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Sandra Phase 2a > GI > Flashcards

GI Flashcards

1
Q

What is an inflammatory bowel disease?

A

Inflammatory Bowel Disease: Autoimmune-mediated intestinal inflammation primarily due to either Crohn’s disease or ulcerative colitis.

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2
Q

What are the 2 types of inflammatory bowel disease

A
  • Crohn’s
  • Ulcerative colitis
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3
Q

Risk Factors for IBD

A
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4
Q

Signs and symtpoms for IBD

A
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5
Q

Differential diagnosis for IBD

A
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6
Q

Investigations for IBD

A
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7
Q

Pathology for IBD

A
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8
Q

Management of IBD

A
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9
Q

Complications and Prognosis of IBD

A
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10
Q

What is irritable bowel syndrome

A

Functional Disorder where there is recurrent abdominal pain + abnormal bowel motility causing constipation and/or diarrhoea

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11
Q

Symptoms of Irritable Bowel Syndrome

A

Abdominal pain, Bloating and Change in bowel habit are classic features of irritable bowel syndrome

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12
Q

Risk Factors for IBS

A
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13
Q

Differential diagnosis of IBS

A

Coeliac Disease
Lactose Intolerance
Inflammatory Bowel Disease - Crohn’s Disease or Ulcerative Collitis
Infective Colitis
Lymphocytic Collagenous Colitis
Colon cancer
Drug effects (e.g. Proton Pump Inhibitors, NSAIDS, metformin)
Choledocholithiasis

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14
Q

Investigations for IBS

A
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15
Q

Pathophysiology of IBS

A

The pathophysiology of IBS is unclear. There are no specific anatomical, endoscopic, microbiological or histological findings that indicate a clear pathophysiology.

According to current understanding, IBS arises due to multiple factors that contribute to alteration of:

The Brain-gut axis: Bidirectional communication between the brain and the GIT. Involves the ANS, the neuroendocrine system and neuroimmune pathways
Gut sensitivity: Sensation of the GIT.
Gut reactivity: Mobility and secretion of the GIT.
Psychological functioning

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16
Q

Treatment for IBS

A

Only a fraction of patients with IBS-like symptoms (∼50%) seek medical care

Education and reassurance
Dietary alterations
Pharmacotherapy
Behavioural and psychological therapy

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17
Q

What is coeliac disease

A

Inflammatory process which occurs in susceptible individuals in response to ingestion of wheat protein (gluten-gliaden)

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18
Q

Small Intestine: Anatomy and Physiology

A

-

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19
Q

Risk Factor for coeliac disease

A

Family history
IgA deficiency
Type 1 diabetes
Autoimmune diseases - autoimmune thyroid, Sjogren’s syndrome, Addison’s disease
Inflammatory Bowel disease
Genetic disorder - Down’s syndrome, Turners syndrome

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20
Q

Clinical Presentation of coeliac disease

A

A 30-year-old woman presents with foul smelling oily diarrhoea, abdominal bloating, fatigue and weight loss. On examination she has papulovesicular lesions on the extensor aspects of her arms - coeliac disease

Splenic atrophy may occur in coeliac disease together with the appearance of Howell-Jolly bodies in erythrocytes

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21
Q

Differential diagnosis for coeliac disease

A

Childhood other food-sensitive enteropathies (milk sensitivity)

Adults

Lymphoma
Whipple’s disease
Crohn’s Disease
Giardiasis
Irritable Bowel Syndrome

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22
Q

Investigations for coeliac disease

A

Gold Standard: Endoscopy

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23
Q

Management for coeliac disease

A

Management is ongoing

Gluten Free diet
Calcium Supplements
Iron Supplements
Vitamins

Coeliac Crisis Management:
Rehydration
Electrolytes
Corticosteroids

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24
Q

Pathology of coeliac disease

A
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25
Q

Complications of coeliac disease

A

Coeliac disease is most associated with osteomalacia, osteporosis, small bowel lymphoma, lactose intolerance

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26
Q

What type of HLA allele is most associated coeliac disease?

A

HLA-DQ2/DQ8

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27
Q

What is gastritis

A

Inflammation of the stomach lining that’s associated with mucosal injury.

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28
Q

isk Factors for Gastritis

A

H. Pylori infection
Alcohol
NSAIDs use
Previous gastric surgery
Autoimmune disease

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29
Q

Causes of gastritis

A

Caused by things that cause inflammation to stomach e.g -
H.Pylori - lives in gastric mucus
Autoimmune gastritis
Viruses e.g. CMV and HSV
Duodenogastric reflux
Crohn’s disease
Mucosal ischaemia
↑ Stomach acid
Aspirin and NSAIDs
Alcohol

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30
Q

Pathophysiology of Gastritis

A
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31
Q

Clinical manifestations for Gastritis

A

Key presentations: Epigastric pain, Recurrent upset stomach

Signs: Abdominal bloating, Haematemesis

Symptoms: Loss of appetite, Vomiting, Indigestion, Nausea

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32
Q

Investigations of gastritis

A
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33
Q

Differential Diagnosis of gastritis

A

Peptic Ulcer disease
GORD
Non-ulcer dyspepsia
Gastric lymphoma
Gastric carcinoma

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34
Q

Treatment for Gastritis

A
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35
Q

Complications gastrits

A

Achloridya
B12 deficiency
Peptic Ulcer disease

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36
Q

What is GORD

A

Gastric Oesphageal Reflux Disease

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37
Q

What are symptoms of GORD caused by?

A

backflow of gastric acid and other gastric contents into oesphagus due to incompetent barriers at the gastroesophageal junction

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38
Q

Anatomy of oesphagus

A
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39
Q

What factors contribute to GORD

A

Decrease in oesphageal sphincter tone

Increase in intra-gastric volume pressure

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40
Q

What factors increase intra-gastric volume pressure

A

Cough
Large meals
Delayed gastric emptying

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41
Q

What factors decrease oesophageal sphincter tone

A

Alcohol
Drugs: Tricyclic antidepressants
Previous surgery
Peptic strictures

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42
Q

Pathological Features of GORD

A

By reflux oesphagitis: develops when mucosal defences are unable to counteract the damage done by acid pepsin and bile. This causes inflammation

Oesphageal strictures: results from fibrosis that causes luminal constriction. Occur in 10% of patients with untreated GORD and distal oesphagous near the squamous columnar junction

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43
Q

Clinical Presentation of GORD

A

Heart Burn: after meal, lying
Acid Brash
Water Brash
Ooynophagia
Chronic cough
Laryngitis
Sinusitis

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44
Q

Investigations-Diagnosis of GORD

A

Young <40
PPI trial

Elderly/not received by medication
1. Endoscopy
2. Barium Swallow
3. 24hr pH monitoring

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45
Q

Lifestyle management for GORD

A

1.weight loss
2. smoking cessation
3. small regular meals
4. avoid meals before sleep
5. avoid:
fizzy drinks
alcohol
coffee
citrus fruits
spicy foods

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46
Q

Pharmacological management for GORD

A

Proton Pump Inhibitor
Antacids
H2 Receptor Blocker

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47
Q

Surgical Management for GORD

A

Only if medical management has failed
1. Nissen’s operation

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48
Q

Complications of GORD

A

Oesophagitis -> metaplasia/dysplasia (Barrett’s oesophagus) -> Adenoma

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49
Q

What is peptic ulcer disease

A

Defect which develops in the mucous membrane of the stomah or duodenum

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50
Q

What are peptic ulcers

A

Having one or more sores in the stomach (gastric ulcers), or in the duodenum (duodenal ulcers)

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51
Q

Stomach: Anatomy and Physiology

A
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52
Q

Risk Factors for peptic ulcer disease

A

H. pylori
NSAIDs
Smoking
>Age
History of peptic ulcer
Family History of peptic ulcer
Alcohol
Patient in ICU on mechanical ventilation or with coagulopathy
Chronic obstructive lung disease
Chronic renal insufficiency

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53
Q

Causes of peptic ulcer disease

A
  1. H.Pylori Bacterial infection:
  2. NSAIDs

3.Zollinger-Ellison Syndrome

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54
Q

Differential diagnosis for peptic ulcer disease

A

Oesophageal Cancer
Gastric Cancer
GORD/GERD
Gallstone Disease
Acute Pancreatitis
Coeliac Disease
Irritable Bowel Syndrome
Pericarditis
Lower lobe Pneumonia
Achalasia

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55
Q

Investigations peptic ulcer disease

A

H.pylori breath test or stool antigen test
Upper Gastro endoscopy
FBC
Fasting serum gastrin level – hypergastrinaemia in Zollinger-Ellison syndrome
Abdominal X-ray
Abdominal CT

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56
Q

Pathophysiology of peptic ulcer disease

A
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57
Q

Complication of peptic ulcer disease

A
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58
Q

Management peptic ulcer disease

A
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59
Q

Symptoms for peptic ulcer disease

A
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60
Q

What is appendicitis

A

Inflammed appendix
Affects 10% of population

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61
Q

Signs and symptoms of appendicitis

A
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62
Q

Differential Diagnosis of appendicitis

A
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63
Q

Investigations of appendicits

A
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64
Q

Management for Appendicitis

A
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65
Q

Complication for appendicitis

A

Perforation
Appendix mass
Appendix abscess
Portal Venous thrombosis
Liver Abscess
Bacteraemia - sepsis
Fistula
Pyelonephritis
PE/DVT following hospitalization

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66
Q

What is diverticular disease

A
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67
Q

What is diverticula/diverticulum?

A

abnormal sac-like protrusion from the wall of a hollow organ

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68
Q

Diverticulosis

A

Diverticulosis: presence of multiple diverticula, not symptomatic

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69
Q

Diverticulitis:

A

inflammation of diverticula

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70
Q

Diverticular Disease:

A

Complication of diverticulosis

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71
Q

What are a true diverticula?

A

Contain all layers of the colonic wall, often right-sided (i.e Merkel’s Diverticulum)

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72
Q

False diverticulum

A

False (acquired) diverticuli: contain mucosa and submucosa, often left-sided (highest pressure)

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73
Q

Merkel’s Diverticulum:

A

A true diverticulum, it is a reminant of proximal part of the yolk-stalk. May present with symptoms in a small majority of patients.

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74
Q

What are most colonic diverticula

A

False

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75
Q

Colon Anatomy and physiology

A
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76
Q

Risk Factor for diverticular disease

A

Age >50
Low fiber diet
Western diet
Obesity
NSAIDs

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77
Q

Signs and symptoms of diverticular disease

A

Clinical Presentation of Diverticular Disease, one of four: Asympstomatic (majority), Painful Diverticular Disease, Bleeding Diverticular Disease or Diverticulitis

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78
Q

Differential diagnosis for diverticular disease

A

Ectopic Pregnancy
Colorectal Cancer
Meckel’s diverticulum
Appendicitis
Inflammatory Bowel Disease
Mesenteric Ischaemia
Pyelonephritis
Urinary Tract infection
Pelvic Inflammatory Disease
Irritable Bowel Syndrome

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79
Q

Investigations for diverticular disease

A

Investigations depend on suspected complication and for diagnosis of diverticular disease. Diverticulosis may be an incidental finding on colonoscopy. Laboratory tests include FBC and CRP to check for bleeding and signs of inflammation/infection/malignancy. CT scan can help identify complications. A Chest x-ray can also be used which may reveal free air under the diaphragm (sign of perforation)

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80
Q

Pathophysiology of diverticular disease

A
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81
Q

Management for diverticular disease

A
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82
Q

Complications of diverticular disease

A
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83
Q

What is Merkels diverticulitis

A

Meckel’s diverticulum is the remnant of the vitellointestinal duct of the embryo. It lies on the antimesenteric border of the ileum and, as an approximation, occurs in 2% of the population, arises 55cm (2 feet) from the caecum, and averages 5 cm (2 inches) in length.

Remember Merkel’s Diverticulum is a true diverticulum

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84
Q

Right Lower-quadrant pain common differential

A
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85
Q

Difference between diverticula vs diverticulosis, diverticultis

A
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86
Q

What is Helicobacter Pylori (H.Pylori)

A

Helicobacter pylori is a Gram-negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease.

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87
Q

How is H.pylori infection spread?

A
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88
Q

Pathology of H.pylroi infection

A
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89
Q

Association of H.pylori

A
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90
Q

Consequence of H.pylori infection

A
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91
Q

Clinical presentation of H.pylori

A
92
Q

Diagnosis of H.pylori infection

A
93
Q

Treatment for H.pylori infection

A

Clarithromycin
Amoxycillin
PPI

94
Q

What is intestinal obstruction

A

A condition that comes from either a mechanical blockage of the bowels or a functional issue (Pseudo) where the bowels no longer propel digested content properly through the G.I tract

95
Q

Several categories have been used to classify differences in the various presentations of intestinal obstruction. Ask yourself:

A

Cardinal features of bowel obstruction present?
Degree of obstruction to flow (partial or complete)
Site of obstruction (small bowel or large bowel)
Mechanical obstruction or ileus?
Absence or presence of intestinal ischemia (simple or strangulated).

96
Q

Cardinal features of bowel obstruction

A

Colicky abdominal pain
Distension
Absolute constipation/obstipation
Nausea and Vomiting

97
Q

Pathophysiology of intestinal obstruction

A

Disruption of the normal flow of intestinal contents leading to proximal dilatation and distal decompression may take 12-24 h to decompress. Therefore passage of faeces and status may occur and the onset of obstruction. Bowel ischemia may occur if blood supply is strangulated or if the bowel wall in ammation leads to venous congestion, bowel wall oedema, and disruption of normal bowel absorptive function can lead to increased intraluminal uid and transudative fluid loss into the peritoneal cavity, electrolyte disturbances.

98
Q

Is it a partial or complete bowel obstruction?

A

Partial Obstruction - still can pass gas +/- diarrhoea
Complete Obstruction - can not pass gas or poo

99
Q

Is it obstruction of the small or large bowel?

A
100
Q

Mechanical obstruction or ileus?

A
101
Q

Radiography Bowel obstruction

A
102
Q

Treatment for intestinal obstruction

A
103
Q

Bowel obstruction table

A
104
Q

What is diarrhoea

A

Loose stools 3< Times per day. 200g/24hr (Not commonly used)

105
Q

Classifications of diarrhoea

A
106
Q

How to distinguish between functional/organic diarrhoea

A
107
Q

Small Bowel vs Large Bowel diarrhoea

A
108
Q

What do you do once you have identified small bowel vs large bowel and Organic vs Functional diarrhoea

A
109
Q

Types of diarrhoea based on pathophisiology

A
110
Q

Gastric cancer

A

Gastric cancer accounts for around 2% of all cancer diagnoses in the developed world, making it much less common than colorectal and slightly less common than oesophageal cancer. It is a cancer of older people (half of patients are > 75 years) are has a male predominance (2:1).

111
Q

Risk Factors of gastric cancer

A
  1. Age - Median age 70
  2. Sex - 2:1 Male: Female
  3. Helicobacter Pylori infection- 60%
  4. Smoking
  5. Alcohol
  6. Obesity
  7. Diet - Pickled/cured/processed
  8. Family History: 10%, 1% syndromic: hereditary diffuse gastric cancer
  9. Pernicious anaemia
  10. Gastritis
112
Q

Most common sites of gastric cancer

A
113
Q

Most common types of gastric cancer

A

95%: Adenocarcinoma
5%: Lymphoma, carcinoid, stromal tumours

114
Q

Signs and symptoms of gastric cancer

A

abdominal pain
typically vague, epigastric pain
may present as dyspepsia
weight loss and anorexia
nausea and vomiting
dysphagia: particularly if the cancer arises in the proximal stomach
overt upper gastrointestinal bleeding is seen only in a minority of patients
if lymphatic spread:
left supraclavicular lymph node (Virchow’s node)
periumbilical nodule (Sister Mary Joseph’s node)

115
Q

Investigations of gastric cancer

A

Endoscopy + Biopsy are the gold standard
CT imaging

Diagnosis: oesophagus-gastro-duodenoscopy with biopsy
signet ring cells may be seen in gastric cancer. They contain a large vacuole of mucin which displaces the nucleus to one side. Higher numbers of signet ring cells are associated with a worse prognosis
staging: CT.

116
Q

How to identify different stages of gastric cancer

A

Stage 3 is most common

117
Q

Survival of gastric cancer

A

West - 30% 5 Year survival
Japan/Korea - 45% 5 Year survival

*Stage 0/1 5 Year survival is ~90%

118
Q

Treatment for gastric cancer

A

surgical options depend on the extent and side but include:
endoscopic mucosal resection
partial gastrectomy
total gastrectomy
chemotherapy

119
Q

Colorectal cancer significance

A

Colon cancer is the second most commonly diagnosed cancer. 1/12 people will develop bowel cancer before the age of 85. However, there are Survival rates are increasing. Early bowel cancer is cured by surgery alone (screening is important!!). If untreated, or diagnosed when distance metastases are present, >98% pf patients die in <5 years.

Cancer of the colon and/or rectum usually at an advanced age. It is an adenoma and the primary site of metastasis is the liver.

120
Q

Risk Factors for Large Bowel Cancer

A

Diet Poor in fiber
Age
Male
Smoking
Family History
Polyposis syndrome: FAP, HNPCC
History of polyps
History of colon cancer
Ulcerative colitis
Crohn’s

121
Q

Differential diagnosis of colorectal cancer

A
122
Q

Clinical Presentation of Colorectal Cancer

A

Clinical Examination

Anaemia
Palpable mass on abdominal examination
Palpable nodular liver (metastasis)
Pigmentation (Peutz-Jeghers syndrome)
Discrete black brown lesion on lips

123
Q

Pathology of Large Bowel Cancer

A

Pathology Colorectal cancer are primarily adenocarcinoma. Coloncancer can be polyploid, ulcerative, stenosing or infiltrative.

Remember Blumer’s shelf: A firm lump felt in the perirectal pouch on rectal examination. It is a rare physical finding in patients with metastatic adenocarcinoma from the GIT usually the stomach.

124
Q

Investigations for large bowel cancer

A

Rectal examination
FBC
Faecal occult blood testing (not done if symptomatic)
Tumour markers
CT imaging
Colonoscopy

Investigation
Remember Screening for colon cancer is available: FOBT. Done yearly after 50yo (Australia).

Diagnosis Colon cancer is usually diagnosed with colonoscopy and biopsy (takes 1-2 days for pathology results)

125
Q

Investigations for staging large bowel cancer

A
126
Q

Treatment for Large bowel cancer

A
127
Q

Complications and prognosis of colorectal cancer

A
128
Q

What is oesophageal cancer, and what are the different types

A

Until recently, oesophageal cancer was most commonly due to squamous cell carcinoma, but the incidence of adenocarcinoma is rising rapidly. Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett’s.

The majority of adenocarcinomas are located near the gastroesophageal junction, whereas squamous cell tumours are most commonly found in the upper two-thirds of the oesophagus.

129
Q

Squamous cell carcinoma orginates

A

in squamous epithelium

130
Q

Risk Factors of squamous cell carcinoma

A

Alcohol
Smoking
Hot fluids

131
Q

Squamous cell carcinoma mutations occur in

A
132
Q

Adenomcarcinoma

A

Originates in columnar glandular epthelium
Affects lower 1/3 of oesphagus
Consequence of GORD

133
Q

Risk Factors of oesphageal cancer

A
134
Q

Symptoms of oesophageal cancer

A

dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough

135
Q

Diagnosis of oesophageal cancer

A

Upper GI endoscopy with biopsy is used for diagnosis
Endoscopic ultrasound is the preferred method for locoregional staging
CT scanning of the chest, abdomen and pelvis is used for initial staging
FDG-PET CT may detect occult metastases if metastases are not seen on the initial staging CT scans.
Laparoscopy is sometimes performed to detect occult peritoneal disease.

136
Q

Treatment for oesophageal cancer

A

The operable disease is best managed by surgical resection - the most common procedure is an Ivor-Lewis type oesophagectomy.
The biggest surgical challenge is an anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis.
In addition to surgical resection, many patients will be treated with adjuvant chemotherapy.

137
Q

What is Meckel’s Diverticulum

A

Abnormal pouch on antimesenteric side of ileum

138
Q

Complications of Meckel’s Diverticulum

A

Diverticulitis

139
Q

Signs and symptoms of Meckel’s Diverticulum

A

Usually asymptomatic
Abdominal pain/distension, melena, vomiting, constipation

140
Q

Diagnosis of Meckel’s Diverticulum

A
141
Q

Treatment for Meckel’s Diverticulum

A
142
Q

What is achalasia?

A

Rare disorder that results from progressive destruction of the ganglion cells in the myenteric plexus in the oesphogeal wall.

The destruction of these cell leads to the inability of the lower oesphageal sphincter to relax and leads to the loss of peristalsis of the distal oesphagus

143
Q

What is the result of achalasia

A

Dilatation of the distal oesphagus

144
Q

Clinical Presentation of achalasia

A

dysphagia of BOTH liquids and solids
typically variation in severity of symptoms
heartburn
regurgitation of food
may lead to cough, aspiration pneumonia etc
malignant change in small number of patients

145
Q

What is a misdiagnosis for achalasia

A

Gastrooesophageal reflux

146
Q

Aetiology of achalasia

A

1.Idiopathic

2.Viral/parasitic cause

3.Autoimmune

4.Neurodegenerative disorder

5.Trypanoma cruzi -> Chagos disease

6.Antibodies against:
-HSV
-HPV
-Rubeola

Remember : Both myenteric antibodies and HSV-1 infection were found in 100% of patients with achalasia

147
Q

Investigations for achalasia

A

1.oesophageal manometry
excessive LOS tone which doesn’t relax on swallowing
considered the most important diagnostic test
2.barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance
3.chest x-ray
wide mediastinum
fluid level

148
Q

Pseudo achalasia

A

Due to an obstructed distal oesophagus from causes other than destruction of the myenteric plexus at the distal oesophagus.

Due to obstruction by a malignant mass, scleroderma, strictures, toxins, reflux malignancies.

Also due to lymphoma, oesophageal carcinoma, gastric carcinoma

Investigations include:
CT
Endoscopic ultrasound

149
Q

Treatment for achalasia

A

1.pneumatic (balloon) dilation is increasingly the preferred first-line option
less invasive and quicker recovery time than surgery
patients should be a low surgical risk as surgery may be required if complications occur

2.surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms

3.intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk

4.drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects

150
Q

What is intestinal ischaemia

A

group of conditions where there is inadequate blood flow to large or small intestine

151
Q

Classifications of intestinal ischaemia

A

Ischaemic collitus: affects large intestine

Acute/Chronic mesenteric ischaemia: Affects small intestine

152
Q

Areas most prone to intestinal ischaemia

A

Splenic Flexture (Griffiths point)
Rectosigmoid junction (Sudeck’s point)

153
Q

Causes of intestinal ischaemia

A

Acute mesenteric ischemia can result from occlusion of a mesenteric vessel arising from an embolus, which may emanate from an atheroma of the aorta or cardiac mural thrombus, or primary thrombosis of a mesenteric vessel, usually at a site of atherosclerotic stenosis. Embolic occlusion is more common in the superior mesenteric artery than the celiac or inferior mesenteric artery, presumably because of the less acute angle of the superior mesenteric artery of the abdominal aorta.

Remember: AF with abdominal pain think mesenteric ischaemia.

154
Q

Signs and symtoms of intestinal ischaemia

A

Depends on severity and time of occlusion

  1. Abdominal pain (95%)
    -Disproportionate to exam
    -Widespread as ischaemia progresses
  2. Nausea/Vomiting
  3. Diarrhoea (Constipation is rare)
  4. Rectal Bleeding

Can be sequence to the symptoms (see pic)

Chronic symptoms
-Slower onset
-Pain 30min after eating: Fear of eating & Weight loss

155
Q

Risk Factors for intestinal ischaemia

A

1.Atherosclerosis
2.Age
3.smoking
4.atrial fibrillation
5.hypercoagulability
6.chronic organ failure

156
Q

Diagnosis for intestinal ischaemia

A

1.HIstory + Physical Exam
2.Lab markers: Leukocytosis, Raised lactate
3.imaging:
-CT (intramural gas, portal venous gass, free air)
-Angiogrpahy
-X-Ray
-Endoscopy

157
Q

Treatment for intestinal ischaemia:

A
158
Q

What is pseudomembranous Colitis

A

Swelling or Inflammation of the large intestine due to disturbance of normal bacterial flora of the colon and an overgrowth of Clostridium difficile (C.diff) bacteria

159
Q

What is pseudomembranous Colitis a common cause of

A

Diarrhoea after antibiotic use

160
Q

Pseudomembranous colitis infection causes

A

Antibiotics: ampicillin, cindamycin, fluoroquinolone, cephalosporins

Healthcare workers: as infection is spread by faeces

161
Q

What is C.difficle bacteria

A

Spore forming, anaerobic, gram positive bacilus.

Pathogenic C.difficile strains produce multiple toxins e.g entertoxins and cytotoxins both of which produce diarrhoea and inflammation in infected patients

162
Q

Pathophysiology of C.difficile

A

anaerobic gram-positive, spore-forming, toxin-producing bacillus
transmission: via the faecal-oral route by ingestion of spores
releases two exotoxins (toxin A and toxin B) that act on intestinal epithelial cells and inflammatory cells resulting in colitis

163
Q

Symptoms of pseudomembranous colitis

A

diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop

164
Q

Investigations for Pseudomembranous colitis

A
165
Q

Management of pseudomembranous colitis

A
166
Q

What is an anal fissure

A

A superficial linear tear in the anoderm distal to the pectinate line (dentate line) commonly caused by passage of hard stool

167
Q

Clinical Presentation of an anal fissure

A
168
Q

Risk Factors for anal fissure

A

Low intake of dietary fiber

169
Q

Differential diagnosis for an anal fissure

A
170
Q

Pathophysiology of an anal fissure

A

Anal fissures usually occur in the anterior or posterior parts of the anus and underlies the internal anal sphincter. Muscles spasm are due to contraction of the internal anal sphincter causing ischaemia → pain

171
Q

Complications for an anal fissure

A

Faecal incontinence due to sphincterotomy

172
Q

Signs and symptoms of an anal fissure

A
173
Q

Diagnosis of an anal fissure

A

History, examination of anal region/rectum

174
Q

Treatment of an anal fissure

A
175
Q

What is an anal fistula

A

abnormal connection of the anorectal epithelial surface to the perineal or vaginal skin.

176
Q

Types of anal fistula

A
177
Q

Signs & Symptoms of anal fistula

A
178
Q

Differential diagnosis of an anal fistula

A

Anal Abscess
Anal fissure
Anal ulcer or sores (secondary to another disease or infection)
Crohn disease

179
Q

Diagnosis of anal fistula

A
180
Q

Pathophysiology of an anal fistula

A
181
Q

Treatment for anal fistula

A
182
Q

Complication of an anal fistula

A

Recurrence
Faecal incontinence from surgery

183
Q

What is a haemorrhoid

A

collections of submucosal, fibrovascular, arteriovenous sinusoids that are part of the normal anorectum

184
Q

Types of haemorrhoid

A
185
Q

Risk factors for haemorrhoid

A

Constipation, a low fibre diet, a high Body Mass Index, pregnancy, and a sedentary lifestyle

186
Q

Complications with haemorrhoid

A

Anaemia
Pain
Heavy bleeding
Chronic unremitting prolapse of mucosal tissue
Strangulation
Ulceration
Thrombosis

187
Q

Signs and symptoms of a haemorrhoid

A
188
Q

Diagnosis of a haemorrhoid

A
189
Q

Treatment of haemorrhoids

A
190
Q

What is an anorectal abscess

A

Collection of pus in the anal/rectal region

Usually an invasion of normal rectal flora

191
Q

Signs and symtpoms of an anorectal abscess

A
192
Q

Investigations for anorectal abscess

A
193
Q

Diagnosis of anorectal abscess

A
194
Q

Pathophisiology of anorectal abscess

A

Usually originates from an infected anal crypt gland

1.Infection of crypts
2.spread through anal duct and gland
3.Infection spreads:
-Submucosal
-Subcutaneous
-Transsphincter
Surrounding tissue

the abscess collects in which ever anatomical space between the gland terminates or whichever path of least resistance is

195
Q

Differential diagnosis of an anorectal abscess

A
196
Q

Management of an anorectal abscess

A
197
Q

Complications of an anal abscess

A
198
Q

What is pilonidal sinus

A

Obstruction of natural hair follicles above the anus

199
Q

Clinical Presentation of pilonidal sinus

A
200
Q

Pilonidal sinus pathophisiology

A
201
Q

Aetiology of pilonidal sinus

A

Congenital

202
Q

Diagnosis of pilonidal sinus

A

Diagnosis of observation

203
Q

Treatment for a pilonidal sinus

A
204
Q

Complication of pilonidal sinus

A

Infection

205
Q

Venn Diagram comparing IBD

A
206
Q

a 20-year-old woman presents with recurrent episodes of abdominal pain associated with bloating. The pain is relieved on defecation. She normal passes 3 loose stools with mucous in the mornings

A

IBS

207
Q

Table comparing diff between IBD

A
208
Q

Diverticulitis classical presentation is:

A

left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)

209
Q

Mesenteric ischaemia: Key question features (lower gastrointestinal disorders)

A

abdominal pain, rectal bleeding, metabolic acidosis

210
Q

Stereotypical histories Crohn’s disease

A

a 20-year-old woman presents with diarrhoea. Over the past few months she has lost weight and suffered with recurrent abdominal pain and mouth ulcers

211
Q

An elderly man complains of dysphagia, halitosis, regurgitation and cough is a stereotypical history for:

A

Pharyngeal pouch

212
Q

Which antibody is most associated with ulcerative colitis?

A

P-ANCA

213
Q

Palpation in LLQ causes pain in RLQ

A

acute appendicitis

214
Q

What type of cancer is most associated with Helicobacter pylori?

A

B cell lymphoma of MALT tissue

215
Q

What type of cancer is most associated with Helicobacter pylori?

A

B cell lymphoma of MALT tissue

216
Q

Strong family history of colorectal and endometrial cancer in a question is most likely to indicate:

A

Hereditary non-polyposis colorectal carcinoma

217
Q

Which one of the following tumour markers is most associated with colorectal cancer?

A

Carcinoembryonic antigen

218
Q

A 17-year-old boy is admitted to hospital with suspected appendicitis. He is found to be maximally tender at McBurney’s point. Where is this located?

A

McBurney’s point is found 2/3rds of the way along an imaginary line that runs from the umbilicus to the anterior superior iliac spine on the right-hand side. The other options do not locate this anatomical site.

219
Q

Pathophysiology of a Mallory-Weiss tear

A

Severe vomiting → painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics

220
Q

Mallory Weiss tear

A
221
Q

Oesphogeal Varices

A

Definition
Epidemiology
Aetiology
Risk Factors

222
Q

Pathophysiology of oesphogeal varices

A

@ oesophagogastric junction, rectum and anterior wall - portal and systemic
capillary beds meet
If portal hypertension, then blood takes path of least resistance i.e. through
systemic circulation - bypasses liver and into heart
∴ causes detoxification and nutrition issues
As portal pressure ↑, can cause oesophagogastric varices to form and rupture
∴ massive haemorrhage
—
As these vessels are not thin, not meant to transport higher pressure blood
∴ rupture
(∴ haematemesis)
(if blood digested = melaena)

223
Q

Clinical Manifestations and Investigations for oesphageal varices

A
224
Q

Differential diagnosis for oesphageal varices

A

Gastroenteritis
Peptic ulcer
Cancer
Mallory-Weiss tear

225
Q

Management for oesphageal varices

A

Blood transfusion if anaemic
Beta blocker to reduce CO ∴ ↓ portal pressure
Nitrate to cause vasodilation ∴ ↓ portal pressure
Terlipressin (ADH analogue) ∴ ↓ portal pressure
Trans-jugular intrahepatic portoclaval shunt (TIPS)
Correct clotting abnormalities w/ vit K and platelet transfusion
Variceal banding - band put around varice using endoscopy

Sandra Phase 2a (17 decks)

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