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Phase 2a > GI/ Liver Diseases > Flashcards

GI/ Liver Diseases Flashcards

1
Q

What is the clinical presentation of GORD?

A 
Acidic taste in mouth
Regurgitation 
Heartburn
Odynophagia 
Bad breath
Bloating or nausea 
Reoccurring cough/hiccups
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2
Q

Briefly describe the pathology of GORD

A

Reflux occurs when acid moves into the oesophegus due to failure of the lower oesophageal sphincter. There is an increased mucosal sensitivity to gastric acids.

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3
Q

What are some risk factors for GORD?

A

Hiatus hernia
Certain foods and drinks (Citrus, fatty foods, spicy foods, alcohol, caffeine)
Large meals before bed
Certain medications (Aspirin, ibuprofen, muscle relaxers, blood pressure medications)
Being overweight
Pregnancy
Smoking

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4
Q

How is GORD diagnosed?

A

Certain diagnostic tests- gastroscopy, barium swallow

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5
Q

What is the epidemiology of GORD?

A

2-3x more common in men, 25% of adults experience heartburn

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6
Q

What are some natural treatments for GORD?

A 
Changes to diet and times of meals
Smoking cessation
Raising head-end of bed
Loose-clothing
BMI management 
Medication review
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7
Q

What are some medications for GORD?

A

Antacids for mild cases
Proton pump inhibitors (Omeprazole)
H2 receptor antagonists (Ranitidine)

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8
Q

What are some complications of GORD?

A

Barrett’s oesophagus which can develop into oesophageal cancer

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9
Q

Where is the appendix found?

A

McBurneys point= 2/3 of the way from the umbilicus to anterior superior iliac spine

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10
Q

What is the epidemiology of acute appendicitis?

A
  • Most common surgical emergency
  • More common in men aged 10-20 yrs
  • Rare before age 2 because the appendix is wider like a cone
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11
Q

What are the causes of acute appendicitis?

A
  • Faecolith (stone made of faeces) = Most common
  • Lymphoid hyperplasia
  • Filarial worms
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12
Q

Briefly explain the pathophysiology of acute appendicits

A

It occurs when the lumen of the appendix becomes obstructed by lymphoid hyperplasia, filarial worms, or a faecolith, resulting in the invasion of gut organisms into the appendix wall. If the appendix ruptures, then the infected and faecal matter will enter the peritoneum causing peritonitis

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13
Q

What is the clinical presentation of acute appendicits?

A
  • Pain in umbilical region that then migrates to mcburneys point after afew hours
  • Inflammation causes a colicky periumbilical pain
  • Anorexia
  • Nausea and vomitting (and occasionally diarrhoea)
  • Constipation
  • Tenderness with guarding
  • Tender mass in right iliac fossa
  • Pyrexia
  • Rosving’s sign
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14
Q

How is acute appendicitis diagnosed?

A

CT= Gold standard
Blood tests= Raised neutrophils and other WBCs, Elevated CRP&ESRs
*******
Ultrasound= Can detect inflamed appendix and appendix mass
- Pregnancy test and urinalysis = exclude pregnancy and UTI

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15
Q

How is acute appendicitis treated?

A

Surgical= Appendicectomy laparoscopically
IV antibiotic pre-op= IV metronidazole and IV cefuroxime
If appendix mass is present= IV fluids and antibiotics over afew weeks, and then appendicectomy

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16
Q

What are the complications of acute appendicitis?

A
  • Perforation= Commoner in faecolith
  • Appendix mass: When an inflamed appendix becomes covered in omentum. Treat with antibiotics
  • Appendix abscess: If appendix mass fails to resolve and instead enlarges. Drain and treat with antibiotics.
  • Adhesions
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17
Q

What is a peptic ulcer?

A

A break in the superficial epithelial cells penetrating down to the muscularis mucosa on the duodenum or stomach

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18
Q

What is the epidemiology of peptic ulcer disease?

A

Duodenal ulcers affect approx 10% of adult population, and 2-3x more common than gastric ulcers. More common in elderly and in developing countries. Decline in incidence in men and increase in women

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19
Q

What are the causes of peptic ulcer disease?

A

H pylori infection, drugs (NSAIDs, steroids), increased gastric acid secretion, smoking, delayed gastric emptying, blood group O

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20
Q

Briefly explain how NSAIDs cause peptic ulcer disease

A

They inhibit cyclooxygenase 1 which is needed for prostaglandin synthesis. Prostaglandins stimulate mucous secretion- therefore NSAIDs= decreased mucosal defence

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21
Q

Briefly explain how H. pylori cause peptic ulcer disease

A

H pylori causes a decrease in duodenal bicarbonate, and secretes urease. Urease splits into CO2 and ammonia, which changes the pH. This causes damages to the mucosa, and causes gastrin secretion. There is therefore an inflammatory response.

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22
Q

What are some possible complications of peptic ulcer disease?

A

Massive hemorrhage, peritonitis, acute pancreatitis

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23
Q

How is peptic ulcer disease diagnosed?

A

If patient is under 55, do non-invasive h pylori testing (Serology, C urea breath test, stool antigen test)
Invasive testing = endoscopy (essential in all alarm patients and those over 55), histology, biopsy urease test

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24
Q

What is the clinical presentation of peptic ulcer disease?

A
  • Recurrent burning epigastric pain in a specific point, typically occurs at night and is worse when hungry
  • Nausea, anorexia and weight loss
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25
Q

How is peptic ulcer disease treated?

A
  • Lifestyle: reduce stress, avoid some foods, reduce smoking
  • Stop NSAIDs
  • Triple therapy for H pylori= PPI (lansoprasole), Two out of metronidazole, bismuth, tetracycline, amoxicillin, clarithromycin
  • H2 antagonists (ranitidine)
  • Surgery if complications arise
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26
Q

What is the epidemiology of IBS?

A
  • Age of onset under 40
  • More common in females
  • Common= Around 1 in 5 show symptoms
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27
Q

What are the main causes of IBS?

A

Depression, anxiety, psychological stress, trauma, GI infection, abuse, eating disorders

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28
Q

What are the 3 types of IBS?

A
  • IBS-C = With constipation
  • IBS-D= With diarrhoea
  • IBS-M= With Both (mixed)
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29
Q

What are the risk factors for IBS?

A
  • Female
  • Previous severe and long diarrhoea
  • High hypochondrial anxiety and neurotic score at time of intial illness
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30
Q

Briefly explain the pathophysiology of IBS?

A

Dysfunction in the brain-gut axis resulting in disorder of intestinal motility and/or visceral hypersensitivity

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31
Q

What are the clinical features of IBS?

A
  • Non intestinal symptoms= painful period, urinary frequency, incomplete bladder emptying, urgency, nocturia, back pain, fatigue
  • Abdominal pain, bloating and change in bowel habit
  • Abdominal pain that is relieved by defecation or is associated with altered stool form/frequency
  • 2 or more of: urgency, mucous in stool, nausea, incomplete evacuation
  • Chronic symptoms and exacerbated by stress
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32
Q

What are the differentials of IBS?

A

Coeliac’s disease, Lactose intolerance, Bile acid malabsorption, IBD, Colorectal cancer

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33
Q

How is IBS diagnosed?

A
  • Clinical features and ruling out differentials
  • Faecal protectin= raised in IBD
  • Colonoscopy to rule out IBD and colorectal cancer
  • FBC for anaemia
  • ESR&CRP for inflammation
  • Coeliac testing (EMA and ETG)
  • Rome III diagnostic criteria= abdominal pain plus 2 or more of change in stool frequency, change in appearance and improvement with exacerbation
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34
Q

What are the lifestyle treatments of IBS?

A

Dietary modifications= Low FODMAP diet

  • In IBS-D= Avoid insoluble fibre
  • In wind and bloating= Increase soluble fibre
  • High water intake (avoid caffeine, fizzy drinks)
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35
Q

What are some pharmacological treatments for IBS?

A
  • Pain/bloating= Antispasmodics
  • Loperamides
  • Constipation= Laxitives (Mavicol or Senna), or linaclotide if it has been over a year and no improvement with other treatments
  • Diarrhoea= Anti-motility
  • Tricyclic antidepressants can be used
  • Psychological therapy
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36
Q

What is the epidemiology of ischaemic colitis?

A
  • Older age group
  • Related to atherosclerosis
  • In young population it is associated with contraceptive pill, thrombophilia, and vasculitis
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37
Q

What are the risk factors for ischaemic colitis?

A

Contraceptive pill, thrombophilia and vasculitis

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38
Q

What are the main causes of ischaemic colitis?

A
  • Thrombosis
  • Emboli
  • Decreased CO and arrhythmias
  • Drugs e.g. oestrogen, ADH, Antihypertensives
  • Surgery
  • Vasculitis
  • Coagulation disorders
  • Idiopathic
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39
Q

Briefly explain the pathophysiology of ischaemic colitis

A

Occlusion of branch of SMA or IMA, often in the older age group. This is most commonly at the splenic flexure.

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40
Q

What are the clinical features of ischaemic colitis

A

Sudden onset at lower left side abdominal pain
Passage of bright red blood with/without diarrhoea
May be signs of shock and underlying cardiovascular disease

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41
Q

How is ischaemic colitis diagnosed?

A
  • Urgent CT scan to exclude perforation
  • Flexible sigmoidoscopy: biopsy shows epithelial cell apoptosis
  • Colonoscopy and biopsy= GOLD STANDARD= done after patient has recovered to exclude stricture formation
  • Barium enema
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42
Q

How is ischaemic colitis treated?

A
  • Normally symptoms of treatment
  • Fluid replacement
  • Antibiotics to reduce infection risk
  • Strictures are common :(
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43
Q

What is the epidemiology of squamous cell carcinoma of the oesophagus?

A

Common in Ethiopia, China, S+E Africa
UK= 5-10 per 100000
Incidence is decreasing
More common in males

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44
Q

What are the causes of squamous cell carcinoma of the oesophagus?

A 
High levels of alcohol
Achalasia 
Tobacco/ Smoking
Obesity
Low fruit, veg and fibre
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45
Q

What is the epidemiology of adenocarcinoma of the oesophagus?

A

45% of oesophageal tumours

Incidence is increasing

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46
Q

What is the aetiology of adenocarcinoma of the oesophagus?

A

Barrett’s oesophagus= Recurrent acid exposure causes squamous epithelium to be replaced by metaplastic columnar mucosa
Previous reflux increase risk by 8

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47
Q

What are the causes of adenocarcinoma of the oesophagus?

A

Smoking/ Tobacco
GORD
Obesity
Barrett’s oesophagus

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48
Q

What are the risk factors for SSC& Adenocarcinoma of the oesophagus?

A

Alcohol, Smoking, Obesity, Achalasia, Diet low in vit A&C, Barrett’s oesophagus

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49
Q

Where does squamous cell carcinoma of the oesophagus normally affect?

A

Upper 2/3 of the oesophagus

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50
Q

Where does adenocarcinoma of the oesophagus normally affect?

A

Lower 1/3 of the oesophagus

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51
Q

What is the clinical presentation of SSC& Adenocarcinoma of the oesophagus?

A
  • Often asymptomatic so when it is found it is V advanced
  • Progressive dysplasia
  • Weight loss, anorexia and lyphadenopathy
  • Pain due to food impaction or infiltration
  • If in upper 1/3 of oesophagus: hoarseness and cough
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52
Q

How is SSC& Adenocarcinoma of the oesophagus diagnosed?

A

Oesophagoscopy with biopsy
Barium swallow
CT/MRI/PET for tumour staging

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53
Q

How is SSC& Adenocarcinoma of the oesophagus treated?

A

Surgical resection combined with chemotherapy +/- radiotherapy
If locally incurable or metastatic then systemic chemotherapy

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54
Q

What is the epidemiology of benign oesophageal tumour?

A

1% of all oesopheageal tumour
Leiomyomas are more common
Also include papillomas, fibrovascular polyps, haemangiomas, lipomas

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55
Q

Briefly explain the pathophysiology of benign oesophageal tumour leiomas

A

Leiomas are smooth muscle tumours arising from the oesophageal wall. They are intact, well encapsulated and are within the overlying mucosa. Slow growing.

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56
Q

What are the clinical features of benign oesophageal tumour ?

A
  • Usually asymptomatic, found incidentally
  • Dysphagia
  • Retrosternal pain
  • Food regurgitation
  • Recurrent chest infections
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57
Q

How is benign oesophageal tumour diagnosed?

A
  • Endoscopy
  • Barium swallow
  • Biopsy
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58
Q

How is benign oesophageal tumour treated?

A
  • Endoscopic removal

- Surgical removal of larger tumours

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59
Q

What is the epidemiology of gastric adenocarcinoma?

A
  • More common in males
  • Incidence increases with age
  • Highest incidence in Eastern Asia, Eastern Europe and South America
  • Incidence of adenoma is decreasing
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60
Q

What are the causes of gastric adenocarcinoma?

A
  • Smoking
  • H. Pylori infection
  • Dietary factors
  • Loss of P53 and APC genes
  • Pernicious anaemia
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61
Q

What are the risk factors for gastric adenocarcinoma?

A

First degree relative with gastric cancer
Smoking
High salts and nitrates
Low fruit, veg and garlic in diet

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62
Q

Briefly explain how H.pylori can cause gastric adenocarcinoma

A

H. pylori causes acute gastritis, which can progress into chronic active gastritis. This causes atrophy, which can then develop into metaplasia, and then dysplasia

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63
Q

What are the two types of gastric adenocarcinoma?

A
  1. Intestinal= Well formed tumours with rolled edges. Often caused by H. Pylori
  2. Diffuse= Poorly undifferentiated cells that tend to infiltrate gastric wall. Worse prognosis
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64
Q

What is the clinical presentation of gastric adenocarcinoma ?

A
  • Often v advanced at presentation
  • Nausea, Anorexia and weight loss
  • Vomitting is frequent and severe if tumour encroaches on the pylorus
  • Dysphagia if in fundus
  • Constant and severe gastric pain
  • Anaemia if blood loss
  • Symptoms if metastatis
  • Palpable lymph nodes
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65
Q

How is gastric adenocarcinoma diagnosed?

A
  • Repeated gastroscopy and biopsy to confirm histologically
  • Endoscopic ultrasound
  • CT/MRI
  • PET scan for metastasis
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66
Q

How is gastric adenocarcinoma treated?

A
  • Nutritional support

- Surgery and combination chemo; Epirubicin + Cisplatin + 5-Fluorouracil known as ECF chemo, and post op Radiotherapy

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67
Q

What is the epidemiology of small intestine tumour?

A
  • Quite rare
  • Adenocarcinoma is most common tumour of SI
  • Lymphomas are most frequently found in ileum and are less common than adenocarcinomas
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68
Q

What are the risk factors for small intestine tumour?

A

Coeliacs and crohn’s disease

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69
Q

How is small intestine tumour treated?

A
  • Surgical resection

- Radiotherapy

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70
Q

What are the clinical features of small intestine tumour?

A
  • Pain, Diarrhoea, anorexia
  • Weight loss
  • Anaemia
  • May be a palpable mass
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71
Q

How is small intestine tumour diagnosed?

A
  • Ultrasound
  • Endoscopic biopsy can histologically confirm
  • CT: Small bowel wall thinning and lymph node involvement
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72
Q

What is the epidemiology of colorectal carcinoma?

A
  • 3rd most common cancer worldwide
  • Usually adenocarcinoma and majority occur in distal colon
  • More common in males and those over 60
  • More common in Western countries
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73
Q

How can you reduce risk of colorectal carcinoma?

A
  • Veg
  • Garlic
  • Milk
  • Exercise
  • Low dose aspirin
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74
Q

What are the risk factors of colorectal carcinoma?

A
  • Increasing age
  • Obesity and diet= Low fibre diet, high sugar, saturated animal fat and red meat
  • Colorectal polps, adenomas
  • Alcohol
  • Smoking
  • Ulcerative collitis
  • Genetic predisposition: Familial adenomatous polyposis, lynch syndrome
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75
Q

What is the clinical presentation of colorectal carcinoma?

A
  • The closer the cancer is to the outside, the more visible blood and mucous
  • Right sided carcinoma= Usually asymptomatic until iron deficiency anemia, may have a mass, low haemoglobin, abdominal pain
  • Left sided and sigmoid carcinoma= Change in bowel habits with blood/mucous
  • Rectal carcinoma= Rectal bleeding and mucous, thinner stool and tenesmus
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76
Q

What are the 4 cardinal signs of colonic obstruction?

A
  • Absolute constipation
  • Colicky abdominal pain
  • Abdominal distension
  • Vomitting
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77
Q

How is colorectal carcinoma diagnosed?

A
  • Faecal occult blood= Used in screening
  • Tumour markers e.g. CEA
  • Colonoscopy (Gold standard)= Allows for biopsy and removal of polyps
  • Double contrast barium enema= Doesn’t require sedation and no risk of perforation
  • CT colonoscopy
  • MRI to determine spread
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78
Q

How is colorectal carcinoma treated?

A
  • Surgery
  • Endoscopic stenting- For palliation in malignant obstruction
  • Radiotherapy
  • Chemotherapy
  • Polyp cancers are removed with colonoscopy
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79
Q

What is the normal pressure of the portal system?

A
  • 5-8 mmHg
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80
Q

Briefly explain the pathophysiology of portal hypertension?

A
  • Following liver injury and fibrogenesis, the contraction of activated myofibroblasts contributes to increased resistance to blood flow
  • This leads to portal hypertension, which leads to splanchnic vasodilation, and a drop in BP
  • This then leads to increased CO, so increased portal flow and formation of collaterals between portal and systemic system
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81
Q

What are the sites of collaterals between portal and systemic system?

A
  • Gastro-oesophageal junction
  • Rectum
  • Left renal vein
  • Diaphragm
  • Retroperitoneum
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82
Q

What are the causes of portal hypertension?

A
  • Pre hepatic= Portal vein thrombosis
  • Intra-hepatic= Cirrhosis, schistosomiasis, sarcoidosis
  • Post hepatic= Right heart failure, constrictive pericarditis, IVC obstruction
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83
Q

What are the clinical features of portal hypertension?

A
  • Often asymptomatic, or only clinical sign being splenomegaly
  • Chronic liver disease features= Haematemesis and malaena, clubbing, palmar erythema, dupuytren’s contracture, spider naevi
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84
Q

What is the epidemiology of chronic pancreatitis?

A
  • Males affected more than females

- Median age of presentation is 55yrs

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85
Q

What are the main causes of chronic pancreatitis?

A
  • Commonest cause in the developed world is long-term alcohol excess
  • CKD
  • Hereditary= defects in trypsinogen gene, cystic fibrosis
  • Autoimmune pancreatitis
  • Idiopathic
  • Trauma
  • Recurrent acute pancreatitis
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86
Q

Briefly explain the pathophysiology of chronic pancreatitis

A
  • Obstruction or reduction in bicarb secretion causes an alkaline pH
  • This causes activation of trypsinogen to trypsin
  • This plugs pancreatic ducts, and is then calcified resulting in obstruction and pancreatic damage
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87
Q

How is chronic pancreatitis diagnosed?

A
  • Serum amylase and lipase: may be elevated, but in advanced disease they may not be
  • MRI with MRCP for more subtle abnormalities
  • Abdominal ultrasound and contrast CT: detects calcification and a dilated pancreatic duct
  • Faecal elastase will be abnormal
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88
Q

What are the clinical features for chronic pancreatitis?

A
  • Epigastric pain that ‘bores’ through to the back: episodic or unremitting. Can be relieved by sitting forward. Exacerbated by alcohol
  • Nausea and vomitting
  • Decreased appetite and weight loss
  • Exocrine dysfunction: malabsorption, steatorrhoea, protein deficiency
  • Endocrine dysfunction: Diabetes
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89
Q

How is chronic pancreatitis treated?

A
  • Alcohol cessation
  • Abdominal pain: NSAIDS, opiates, tricyclic antidepressants
  • Duct drainage
  • Shock wave lithotripsy to fragment gallstones
  • Steatorrhea: pancreatic enzyme supplements, PPI
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90
Q

What is the epidemiology of acute mesenteric ischaemia?

A
  • Usually seen in over 50s
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91
Q

What are the causes of acute mesenteric ischaemia?

A
  • SMA thrombosis (commonest)
  • SMA embolism= due to AF
  • Mesenteric vein thrombosis
  • Non-occlusive disease
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92
Q

What are the clinical features of acute mesenteric ischaemia?

A
  • Acute severe abdominal pain (constant, central or around right iliac fossa)
  • No abdominal signs
  • Rapid hypovolaemia resulting in shock- pale skin, weak rapid pulse, reduced urine output, confusion
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93
Q

How is acute mesenteric ischaemia diagnosed?

A
  • Abdominal x ray= rules out other pathology
  • CT/MRI angiography= Can see a blockage
  • Laparotomy
  • Bloods= increased Hb and WCC, persistant metabolic acidosis
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94
Q

How is acute mesenteric ischaemia treated?

A
  • Fluid resuscitation
  • Antibiotics e.g. IV gentamycin and IV metronidazole
  • IV Heparin to reduce clotting
  • Surgery to remove dead bowel
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95
Q

What are the complications of acute mesenteric ischaemia?

A
  • Septic peritonitis

- Systemic inflammatory response syndrome

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96
Q

What is the epidemiology of large bowel obstruction?

A
  • Accounts for 25% of all intestinal obstruction
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97
Q

What are the main causes of large bowel obstruction?

A
  • 90% due to colorectal malignancy

- Volvulus in sigmoid colon

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98
Q

Briefly explain the pathophysiology of large bowel obstruction

A
  • The colon proximal to the obstruction dilates
  • Increased pressure and decreased blood flow
  • Full thickness necrosis as well as perforation
  • If it is do to a volvus, there is a twist resulting in a closed loop and increased pressure instead of an obstruction
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99
Q

What are the clinical features of large bowel obstruction?

A
  • Abdominal pain that is more constant than in SBO. Usually in left iliac fossa
  • Abdominal distension
  • Bowel sounds are normal, then increased, then quiet later
  • Palpable mass
  • Late vomitting (later than SBO), early Constipation (earlier than in SBO)
  • Nausea, fullness, bloating
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100
Q

How is large bowel obstruction diagnosed?

A
  1. Abdominal X ray= Peripheral gas shadows proximal to the blockage
  2. CT= Gold standard
  3. FBC= Low Hb
  4. Digital rectal exam
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101
Q

What is the epidemiology of small bowel obstruction?

A
  • Accounts for 60-75% of intestinal obstruction
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102
Q

What are the main causes of small bowel obstruction?

A
  • Adhesions (60% of SBOs) usually secondary to previous abdominal surgery
  • Hernia
  • Malignancy
  • Crohn’s disease
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103
Q

Briefly explain the pathophysiology of small bowel obstruction

A
  • Obstruction of the bowel leading to bowel distension
  • Proximal dilation above the block, resulting in increased secretions and swallowed air in the small bowel. Also decreased absorption, and increased pressure
  • Untreated, it leads to ischaemia, necrosis or inflammation
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104
Q

What are the clinical features of small bowel obstruction?

A
  • Pain= initially colicky, then diffuse
  • Profuse vomitting that follows pain= more rapid than LBO
  • Less distension as compared to LBO
  • Tenderness
  • Constipation with no passage of wind
  • Increased bowel sounds= Tinkling
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105
Q

How is SBO/LBO treated?

A
  • Aggressive fluid resuscitation
  • Bowel decompression= drip and suck
  • Analgesia and antiemetic
  • Antibiotics
  • Laparotomic surgery to remove obstruction
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106
Q

How is small bowel obstruction diagnosed?

A
  1. Abdominal X ray: shows central gas shadows that completely cross the lumen and no gas in the large bowel
  2. Examination of hernia orifices and rectum
  3. FBC is essential
  4. CT= gold standard
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107
Q

What causes pseudo-obstruction?

A
  • Intra-abdominal trauma
  • Post operative states e.g. paralytic ileus
  • Intra-abdominal sepsis
  • Pneumonia
  • Drugs e.g. opiates
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108
Q

What are the clinical features of pseudo-obstruction?

A

Patients present with rapid and progressive abdominal distention and pain
Identical presentation to SBO/LBO dependent on where the issue is

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109
Q

How is pseudo-obstruction diagnosed?

A

X ray shows a large, gas filled bowel

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110
Q

How is pseudo-obstruction treated?

A

Treat underlying cause

IV neostigmine

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111
Q

What is malabsorption?

A
  • The failure to fully absorb nutrients either because of the destruction to epithelium or due to a problem in the lumen
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112
Q

What are the causes of malabsorption?

A
  • Defective intraluminal digestion= pancreatitis, defective bile secretion
  • Insufficient absorptive area= Coeliac disease, Crohns, giardia lambila, surgery
  • Lack of digestive enzymes= Lactose intolerance, bacterial overgrowth
  • Defective epithelial transport
  • Lymphatic obstruction
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113
Q

How does pancreatitis cause malabsorption?

A
  • There is damage to most of the glandular pancreas

- Less or no enzymes are released

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114
Q

How does coeliac disease cause malabsorption?

A
  • Villi are very short if present at all sinse there is villous atrophy and crypt hyperplasia
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115
Q

How does Crohn’s cause malabsorption?

A
  • Causes inflammatory damage to the lining of the bowel resulting in cobblestone mucosa with significant reduction of absorptive surface area
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116
Q

How does Giardia lambila cause malabsorption?

A
  • Extensive surface parasitisation of the villi and microvilli. Parasites coat the surface, so food cannot be absorbed.
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117
Q

Briefly explain the pathophysiology of lactose intolerance

A
  • There is disaccharidase deficiency so cannot break down lactose in milk into glucose
  • The undigested lactose passes into the colon where it is then eaten up by bacteria
  • CO2 is released leading to wind and diarrhoea
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118
Q

What is the epidemiology of hepatocellular carcinoma?

A
  • 5th most common cancer worldwide
  • Accounts of 90% of live primaries
  • Common in china
  • More common in males
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119
Q

What are the risk factors of hepatocellular carcinoma?

A
  • Carriers of HBV and HCV have very high risk of developing HCC
  • Associated with cirrhosis
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120
Q

What are the clinical features of hepatocellular carcinoma?

A
  • Weight loss and anorexia
  • Fever
  • Fatigue
  • Jaundice
  • Ache in right hypochondrium
  • Ascites
  • Enlarged, irregular, tender liver
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121
Q

How is hepatocellular carcinoma diagnosed?

A
  • Serum alpha-fetoprotein may be raised
  • Ultrasound showing filling defects in 90% of cases
  • Enhanced CT: can diagnose if it is a large lesion
  • Liver biopsy
122
Q

How is hepatocellular carcinoma treated?

A
  • Surgical resection of isolated lesion
  • Liver transplant is only chance of cure
  • Prevention: widespread vaccination against HBV to reduce HCC incidence
123
Q

What is the epidemiology of pancreatic adenocarcinoma?

A
  • Typical patient is male above 60 yrs

- Typically occurs in the pancreatic head

124
Q

What are the risk factors of pancreatic adenocarcinoma?

A
  • Smoking
  • Excess alcohol/ caffeine
  • Excessive aspirin intake
  • Diabetes
  • Chronic pancreatitis
  • Family history
125
Q

What are the clinical features of pancreatic adenocarcinoma?

A
  • Anorexia
  • Weight loss
  • Diabetes
  • Acute pancreatitis
  • Head of pancreas: painless obstructive jaundice
  • Body and tail of pancreas: Epigastric pain which radiates to the back and is relieved by sitting forward
126
Q

How is pancreatic adenocarcinoma treated?

A
  • Surgery

- Palliative therapy: opiates, palliation of jaundice using stenting, nutritional supplements

127
Q

How is pancreatic adenocarcinoma diagnosed?

A
  • Usually present quite late
  • Cholestatic jaundice is non-specific but helps assess prognosis
  • Transabdominal ultrasound and CT to find pancreatic mass. Also can guide biopsy and help with staging.
128
Q

What is the epidemiology of gallstones?

A
  • May present at any age but unusual before 30s

- Increase in prevalence with age

129
Q

What are the main causes of gallstones?

A
  • Obesity and rapid weight loss
  • DM
  • Contraceptive pill
  • Liver cirrhosis
130
Q

What are the risk factors of gallstones?

A
  • Female
  • Fat
  • Fertile
  • Smoking
131
Q

What are the clinical features for gallstones?

A
  • Majority of gallstones are asymptomatic

- If they become symptomatic, they cause biliary colic or acute cholecystitis

132
Q

What are the two types of gallstones?

A
  • Cholesterol stones

- Pigment stones

133
Q

What are the complications of gallstones?

A
  • Jaundice
  • Acute cholecystitis
  • Pancreatitis
  • Gallstone ileus
  • Empyema
  • Cholangitis
134
Q

What are pigment gallstones made of?

A
  • Bilirubin polymers and calcium bilirubinate
135
Q

What are cholesterol gallstones made of?

A

Cholesterol, bile salts and phospholipids

136
Q

What are the clinical features of biliary colic?

A
  • Pain is sudden onset, severe but constant with crescendo characteristic
  • Usually pain starts mid evening and lasts until the early hours
  • Usually epigastrum pain but there may be a right upper quadrant component
  • Radiation of pain into right shoulder and right subscapular pain
  • Nausea and vomitting in severe attacks
137
Q

How is biliary colic diagnosed?

A
  • Unlikely to be associated with significant abnormality of lab test
  • Abdominal ultrasound
138
Q

How is biliary colic treated?

A
  • Laparoscopic cholecystectomy
  • Stone dissolution with oral ursodeoxycholic acid or cholesterol lowering agents
  • Shock wave lithrotripsy
139
Q

What is Wilson’s disease?

A

Rare inherited disorder of biliary copper excretion with too much copper in the liver and CNS

140
Q

What are the risk factors for Wilson’s disease?

A

Family history

141
Q

Briefly explain the pathophysiology of Wilson’s disease

A

A very rare inborn error of copper metabolism that results in copper deposition in various organs, including the liver and the basal ganglia.

142
Q

What are the clinical features of Wilson’s disease?

A
  • Children present with hepatic problems
  • Young adults tend to present with more CNS problems eg. tremor, dysphagia etc
  • Reduced memory
  • Kayser-Fleischer ring= green brown pigment at the corneoscleral junction
143
Q

How is Wilson’s disease diagnosed?

A
  • Serum copper and caeruloplasmin are reduced/ normal
  • 24hr urine copper is high
  • Liver biopsy shows increased hepatic copper, hepatitis and cirrhosis
  • Haemolysis and anaemia
  • MRI will show basal ganglia and cerebellar dysfunction
144
Q

How is Wilson’s disease treated?

A
  • Avoid food high in copper

- Lifelong chelating agent e.g. pencillamine

145
Q

What are the clinical features of cholecystitis?

A
  • Initially, continuous epigastric pain
  • Progression with severe localised right upper quadrant pain
  • Pain is associated with tenderness and muscle guarding or rigidity
  • Vomitting, fever and local peritonitis
  • Infammatory component
  • Can lead to obstructive jaundice and cholangitis
146
Q

How is cholecystitis diagnosed?

A
  • Blood tests: Raised WCC and CRP. Increased serum bilirubin, alk phosphatase and aminotransferase
  • Abdominal ultrasound: Thick walled, shrunken gallbladder, pericholecystic fluid, stones
  • Examination: Right upper quadrant tenderness, Murphy’s sign
147
Q

How is cholecystitis treated?

A
  • Nil by mouth
  • IV fluids
  • Opiate analgesia
  • IV antibiotics e.g. cefuroxime or ceftriaxone
  • Cholecystectomy after a few days to allow symptoms to subside
148
Q

What is ascending cholangitis?

A

An infection of the biliary tree and most often occurs secondary to common bile duct obstruction by gallstones

149
Q

What are the clinical features of ascending cholangitis?

A
  • Biliary colic

- Fever, jaundice, right upper quadrant pain

150
Q

How is ascending cholangitis diagnosed?

A
  • Blood tests= Increased neutrophil count, increased ESR and CRP, increased serum bilirubin-bile obstruction, increased serum alk phosphatase, increased aminotransferase
  • Transabdominal ultrasound
  • Magnetic resonance cholangiography
  • CT
151
Q

How is ascending cholangitis treated?

A
  • IV antibiotics e.g. cefotaxime and metronidazole
  • Urgent biliary drainage
  • Surgery is required for larger stones
152
Q

What are varices?

A

Dilated veins at the junction between the portal and systemic venous systems leading to variceal haemorrhage

153
Q

What are the clinical features of varices?

A
  • Haematemesis
  • Abdominal pain
  • Rectal bleeding
  • Liver disease= Jaundice, increased bruising, ascites
  • Pallor
  • Shock
  • Splenomegaly
  • Hyponatraemia
154
Q

Briefly explain the pathophysiology of varices

A

Liver disease leads to high pressure in the portal vein. This leads to veins at the junction with the systemic venous system (varices). This causes damage and can lead to bleeding from the varices into the oesophagus.

155
Q

What are the risk factors for varices?

A
  • Cirrhosis
  • Portal hypertension
  • Schistosmiasis infection
  • Alcoholism
156
Q

What are the causes of varices?

A
  • Portal hypertension= caused by alcoholism and viral cirrhosis
  • Thrombosis in portal/ splenic vein
157
Q

How is varices diagnosed?

A

Endoscopy to find bleeding source

158
Q

How are varices treated?

A
  • Treat shock
  • Vasoactive drugs (IV terlipressin), endoscopic band ligation and antibiotics
  • Can obturate with glue like substance
159
Q

What are some possible complications of varices?

A

70% chance of rebleeding

Significant risk of death

160
Q

What are the causes of haemochromatosis?

A
  • HFE gene mutation
  • High intake of iron and chelating agents
  • Alcohol
161
Q

What is the epidemiology of haemochromatosis?

A
  • More common in men as menstrual blood is protective
162
Q

Briefly explain the pathophysiology of haemochromatosis

A

Increased iron absorption. Excess iron is then gradually taken up by the liver and other tissue over a long period. The iron itself precipitates fibrosis.

163
Q

What are the clinical features of haemochromatosis?

A
  • Early on there is tiredness and arthralgia
  • Hypogonadism
  • Slate grey skin pigmentation, signs of chronic liver disease
  • Osteoporosis
  • Cardiac manifestations= Heart failure, cardiomyopathy
  • In gross iron overload there is a classical triad= Bronze skin pigmentation, hepatomegaly, DM
164
Q

How is haemochromatosis diagnosed?

A
  • Homozygous= Raised serum iron, raised serum ferritin
  • Heterozygotes= Slightly raised serum iron transferrin saturation or ferritin
  • MRI= Detects iron overload
  • Liver biopsy= Can establish extent of damage
  • ECG/ ECHO if cardiomyopathy
165
Q

How is haemochromatosis treated?

A
  • Lifelong venesection
  • Testosterone replacement
  • If venesection not tolerated, chelation therapy
  • Diet low in iron
  • Avoid fruit and white wine
  • Screening
166
Q

What are the main causes of acute pancreatitis?

A 
I= Idiopathic
G= Gallstones (majority)
E= Ethanol
T= Trauma
S= Steroids
M= Mumps
A= Autoimmune
S= Scorpion venom
H= Hyperlipidaemia
E= ERCP
D= Drugs e.g. azathioprine, furosemide, corticosteroids, NSAIDS, ACE inhibitors
167
Q

What are the clinical features of acute pancreatitis?

A
  • Severe epigastric or central abdominal pain that radiates to back
  • Anorexia, nausea and vomitting= dehydration and hypotension
  • Tachycardia
  • Fever
  • Jaundice
  • Periumbilical ecchymosis= Cullens sign
  • Left flank Bruising= Grey Turners sign
168
Q

How is acute pancreatitis diagnosed?

A
  • Serum amylase= 3x more than normal
  • Lipase levels rising
  • Excluding differentials and seeing extent of damage; erect CXR, Contrast enhanced CT, Abdominal ultrasound, MRI
169
Q

How is acute pancreatitis treated?

A
  • Mild= Pain relief (IV pethidine or IV morphine), IV fluid
  • Severe= IV antibiotics if necrotising, feed with enteral nutrition, monitor for complications
  • Drainage of collections may be required
170
Q

What are the complications of acute pancreatitis?

A

Systemic inflammatory response syndrome

171
Q

What is gastritis?

A

Inflammation of the gastric mucosa

172
Q

What causes gastritis?

A
  • Most commonly H pylori infection

- Also possible: autoimmune gastritis, viruses, duodeno-gastric reflux, alcohol, some medications

173
Q

What are the clinical features of gastritis?

A
  • Usually asymptomatic
  • Sometimes functional dyspepsia
  • Upper abdominal pain
  • Nausea and vomitting
  • Haematemesis
174
Q

How is gastritis diagnosed?

A
  • Endoscopy: can appear reddened or normal
  • Histological changes: detected through biopsy
  • Blood tests, stool tests- inflammation or erosions
  • Faecal occult blood tests, faecal calprotecin
  • H pylori urea breath tests
175
Q

How is gastritis treated?

A
  • Eradication of H pylori= Triple therapy
  • Remove causative agents such as alcohol
  • Reduce stress
  • H2 Antagonists= reduce acid release
  • PPIs= Reduce acid release (can be preventative)
  • Antacids
176
Q

What are the clinical features of Hep A?

A
  • Viraemia= patient feels unwell with non specific symptoms (nausea, fever, malaise)
  • After 1-2 weeks, patient becomes jaundiced
  • Hepatosplenomegaly
  • Normally is over within 3-6 weeks
177
Q

How is Hep A diagnosed?

A
  • Liver biochemistry (prodromal stage)= Bilirubinaemia and increased urinary urobilinogen, raised serum AST or ALT
  • Once jaundice has presented: Serum bilirubin reflects jaundice
  • Blood tests: leucopenia, reduced WCC, Raised ESR
  • Viral markers: Anti Hep A antibodies, IgM in acute infection
178
Q

How is Hep A treated?

A
  • Supportive treatment
  • Avoid alcohol and sex
  • Monitor liver function to spot fulminant hepatic failure
  • Manage close contacts by giving normal human immunoglobulin for Hep A
179
Q

What are the clinical features of Hep B?

A
  • Viraemia= patient feels unwell with non specific symptoms (nausea, fever, malaise)
  • There may be rashes
  • After 1-2 weeks, patient becomes jaundiced
  • Hepatosplenomegaly
  • Normally over quickly
  • In chronic HBV, can result in cirrhosis, liver failure and carcinoma
180
Q

How is Hep B diagnosed?

A
  • HBsAg is present 1-6 mnth after exposure
  • HBsAg presence for more than 6 month implies carrier status
  • Anti-HBs= antibodies to Hep B
181
Q

How is Hep B treated?

A
  • Acute= supportive, avoid alcohol and sex, manage close contacts, monitor liver function
  • Chronic= SC pegylated interferon -alpha-2A
182
Q

What are the clinical features of Hep C?

A
  • Most acute infections are asymptomatic
  • 10% Have mild influenza like illness with jaundice and a rise in ALT and ASTs
  • In chronic= cirrhosis, liver failure, hepatocellular carcinoma
183
Q

How is Hep C diagnosed?

A
  • HCV antibody presents within 4-6 weeks

- HCV RNA: Indicates current infection

184
Q

How is Hep C treated?

A
  • Acute HCV: Supportive treatment
  • Antivirals
  • Triple therapy with direct acting antivirals
185
Q

Which types of hepatitis can be both acute and chronic?

186
Q

Which types of hepatitis are a DNA virus?

187
Q

Which types of hepatits are a RNA virus?

A

A, D (Incomplete Hep B dna virus), C (RNA flavivirus)

188
Q

What are the main causes of alcoholic liver disease?

A

Alcohol
Genetic predisposition
Immunological mechanisms

189
Q

How does alcohol lead to a fatty liver and cirrhosis?

A
  • Metabolism of alcohol produces fat in the liver
  • This is minimal with small amounts, but larger amounts causes fat swelling (Steatosis)
  • In some cases collagen is laid down around central hepatic veins= cirrhosis
190
Q

What are the clinical features of alcoholic fatty liver disease?

A
  • Often asymptomatic
  • Vague abdominal symptoms due to general effects of alcohol
  • Hepatomegaly
191
Q

What are the clinical features of alcoholic cirrhosis?

A
  • Patient can be very well with few symptoms
  • On examination, there are usually signs of chronic liver disease
  • Features of alcohol dependance
192
Q

What are the clinical features of alcoholic hepatitis?

A
  • Patient may be well- hepatitis only on biopsy
  • Mild= moderate symptoms of ill health with mild jaundice, signs of chronic liver disease
  • Severe= Abdominal pain and high fever due to necrosis. Severe jaundice, hepatomegaly and ascites with ankle oedema.
193
Q

How is alcoholic liver disease diagnosed?

A
  • High MCV indicates heavy drinking
  • Fatty liver= high ALT and AST. Ultrasound or CT will demonstrate fatty liver (as well as histology)
  • Hepatitis= Leucocytosis. Elevated bilirubin, high AST&ALT, high alk phos and prothrombin time
  • CT to show cirrhosis
194
Q

How is alcoholic liver disease treated?

A
  • Stop alcohol (use diazepam for DT)
  • Diet high in vitamins and protein
  • Alcoholic hepatitis= steroids for short term benefit
  • Alcholic cirrhosis= Reduce salt intake, liver transplant
195
Q

What are the most common viral causes of diarrhoea?

A
  • Rotavirus (more common in children)
  • Norovirus
  • Adenovirus
  • Astrovirus
196
Q

What are the most common bacterial causes of diarrhoea?

A
  • Campylobacter jejuni
  • E coli
  • Salmonella
  • Shigella
197
Q

What parasite causes diarrhoea?

A
  • Giardia lamblia
198
Q

What is C. Difficile?

A
  • Gram-positive spore forming bacteria
  • Can give rise to pseudomembranous colitis where C.diff replaces gut flora= diarrhoea
  • Due to antibiotic use (Beginning with C)
199
Q

How is C. Difficile treated?

A
  • Metronidazole or Oral vancomycin
  • Stool transplant
  • Stop C antibiotic
200
Q

How is infective diarrhoea treated?

A
  • Oral rehydration and avoid high sugar drinks
  • Anti-emetics to treat vomitting (metoclopramide)
  • Antibiotics
  • Anti motility agents
201
Q

What are the clinical features of liver failure?

A
  • Hepatic encephalopathy
  • Abnormal bleeding
  • Ascites
  • Jaundice
  • Mental state shows drowsiness and confusion due to cerebral oedema
202
Q

What causes liver failure?

A
  • Toxins= alcohol, paracetamol
  • Infections= Hepatitis, EBV, CMV
  • Neoplasia
  • Metabolic= Wilsons, haemochromatosis
  • Other= Acute fatty liver of pregnancy, ischaemia, autoimmune causes
203
Q

What is the most common acute cause of liver failure?

A

Paracetamol poisoning

204
Q

How is liver failure diagnosed?

A
  • Raised bilirubin. Low glucose. Low coagulation factors. High PTT. High ammonia
  • Imaging= EEG, Ultrasound, CXR, Doppler ultrasound
  • Microbiology for infection
205
Q

How is liver failure treated?

A
  • Treat cause
  • Treat symptoms
  • Liver transplant in severe cases
206
Q

What is diverticulosis?

A

Presence of diverticula

207
Q

What is diverticular disease?

A

Diverticula are symptomatic

208
Q

What is diverticulitis?

A

Inflammation of diverticulum

209
Q

What are the main causes of diverticula?

A
  • Low fibre diet= Commonly eaten in developed countries, rare in rural Africa
  • Obesity
  • Smoking
  • NSAIDs
210
Q

Briefly explain the pathophysiology of diverticula

A

Herniation of mucosa through weakened muscular walls near blood vessels. Can lead to perforation, fistula formation, with bladder, intestinal or vaginal obstruction.

211
Q

What are the clinical features of diverticula?

A
  • Asymptomatic in 95% of cases
  • Can be pain, constipation, bleeding or diverticulitis
  • Severe cases: left iliac fossa pain, fever, nausea
212
Q

How are diverticula diagnosed?

A
  • Blood tests: polymorphonuclear leucocytes, ESR&CRP raised
  • CT colonography: will show colonic wall thickening and diverticula
  • Pericolic collections and abscesses
213
Q

How is diverticular disease treated?

A
  • Well balanced high fibre diet with smooth muscle relaxants
214
Q

How is acute diverticulitis treated?

A
  • Mild attacks can be treated with oral antibiotics e.g. ciprofloxacin
  • Bowel rest, IV fluids
  • Surgical resection is occasionally required
215
Q

What are the clinical features of coeliac disease?

A
  • Approx 1/3 are asymptomatic
  • Persistent GI symptoms
  • Faltering growth
  • Prolonged fatigue
  • Unexplained weight loss
  • Severe mouth ulcers
  • Anaemia
  • IBS
  • Osteoporosis
216
Q

What are the risk factors for coeliac disease?

A
  • Other autoimmune disease
  • IgA deficiency
  • Breast feeding
  • Rotovirus infection in infancy
217
Q

How is coeliac disease diagnosed?

A
  • IgA tissue transglutaminase antibodies have a very high sensitivity and specificity for coeliacs. Also endomysial antibodies
  • Distal duodenal biopsy: histological changes
  • FBC: Low Hb, Low B12, Low ferritin
218
Q

How is coeliac disease treated?

A
  • Gluten free diet
  • Nutritional supplement as required
  • DEXA scan to monitor osteoporotic risk
219
Q

What are the risk factors for Crohn’s disease?

A
  • Genetic association
  • Female
  • NSAIDS
  • Chronic stress and depression
  • Good hygiene
220
Q

What are the clinical features of Crohn’s disease?

A
  • Diarrhoea with urgency, bleeding and pain
  • Abdominal pain, weight loss and anorexia
  • Malaise
  • Lethargy
  • Perianal abscess
  • Extraintestinal signs= oral ulcers, clubbing, skin and eye problems
221
Q

How is Crohn’s disease diagnosed?

A
  • Examination= tenderness of right iliac fossa
  • Bloods= anaemia, raised ESR&CRP, Raised WCC and platelets, hypoalbuminaemia if severe, liver biochemistry may be abnormal
  • Faecal calprotectin= Indicates IBD but not specific
  • Colonoscopy= Biopsy will see spot lesions and inflammation
222
Q

How is Crohn’s disease treated?

A
  • Stop smoking
  • Corticosteroids to induce remission
  • Thiopurines to maintain remission
  • Anti TNF alpha
  • 80% require surgery at some point. Temporary ileostomy to allow time for affected areas to rest, or resection at worst areas.
223
Q

What are the risk factors for ulcerative colitis?

A
  • Smoking is protective
  • Aged 15-30
  • Family history
  • NSAIDs
  • Chronic stress and depression
224
Q

What are the clinical features of ulcerative colitis?

A
  • Restricted pain in lower left quadrant. Cramps
  • Episodic or chronic diarrhoea with blood and mucous. Urgency and incontinence
  • Acute= Fever, tachy, tender distended abdomen
  • Extraintestinal signs= Clubbing, aphthous oral ulcers, erythma nodusum and amyloidosis
225
Q

What is the macroscopic appearance of ulcerative colitis?

A
  • Begins in the rectum and extends without skips
  • Mucosa looks redenned and inflamed. It bleeds easily
  • Ulcers and pseudopolyps in severe disease
226
Q

What is the microscopic appearance of ulcerative colitis?

A
  • Mucosal inflammation= doesnt go deeper
  • No granulomata
  • Depleted goblet cells
  • Increased crypt abscesses
227
Q

How is ulcerative colitis diagnosed?

A
  • Blood tests= WCC and platelets raised in moderate/severe attacks
  • Iron deficiency anaemia. ESR and CRP raised. Liver biochemistry may be abnormal. Hypoalbuminaemia in severe disease. pANCA may be positive
  • Faecal calprotectin= indicates IBD but non specific
  • Colonoscopy with mucosal biopsy is gold standard.
228
Q

How is ulcerative colitis treated?

A
  • 5-Aminosalicylic acid= drug of choice for remission and relapse prevention
  • Glucocorticoids if don’t respond to 5asa
  • Surgery if severe disease
229
Q

What is the macroscopic appearance of Crohn’s disease?

A
  • Not continuous.
  • Thickened area of bowel
  • Cobblestone appearance due to ulcers and fissures
  • Can affect any part of GI tract
230
Q

What is the microscopic appearance of Crohn’s disease?

A
  • Inflammation extends through all layers of the bowel
  • Increase in chronic inflammatory cells and there is lymphoid hyperplasia
  • Granulomas present in 50-60%
231
Q

What are the main causes of peritonitis?

A
  • Bacterial= E coli, klebsiella, staph aureus

- Chemical= Bile or clotted blood

232
Q

What are the clinical features of peritonitis?

A
  • Perforation= Sudden onset with acute severe abdominal pain followed by general collapse and shock
  • Poorly localised, then moving to one point on the the abdomen
  • Pain is relieved by staying still
233
Q

How is peritonitis diagnosed?

A
  • Blood tests= Raised WCC and CRP, Serum amylase to exclude pancreatitis, HCG to rule out pregnancy
  • Erect CXR to see free air under diaphragm which indicates perforated colon
  • Abdominal X ray to exclude bowel obstruction
234
Q

How is peritonitis treated?

A
  • ABC
  • Treat underlying cause rapidly
  • IV fluids
  • IV antibiotics e.g. cefuroxime and metronidazole
  • Surgical cleaning of abdominal cavity
235
Q

What antibiotic is used against enterobacteriaciae?

A

Beta lactam antibiotics such as cefuroxime

236
Q

What antibiotic is used against anaerobes?

A

Metronidazole

237
Q

What is Rosvings sign?

A

When you press on the left illiac fossa, there will be pain in the right illiac fossa

= Appendicitis

238
Q

What are the clinical features of alpha-1-antitrypsin deficiency in the liver?

A
  • Neonates may present jaundice and hepatitis

- A rare cause of cirrhosis

239
Q

What is a Mallory-Weiss tear?

A

A linear mucosal tear occurring at the oesophogastric junction and produced by a sudden increase in intra-abdominal pressure

240
Q

What is the epidemiology of Mallory-Weiss tear?

A

Most common in males, seen mainly in age 20-50

241
Q

What are the risk factors for Mallory-Weiss tears?

A
  • Alcoholism
  • Forceful vomitting
  • Eating disorders
  • Male
  • NSAID abuse
242
Q

What are the clinical features of Mallory-Weiss tears?

A
  • Vomitting
  • Haematemesis after vomitting
  • Retching
  • Postural hypotension
  • Dizziness
243
Q

How is Mallory-Weiss tears diagnosed?

244
Q

How are Mallory-Weiss tears treated?

A
  • Most bleeds are minor and heal in 24 hrs

- Surgery if very large tear

245
Q

What is the epidemiology of perianal abscesses?

A

2/3x more common in gay sex and those who have anal sex

246
Q

What are the clinical features of perianal abscesses?

A
  • Painful swelling
  • Tender
  • Discharge
247
Q

How are perianal abscesses diagnosed?

A
  • MRI

- Endoanal ultrasound

248
Q

How are perianal abscesses treated?

A
  • Surgical excision

- Drainage with antibiotics

249
Q

What is a fissure-in-ano?

A

Painful tear in the sensitive skin-lined lower anal canal, resulting in pain on defecation

250
Q

What is the epidemiology of fissure-in-ano?

A
  • 90% are posterior

- Females affected more than males

251
Q

What are the main causes of fissure-in-ano?

A
  • Hard faeces

- Spasm

252
Q

What are the clinical features of fissure-in-ano?

A
  • Extreme pain, especially on daefecation

- Bleeding

253
Q

How are fissure-in-ano diagnosed?

A
  • History

- Perianal inspection

254
Q

How are fissure-in-ano treated?

A
  • Increase dietary fibre and fluids to make stools softer
  • Lidocaine ointment and GTN ointment
  • Botox injection (2nd line)
255
Q

What are the causes of cirrhosis?

A
  • Common causes; Chronic alcohol abuse, NAFLD, Hepatitis

- Rare causes; PBC, Autoimmune hepatitis, haemochromatosis, Wilson’s disease, Alpha-1-antitrypsin deficiency

256
Q

What are the clinical features of cirrhosis?

A
  • Leuconychia
  • Clubbing, palmar erythema
  • Dupuytren’s contracture
  • Spider naevi
  • Xanthelasma
  • Loss of body hair
  • Hepatomegaly, bruising
  • Peripheral oedema
  • Abdo pain due to ascites
257
Q

How is cirrhosis diagnosed?

A
  • Child-Pugh classification= Ascites, encephalopathy, high bilirubin, low albumin, long PTT
  • Liver biopsy= gold standard
  • Liver biochemistry= May be normal, increased AST and ALT
  • Ultrasound and CT
258
Q

How is cirrhosis treated?

A
  • Good nutrition, reduce salt, alcohol abstinence, avoid NSAIDs
  • 6 monthly ultrasound for HCC
  • Treat underlying cause
  • Liver transplant
259
Q

What are the possible complications of cirrhosis?

A
  • Fall in clotting factors X, IX, VII, II
  • Encephalopathy
  • Portal hypertension
260
Q

Briefly explain how cirrhosis occurs

A

Chronic liver injury causes fibrosis and activation of stellate and kupffer cells. This releases inflammatory mediators, and increased myofibroblasts leads to progressive collagen matrix deposition resulting in fibrosis and scar tissue, causing reduced liver function.

261
Q

What is ascites?

A

Ascites is the accumulation of free fluid in the peritoneal cavity

262
Q

What are the main causes of ascites?

A
  • Local inflammation; peritonitis, intra abdominal surgery, abdominal cancers (ovarian)
  • Low protein; Nephrotic syndrome, malnutrition
  • Low flow; Cirrhosis, portal hypertension, Cardiac failure
263
Q

What are the risk factors for ascites?

A
  • High sodium diet
  • HCC
  • Splanchnic vein thrombosis resulting in portal hypertension
264
Q

What are the clinical features of ascites?

A
  • Distended abdomen
  • Fullness in the flanks and shifting dullness
  • Mild abdominal pain
  • Itching due to jaundice
  • Peripheral oedema
265
Q

How is ascites diagnosed?

A
  • Presence of fluid is confirmed by shifting dullness
  • Diagnostic aspiration of 10-20ml of fluid using ascitic tap for raised WCC
  • Protein measurement of fluid from tap
266
Q

How is ascites treated?

A
  • Treat underlying cause
  • Reduce sodium to help liver and reduce fluid retention
  • Increase renal sodium excretion
  • Diuretic= aldosterone antagonist (spironlactone)
  • Drain fluid
267
Q

What is the epidemiology of inguinal hernia?

A
  • Commonest type of hernia
  • More common in males over 40
  • Accounts for 70% of all abdominal hernia
268
Q

What are the risk factors for inguinal hernia?

A
  • Male
  • Chronic cough
  • Constipation
  • Urinary obstruction
  • Heavy lifting
  • Ascites
  • Past abdominal surgery
269
Q

Are direct or indirect inguinal hernias more common?

270
Q

Are direct or indirect inguinal hernias medial to the inferior epigastric vessles?

A

Direct (Lateral is indirect)

271
Q

Are direct or indirect inguinal hernias more likely to strangulate?

272
Q

How are inguinal hernias treated?

A
  • Medically; use of truss to contain and prevent further progression
  • Surgery
273
Q

List some types of hernia

A
  • Inguinal
  • Femoral
  • Incisional
  • Hiatus
274
Q

What is a femoral hernia?

A

Bowel comes through the femoral canal below the inguinal ligament

275
Q

How are femoral hernias treated?

A
  • Surgical repair
  • Herniotomy- ligation and excision of the sac
  • Herniorrhaphy
276
Q

A woman presents with a lump in the upper medial right thigh which appears to point down the leg. It is very painful, and cannot reduce. What is it likely to be?

A

Strangulating femoral hernia

277
Q

What is an incisional hernia

A

Occurs when tissue protrudes through a weak surgical scar. Often a complication of abdominal surgery.

278
Q

What are the 2 types of hiatus hernia?

A
  • Sliding hiatus hernia

- Rolling or para-oesophageal hiatus

279
Q

What is the difference between a sliding, and a rolling hiatus hernia?

A

Sliding occurs when the gastro-oesophageal slides up and lies above the diaphragm, but a rolling is where the gastro-oesophageal junction remains in the abdomen

280
Q

How is hiatus hernia diagnosed?

A
  • Barium swallow

- Upper GI endoscopy

281
Q

How is hiatus hernia treated?

A

Lose weight, treat reflux symptoms, surgery to prevent strangulation

282
Q

What causes haemorrhoids?

A
  • Constipation with prolonged straining

- Minor causing; congestion from pelvic tumour, pregnancy, CCF, portal hypertension

283
Q

Breifly explain the pathophysiology of haemorrhoids

A

Vascular cushions protrude through tight anus and becomes more congested. Hypertrophy occurs, but this causes the vascular cushions to protrude more readily. Protrusions may then strangulate.

284
Q

What are the clinical features of haemorrhoids?

A
  • Bright red rectal bleeding
  • Mucous discharge
  • Severe anaemia
  • Weight loss, tenesmus, change in bowel habit
285
Q

How are haemorrhoids diagnosed?

A

PR Exam

Protoscy for internal haemorrhoids

286
Q

How are haemorrhoids treated?

A
  • Medical; increase fluid and fibre intake +/- topical analgesics
  • Rubber band ligation
  • Sclerosants
  • Surgical haemorrhoidectomy
287
Q

What is the epidemiology of primary biliary cholangitis?

A

Women aged 40-50yrs

288
Q

What are the risk factors for primary biliary cholangitis?

A
  • +ve family history
  • Many UTIs
  • Smoking
  • Past pregnancy
  • Other autoimmune disease
  • Use of nail polish
289
Q

Briefly explain the pathophysiology of primary biliary cholangitis

A

Interlobar bile ducts are damaged by chronic autoimmune granulomatous inflammation resulting in cholestasis which may lead to fibrosis, cirrhosis and portal hypertension. Serum anti-mitochondrial antibodies found in almost all patients.

290
Q

What are the clinical features of primary biliary cholangitis?

A
  • Asymptomatic patients are discovered on routine examination or screening and may have hepatomegaly, increased alk phos, or anti-mitochondrial antibodies
  • Pruritus is often earliest symptom
  • Lethargy and fatigue
  • Pigmented xanthelasma on eyelids
291
Q

How is primary biliary cholangitis diagnosed?

A
  • Bloods; increased alk phos, increased serum cholesterol, AMAs, raised serum IgM
  • Liver biopsy; Portal tract infiltrate of plasma cells and lymphocytes, portal tract fibrosis, damage to and loss of small bile ducts
  • Ultrasound; Can show a diffuse alteration in liver architecture
292
Q

How is primary biliary cholangitis treated?

A
  • Ursodeoxycholic acid
  • Vitamin supplements
  • Bisphosphonates for osteoporosis
  • Pruritus; cholestyramine or naloxone
  • Liver transplant
293
Q

What are the possible complications of primary biliary cholangitis?

A
  • Cirrhosis
  • Osteoporosis
  • Malabsorption of fat soluble vitamins
  • Decreased bilirubin
294
Q

What is primary sclerosing cholangitis?

A

Chronic inflammation and fibrosis of the bile ducts

295
Q

What are the clinical features of primary sclerosing cholangitis?

A
  • May be asymptomatic- usually found incidentally

- Charcot’s triad; Fever, RUQ pain and jaundice

296
Q

What is the epidemiology of primary sclerosing cholangitis?

A
  • 75% have association with ulcerative collitis
  • Males
  • Median age 35 yrs
297
Q

What are the complications of primary sclerosing cholangitis?

A
  • Eventual liver failure

- 15% get cholangiocarcinoma

298
Q

Briefly explain the pathophysiology of primary sclerosing cholangitis?

A

Progressive obliterative fibrosis in the intra and extra hepatic ducts can cause strictures of the ducts= cholestatic jaundice and RUQ pain. Eventually leads to cirrhosis

299
Q

What is the aetiology of primary sclerosing cholangitis?

A
  • Generally unknown
  • Possibly genetic, lymphocyte recruitment, portal bacteraemia and bile salt toxicity
  • Secondary; can be secondary to infection, thrombosis or iatrogenic
300
Q

How is primary sclerosing cholangitis diagnosed?

A
  • Ultrasound; may show bile duct dilation
  • ERCP; Can help, but invasive
  • LFT; Elevated ALP or GGT. Serum transaminase levels can be normal to several times normal. Serum albumin drops with progression
301
Q

How is primary sclerosing cholangitis treated?

A
  • Usually manage symptoms of liver failure (eventual transplant)
  • ERCP can dilate some extra-hepatic strictures to slow progression
  • High dose ursodeoxycholic acid can slow progression

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