo pain+ anaemia
    • Raised platelets + sx of GI Ca
    • N/V + Sx GI Ca
124
Q

What is the criteria for dyspepsia?

A

> 1 of the following:

  • Postprandial fullness.
  • Early satiation.
  • Epigastric pain/burning.
125
Q

Give 5 causes of dyspepsia.

A
  1. Excess acid.
  2. Prolonged NSAIDS.
  3. Large volume meals.
  4. Obesity.
  5. Smoking/alcohol.
  6. Pregnancy.
126
Q

Give 5 red flag symptoms that you might detect when taking a history from someone with dyspepsia.

A
  1. Unexplained weight loss.
  2. Anaemia.
  3. Dysphagia.
  4. Upper abdominal mass.
  5. Persistent vomiting.
127
Q

What investigations might you do in someone with dyspepsia?

A
  1. Endoscopy.
  2. Gastroscopy.
  3. Barium swallow.
  4. Capsule endoscopy.
128
Q

What is the management for dyspepsia if the red flag criteria has been met?

A
  1. Suspend NSAID use and review medication.
  2. Endoscopy.
  3. Refer malignancy to specialist.
129
Q

What is the management for dyspepsia without red flag symptoms?

A
  1. Review medication.
  2. Lifestyle advice.
  3. Full dose PPI for 1 month.
  4. Test and treat h.pylori infection
130
Q

What kind of lifestyle advice might you give to someone with dyspepsia?

A
  1. Lose weight.
  2. Stop smoking.
  3. Cut down alcohol.
  4. Dietary modification.
131
Q

Describe the treatment for GORD.

A
  1. PPI.
  2. Lifestyle modification.
  3. Anti-reflux surgery.
132
Q

What is GORD?

A

Prolonged or recurrent reflux of the gastric contents into the oesophagus

133
Q

Give a potential consequence of anterior ulcer haemorrhage.

A

Acute peritonitis.

134
Q

Give a potential consequence of posterior ulcer haemorrhage.

A

Pancreatitis.

135
Q

What are RF for GORD?

A
  1. Being male
  2. Smoking
  3. Hiatus hernia
  4. Increased abdominal pressure (pregnancy, obesity)
136
Q

Give an example of a PPI and how it works.

A

Lanzoprazole

PPIs inhibit gastric hydrogen release, preventing production of gastric acid

137
Q

What is ascites?

A

An accumulation of fluid in the peritoneal cavity that leads to abdominal distension.

138
Q

Give 4 pathophysiological causes of ascites and an example for each.

A
  1. Local inflammation e.g. peritonitis.
  2. Leaky vessels e.g. imbalance between hydrostatic and oncotic pressures.
  3. Low flow e.g. CIRRHOSIS (main cause), thrombosis, cardiac failure.
  4. Low protein e.g. hypoalbuminaemia
139
Q

Describe the pathogenesis of ascites.

A
  1. Increased intra-hepatic resistance leads to portal hypertension -> ascites.
  2. Systemic vasodilation leads to secretion of RAAS, NAd and ADH -> fluid retention.
  3. Low serum albumin also leads to ascites.
140
Q

What can cause ascites?

A
  1. Haemorrhoids
  2. Cholangiocarcinoma
  3. Alcoholic Liver Disease
  4. Liver failure
  5. Hepatocellular carcinoma
141
Q

What is peritonitis?

A
  • Inflammation of the peritoneum due to infection

- as a result of entry of blood, air, bacteria or GI contents (Faeces or bile)

142
Q

What are the symptoms of peritonitis?

A
  1. Dull pain that becomes sharp
  2. Pain worse on coughing/moving
  3. Tenderness
  4. Systemic symptoms e.g. RIGOR, fever, nausea
143
Q

What are the causes of peritonitis?

A

A - Appendicitis: umbilicus to RIF pain
E - Ectopic Pregnancy: low abdo pain, sudden onset, tachycardia, low bp
I - Infection with TB/perforated organ
O - Obstruction: colicky pain, history of abdominal surgery
U - Ulcer: epigastric pain radiating to shoulder

Peritoneal Dialysis

144
Q

Name a bacteria that can cause spontaneous bacterial peritonitis.

A
  1. E.coli.

2. S.pneumoniae.

145
Q

How can spontaneous bacterial peritonitis be diagnosed?

A

By looking for the presence of neutrophils in ascitic fluid.

146
Q

What investigations would you carry out on a patient with suspected peritonitis?

A
  1. Clinical examination: rigid and guarding, laying still
  2. AXR: dilated bowel, flat fluid level, gas under diaphragm
  3. Bloods: FBCs, U&Es, LFTs, clotting
  4. Ascitic Tap: high neutrophil count
147
Q

What complication should you be cautious of in a patient with peritonitis?

A

SEPSIS

peritoneum is thin, has a large SA and is well drained by lymphatics. Suspect Sepsis if bp is low

148
Q

What is the management for ascites?

A
  1. Treat underlying cause
  2. Consider diuretics/ salt&fluid restriction
  3. Paracentesis
  4. Portosystemic shunt
149
Q

Describe the treatment for spontaneous bacterial peritonitis.

A

Cefotaxime and metronidazole.

150
Q

Give 5 symptoms of ruptured varices.

A
  1. Haematemesis.
  2. Melaena.
  3. Abdominal pain.
  4. Dysphagia.
  5. Anaemia.
151
Q

What are causes of haematemesis?

A
  1. Mallory-Weiss tear
  2. Severe GORD
  3. Oesophageal varices (often caused by ALD)
  4. Peptic ulcer
152
Q

Portal hypertension can lead to varices. Explain why.

A
  1. Obstruction to portal blood flow e.g. cirrhosis leads to portal hypertension.
  2. When the portal venous pressure rises above 10 mmHg the sites of portosystemic anastomoses dilate.
  3. It also causes splenomegaly.
153
Q

How would you manage a patient with haematemesis?

A
  1. Identify cause on clinical history/endoscopy
  2. Resuscitate
  3. Maintain airway
  4. Treat shock/ underlying cause
154
Q

On clinical presentation how could you tell the difference between a gastric and duodenal ulcer?

A 
Gastric = acute/ weight loss/ afraid to eat/ vomiting
Duodenal = pain relieved by eating/ can take weeks to present
155
Q

How would you treat a patient with H Pylori -ve peptic ulcers?

A
  1. STOP NSAIDS
  2. PPI (lanzoprasole)
  3. H2 blocker (ranitidine)
156
Q

What is appendicitis?

A

Inflammation of the appendix

157
Q

What is the pathophysiology of appendicitis?

A
  1. Obstruction of lumen causes gut flora to invade appendix wall
  2. Appendix becomes inflamed and infected
  3. If appendix ruptures it can lead to peritonitis
158
Q

What are the presenting features of appendicitis?

A
  1. Pain: umbilicus -> right iliac fossa,
    - Tender with guarding
  2. General: Nausea, localised tenderness, diarrhoea/constipation, pyrexia
159
Q

What investigations would you carry out on a suspected appendicitis?

A
  1. Inflammatory markers raised but not specific

2. CT = GOLD STANDARD

160
Q

What is acute pancreatitis?

A

An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase).

161
Q

What are the 3 different types of acute pancreatitis?

A
  1. 70% are oedematous; acute fluid collection.
  2. 25% are necrotising.
  3. 5% are hemorrhagic.
162
Q

Give the causes of acute pancreatitis.

A

Idiopathic

Gall stones
Ethanol abuse
Trauma

Steroids
Mumps
Auto-immune
Scorpion sting
Hypertriglycerides/hypercalcaemia
ERCP
Drugs
163
Q

What are the presenting symptoms of acute pancreatitis?

A
  1. Epigastric pain radiating to back
  2. Relieved by sitting forward
  3. Guarding and rigidity
  4. Nausea and vomiting
  5. Jaundice
164
Q

What are the two distinctive signs of acute pancreatitis?

A

Cullen’s sign - periumbilical bruising

Grey Turner’s sign - flank bruising

165
Q

How can acute pancreatitis be diagnosed?

A

Pancreatitis is diagnosed on the basis of 2 out of 3 of the following:

  1. Characteristic severe epigastric pain radiating to the back.
  2. Raised serum amylase.
  3. Abdominal CT scan pathology.
166
Q

Name a scoring system that can be used a prognostic tool in acute pancreatitis.

A

The abbreviated glasgow scoring system.

167
Q

What 8 points make up the glasgow scoring system?

A 
PaO2 < 8kPa.
Age > 55 years. 
Neutrophils > 15x10^9. 
Calcium < 2mmol/L. 
Raised urea > 15mmol/L. 
Elevated enzymes. 
Albumin < 32g/L. 
Sugar - serum glucose > 15mmol/L.
168
Q

Describe the treatment for acute pancreatitis.

A
  1. ANALGESIA!
  2. Catheterise and ABC approach for shock patients.
  3. Drainage of oedematous fluid collections.
  4. Antibiotics.
  5. Nutrition.
  6. Bowel rest.
169
Q

Give 2 potential complications of acute pancreatitis.

A
  1. Systemic inflammatory response syndrome.

2. Multiple organ dysfunction.

170
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas leads to irreversible damage.

171
Q

Describe the pathogenesis of chronic pancreatitis.

A

The pathogenesis is not fully understood but the current theory is that pancreatic duct obstruction leads to activation of pancreatic enzymes -> necrosis -> fibrosis.

172
Q

Describe how alcohol can cause chronic pancreatitis.

A

Alcohol -> proteins precipitate in the ductal structure of the pancreas (obstruction) -> pancreatic fibrosis.

173
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

A

IgG4.

174
Q

How is autoimmune chronic pancreatitis treated?

A

It is very steroid responsive.

175
Q

Give 5 symptoms of chronic pancreatitis.

A
  1. Severe abdominal pain.
  2. Epigastric pain radiating to the back.
  3. Nausea, vomiting.
  4. Decreased appetite.
  5. Exocrine/endocrine dysfunction.
176
Q

A sign of chronic pancreatitis is exocrine dysfunction. What can be a consequence of this?

A
  1. Malabsorption.
  2. Weight loss.
  3. Diarrhoea.
  4. Steatorrhoea.
177
Q

A sign of chronic pancreatitis is endocrine dysfunction. What can be a consequence of this?

A

DM

MY PHASE 2A MEDICINE (14 decks)

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