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Phase 2a Medicine > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

What is GORD

A

Gastro-oesophageal reflux disease

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2
Q

What is the pathology of GORD

A

Caused by reflux of stomach contents into the oesophagus.

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3
Q

What are 7 causes of GORD

A

Lower oesophageal sphincter hypotension
Hiatus hernia
Oesophageal dysmotility
Obesity
Gastric acid hypersecretion
Delayed gastric emptying
Smoking, alcohol, pregnancy, drugs.

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4
Q

What are the 5 oesophageal clinical manifestations of GORD

A

Heartburn (burning, retrosternal discomfort after meals)
Belching
Acid brash (acid regurgitation)
Waterbrash
Odynophagia (swallowing pain)

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5
Q

What are the 4 extra-oesophageal clinical manifestations of GORD

A

Nocturnal asthma
Chronic cough
Laryngitis
Sinusitis

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6
Q

What are 2 differential diagnoses for GORD

A

Oesophagitis from corrosives, NSAIDs, herpes
Duodenal or gastric ulcers

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7
Q

What are 3 investigations for GORD

A

Endoscopy if dysphagia
24h oesophageal pH monitoring
Manometry help diagnose GORD when endoscopy is normal

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8
Q

What are the lifestyle changes for management of GORD

A

Weight loss
Smoking cessation
Small, regular meals
Reduce hot drinks, alcohol, citrus fruits, tomatoes, onions, fizzy drinks

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9
Q

What are 3 types of drugs used for GORD

A

Antacids
H2 receptor antagonists e.g. ranitidine
Proton pump inhibitor – lansoprazole

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10
Q

What is peptic ulceration

A

A break in the inner lining of the stomach, first part of the small intestine or sometimes the lower oesophagus.

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11
Q

What are 2 pathological causes of Peptic ulceration

A

Inflammation caused by the bacteria H.pylori
Erosion from stomach acids.

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12
Q

What are the 6 clinical manifestations of peptic ulceration

A

Epigastric pain often related to hunger, specific foods, or time of day
Fullness after meals
Heart burn (retrosternal pain)
Tender epigastrium
ALARM symptoms
Swallowing difficulty

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13
Q

What are the ALARM symptoms

A

for peptic ulceration
Anaemia
Loss of weight
Anorexia
Recent onset
Melaena/haematemesis (vomit/ faeces containing blood)

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14
Q

What are the tests for h.pylori

A

Urea breath test, serology, stool antigen test

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15
Q

What is the treatment for h.pylori

A

appropriate Proton Pump Inhibitor and 2 antibiotic combination
e.g.
Lansoprazole with clarithromycin and metronidazole.

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16
Q

What are the 5 risk factors for duodenal ulcer

A

H.pylori, drugs
increased gastric acid secretion and emptying, blood group O

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17
Q

What are 4 symptoms and signs for Duodenal ulcer

A

Asymptomatic
Epigastric pain
Weight loss
Epigastric tenderness

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18
Q

What are the tests for duodenal ulcer

A

Upper GI endoscopy
Test for H. pylori

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19
Q

What are 2 differential diagnoses for duodenal ulcers

A

Non-ulcer dyspepsia
Duodenal Crohn’s

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20
Q

What are 4 risk factors for gastric ulcers

A

H.pylori, smoking, NSAIDs
Age

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21
Q

What are 3 symptoms for gastric ulcer

A

Asymptomatic
Epigastric pain
Weight loss

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22
Q

What is the investigation for gastric ulcer

A

Upper GI endoscopy to exclude malignancy

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23
Q

What is the treatment for gastric ulcer

A

Proton pump inhibitors

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24
Q

What is the overall treatment for peptic ulcers

A

Lifestyle: decrease alcohol and tobacco use
H.pylori eradication
Drugs to reduce acid: Proton pump inhibitors are effective e.g. lansoprazole
Drug-induced ulcers: stop drug if possible.

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25
Q

what are Oesophago-gastric varices

A

Submucosal venous dilatations secondary to high portal pressures.

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26
Q

What is the complication of Oesophago-gastric varices

A

Bleeding can be brisk, particularly if underlying coagulopathy secondary to loss of hepatic synthesis of clotting factors.

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27
Q

What are 3 causes of oesophago-gastric varices

A

Cirrhosis
Thrombosis
Parasitic infection

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28
Q

What is a pre-hepatic cause of portal hypertension

A

thrombosis (portal or splenic vein)

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29
Q

What are 5 intra-hepatic causes of portal hypertension

A

cirrhosis, schistosomiasis, sarcoid, myeloproliferative diseases, congenital hepatic fibrosis

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30
Q

What are 4 post-hepatic causes of portal hypertension

A

Budd-Chiari syndrome, right heart failure, constrictive pericarditis, veno-occlusive disease

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31
Q

What are 3 Risk factors for variceal bleeds

A

High portal pressure
Variceal size
Endoscopic features of the variceal wall and advanced liver disease

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32
Q

What are 4 symptoms of oesophago-gastric varices

A

Only symptomatic if they bleed;
Vomiting large amounts of blood
Black, tarry or bloody stools
Light headedness
Loss of consciousness in severe cases

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33
Q

What are 3 prevention methods for Oesophago-gastric varices

A

Don’t drink alcohol
Healthy diet and weight
Reduce risk of hepatitis – don’t share needles or have unprotected sex

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34
Q

What are the 2 management options for Oesophago-gastric varices

A

Endoscopic banding or sclerotherapy

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35
Q

What is haematemesis

A

vomiting of blood. It may be bright red or look like coffee grounds.

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36
Q

What is malaena

A

black motions, often like tar, and has a characteristic smell of altered blood

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37
Q

What are 4 common and 3 rare causes for upper GI bleeds

A

Peptic ulcers
Oesophageal varices
Mallory-Weiss tear
Gastritis/ oesophagitis

Bleeding disorders
Portal hypertensive gastropathy
Meckel’s diverticulum

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38
Q

What is a Mallory- Weiss tear

A

a tear in the mucous membrane where the oesophagus meets the stomach

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39
Q

What is the cause of a Mallory-Weiss tear

A

Persistent vomiting/retching causes haematemesis via an oesophageal mucosal tear.

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40
Q

What is the management of a mallory-weiss tear

A

Endoscopy to stop the bleeding.
Endoscopic haemostasis: 2 of clips, cautery, adrenaline.

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41
Q

What is Gastritis

A

Inflammation of the lining of the stomach.

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42
Q

What are 4 causes of gastritis

A

Irritation due to excessive alcohol use, chronic vomiting, stress, or the use of certain medications such as aspirin.
Helicobacter pylori
Bile reflux: a backflow of bile into the stomach from the bile tract
Infections caused by bacteria and viruses

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43
Q

what are 4 risk factors for gastritis

A

Alcohol
NSAIDs
H.pylori
Reflux hernia

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44
Q

4 symptoms of gastritis

A

Epigastric pain
Vomiting
Indigestion (dyspepsia)
Abdominal bloating

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45
Q

3 investigations for gastritis

A

Upper GI endoscopy
Blood tests: anaemia and H.pylori infection
Faecal occult blood tests – presence of blood in your stool.

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46
Q

3 management options for gastritis

A

H2 receptor antagonists e.g. ranitidine
Proton pump inhibitors
Avoid hot and spicy foods

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47
Q

what is Coeliac disease

A

A disease in which the small intestine is hypersensitive to gluten, leading to difficulty in digesting food.

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48
Q

pathology of coeliac disease

A

T-cell responses to gluten in the small bowel causes villous atrophy and malabsorption.

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49
Q

9 clinical manifestations of coeliac disease

A

Stinking stools/steatorrhea
Diarrhoea
Bloating
Abdominal pain
Nausea and vomiting
Aphthous ulcers
Angular stomatitis
Weight loss, fatigue, weakness
Dermatitis herpetiformis

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50
Q

3 investigations for coeliac disease

A

Low Hb, B12 and ferritin
Antibodies: anti-transglutaminase is single preferred test – check IgA levels to exclude subclass deficiency.
Where serology positive or high index of suspicion proceed to duodenal biopsy while on a gluten-containing diet; expect subtotal villous atrophy

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51
Q

4 management options for coeliac disease

A

Lifelong gluten-free diet – rice, maize, soya, potatoes, and sugar are OK
Limited consumption of oats may be tolerated in patients with mild disease.
Gluten-free biscuits, flour, bread and pasta are prescribeable.
Monitor response by symptoms and repeat serology.

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52
Q

3 complications of coeliac disease

A

Anaemia
Dermatitis herpetiformis
Osteopenia/ osteoporosis

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53
Q

what is malabsorption

A

The small intestine can’t absorb enough of certain nutrients and fluids. Malabsorption of protein, fat and carbohydrate leads to weight loss and malnutrition.

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54
Q

5 causes of malabsorption

A

Coeliac disease – reduced surface area
Chronic pancreatitis
Crohn’s disease
Pancreatic insufficiency – poor intraluminal digestion
Infection – lymphatic obstruction

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55
Q

5 symptoms of malabsorption

A

Diarrhoea
Weight loss
Lethargy
Steatorrhea
Bloating

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56
Q

4 signs of malabsorption

A

Anaemia
Bleeding disorders (low vit K)
Oedema
Metabolic bone disease

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57
Q

3 investigations for malabsorption

A

FBC: low Ca2+, Fe, B12 and folate
Lipid profile: coeliac tests
Stool: Sudan stain for fat globules

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58
Q

2 management steps for malabsorption

A

Correction of nutritional deficiencies
Treatment of causative diseases

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59
Q

What is Inflammatory bowel disease

A

Inflammatory bowel disease is a term mainly used to describe two conditions: ulcerative colitis and Crohn’s disease. These are long term conditions that involve inflammation of the gut.

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60
Q

What is the main difference between crohns and ulcerative colitis

A

Crohn’s disease favours the ileum, but can occur anywhere along the intestinal tract.
Ulcerative colitis affects the colon (large intestine) only.

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61
Q

What is crohns disease

A

A chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus (especially terminal ileum).

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62
Q

What are skip lesions

A

unaffected bowel between areas of active disease (crohns)

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63
Q

pathology of crohns

A

An inappropriate immune response against the gut flora in a genetically susceptible individual. Smoking increases the risk.

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64
Q

4 symptoms of crohns

A

Diarrhoea
Abdominal pain
Weight loss/failure to thrive
Systemic symptoms: fatigue, fever, malaise, anorexia

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65
Q

5 signs of crohns

A

Bowel ulceration
Abdominal tenderness/mass
Perianal abscess/fistulae/skin tags
Anal strictures
Clubbing, skin, joint and eye problems

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66
Q

5 complications of crohns

A

Small bowel obstruction
Toxic dilatation
Abscess formation
Fistulae
Malnutrition

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67
Q

first line investigations for crohns

A

FBC: raised WCC, platelets, CRP&ESR, anaemia. Faecal calprotectin raised (indicates IBD). pANCA negative. Stool samples (rule out infection). LFTs: hypoalbuminemia. Low iron, vitamin B12 and folate (B9) levels.

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68
Q

2 lifestyle management options for crohns

A

Quit smoking
Optimise nutrition

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69
Q

management plan for mild-moderate crohns

A

Prednisolone PO, plan maintenance therapy
Azathioprine
Biologics
Nutrition
Surgery

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70
Q

management plan for severe crohns

A

Admit for IV hydration/ electrolyte replacement; IV steroids e.g. hydrocortisone
Monitor pulse, BP, temperature, record stool frequency/character
Physical examination daily, and FBC, ESR, CRP, AXR
Consider need for blood transfusion

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71
Q

What is ulcerative colitis

A

A relapsing and remitting inflammatory disorder of the colonic mucosa.
It may affect just the rectum or extend to involve part of the colon or the entire colon.

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72
Q

Cause of UC

A

Inappropriate mucosal immune response to luminal bacteria. Smoking appears to decrease the risk of UC.

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73
Q

pathology of UC

A

Hyperaemic/ haemorrhagic colonic mucosa +/- pseudopolyps formed by inflammation.

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74
Q

5 symptoms of UC

A

Episodic or chronic diarrhoea
Crampy abdominal discomfort
Bowel frequency relates to severity
Urgency/tenesmus – proctitis
Systemic symptoms: fever, malaise, anorexia, weight loss

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75
Q

6 signs of UC

A

May be none
Acute, severe UC – fever, tachycardia, tender distended abdomen
Extra-intestinal signs:
Clubbing
Aphthous oral ulcers
Conjunctivitis

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76
Q

3 investigations for UC

A

Blood: FBC, ESR, CRP, U&E, LFT, blood culture
Stool: to exclude Campylobacter, C.difficile
Faecal calprotectin: a simple, non-invasive test for GI inflammation with high sensitivity.

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77
Q

2 complications of acute UC

A

Toxic dilatation of colon with risk of perforation
Venous thromboembolism

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78
Q

2 complications of chronic UC

A

Colonic cancer
Neoplasms in mucosa

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79
Q

Management of mild UC

A

Mesalamine is the mainstay for remission-induction/maintenance
Prednisolone

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80
Q

management of moderate UC

A

Induce remission oral prednisolone

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81
Q

management of severe UC

A

IV hydration/ electrolyte replacement
Monitor pulse, BP, temperature, record stool frequency/character
Physical examination daily, and FBC, ESR, CRP, AXR

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82
Q

What is IBS

A

Irritable bowel syndrome
A mixed group of abdominal symptoms for which no organic cause can be found.
Most are probably due to disorders of intestinal motility, enhanced visceral perception or microbial dysbiosis.

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83
Q

5 clinical manifestations of IBS

A

Urgency
Abdominal bloating/distension
Worsening of symptoms after food
Symptoms are chronic >6 months and often exacerbated by stress, menstruation or gastroenteritis.
Examination may be normal but general abdominal tenderness is common

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84
Q

3 investigations for IBS

A

FBC, CRP, ESR, U&E
Coeliac screen
Faecal calprotectin

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85
Q

Diagnosis criteria for IBS

A

Only diagnose IBS if recurrent abdominal pain associated with at least 2 of:
Relief by defecation
Altered stool form
Altered bowel frequency (constipation/diarrhoea)

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86
Q

3 differential diagnoses for IBS

A

Colonic cancer
Inflammatory bowel disease – Crohn’s, UC
Coeliac disease

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87
Q

What is the overall management plan for IBS

A

Should focus on controlling symptoms, initially using lifestyle/dietary measures, then cognitive therapy or pharmacotherapy if required

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88
Q

treatment of constipation in IBS

A

ensure adequate water and fibre intake and promote physical activity.

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89
Q

treatment of diarrhoea in IBS

A

avoid sorbitol sweeteners, alcohol and caffeine. Reduce dietary fibre content, encourage patients to identify their own trigger foods.

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90
Q

Treatment of Colic/bloating in IBS

A

oral antispasmodics. Combination probiotics in sufficient doses may help flatulence or bloating. Less alcohol intake.

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91
Q

treatment of Psychological symptoms/visceral hypersensitivity for IBS

A

emphasize the positive. Sinister pathology has been excluded and symptoms tend to improve over time. Consider CBT and hypnosis.

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92
Q

What are Gastro-intestinal infections (gastroenteritis)

A

diarrhoea +/- vomiting due to enteric infection with viruses, bacteria or parasites.

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93
Q

What is Norovirus

A

Single-stranded RNA virus. Highly infectious. Transmission by contact with infected people, environment, food.
Most common cause of infectious GI disease in England.
Presents 12-48hr after exposure, lasting 24-72h.

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94
Q

4 symptoms of norovirus

A

Acute-onset vomiting, watery diarrhoea, cramps, nausea.

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95
Q

2 investigations for norovirus

A

clinical, stool sample reverse transcriptase PCR

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96
Q

3 treatments for norovirus

A

supportive, anti-motility agents, usually self-limiting.

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97
Q

What is rotavirus

A

Double-stranded RNA virus.
Commonest cause of gastroenteritis in children.

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98
Q

Presentation of rotavirus

A

incubation 2day. Watery diarrhoea and vomiting for 3-8d, fever, abdominal pain

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99
Q

2 investigations for rotavirus

A

clinical, antigen in stool

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100
Q

2 treatments for rotavirus

A

supportive. Routine vaccination in UK

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101
Q

What is Enterotoxigenic E.coli

A

Gram -ve anaerobe
Disease due to heat-stable or heat labile toxin which stimulates Na+, Cl- and water efflux into gut lumen

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102
Q

presentation of Enterotoxigenic E.coli

A

incubation 1-3days. Watery diarrhoea, cramps lasts 3-4 days

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103
Q

2 investigations for Enterotoxigenic E.coli

A

clinical, identification of toxin from stool culture.

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104
Q

treatment for Enterotoxigenic E.coli

A

supportive, self-limiting

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105
Q

Prevention of travellers diarrhoea

A

boil water, cool thoroughly, peel fruit and vegetables. Avoid ice, salads, shellfish. Drink with a straw.

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106
Q

presentation of E.coli

A

watery diarrhoea preceded by cramps and nausea

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107
Q

presentation of giardia lamblia

A

upper GI symptoms e.g. bloating, belching

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108
Q

presentation of Campylobacter jejuni and Shigella

A

colitic symptoms, urgency, cramps.

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109
Q

Diagnosis criteria for travellers diarrhoea

A

3 or more unformed stools per day plus one of the following:
Abdominal pain
Cramps
Nausea
Vomiting
Dysentery

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110
Q

3 treatment steps for travellers diarrhoea

A

Oral rehydration. Clear fluid or oral rehydration salts.
Antimotility agents e.g. loperamide
Antibiotics

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111
Q

define Acute diarrhoea

A

3 episodes partially formed or watery stool/day for <14d

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112
Q

define dysentry

A

infectious gastroenteritis with bloody diarrhoea

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113
Q

define Persistent diarrhoea

A

acutely starting diarrhoea lasting >14d

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114
Q

define Traveller’s diarrhoea

A

Traveller’s diarrhoea: starting during, or shortly after, foreign travel

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115
Q

define Food poisoning

A

disease caused by consumption of food/wate

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115
Q

What is campylobacter

A

Gram -ve, spiral-shaped rod

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115
Q

7 infective causes of diarrhoea

A

Rotavirus/norovirus most common in the UK
Campylobacter
Shigella
Salmonella
S.aureus
E.coli
C.diff

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116
Q

presentation of campylobacter

A

incubation 1-10d. Bloody diarrhoea, pain, fever, headache.

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117
Q

5 complications of camylobacter

A

bacteraemia, hepatitis, pancreatitis, miscarriage, reactive arthritis

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118
Q

2 investigations for campylobacter

A

stool culture. PCR/enzyme immunoassay.

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119
Q

treatment plan for campylobacter

A

supportive. Antibiotics only in invasive cases, refer to local sensitivities.

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120
Q

6 key points of history for diarrhoea

A

Onset/duration
Characteristics of stool
Food/drink
Travel
Fresh water/ swimming
Medications

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121
Q

how does onset/duration change diagnosis of diarrhoea

A

Acute – viral/bacterial
Chronic – parasites and non-infectious causes

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122
Q

how does Characteristics of stool change diagnosis of diarrhoea

A

Floating: fat content – malabsorption, coeliac
Blood or mucus: inflammatory/invasive infection/ cancer
Watery: small bowel infection

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123
Q

how does food/drink affect diagnosis of diarrhoea

A

Meat – campylobacter
Rice – bacillus cereus
Poultry – salmonella
Shellfish – norovirus, v.parahaemolyticus

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124
Q

how does travel history change diarrhoea diagnosis

A

No cholera in the UK – traveller’s diarrhoea

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125
Q

how does fresh water/swimming change diarrhoea diagnosis

A

crypto, giardia, aeromonas

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126
Q

how does medication history change diarrhoea diagnosis

A

Recent antibiotics – C.diff or side effects

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127
Q
A
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128
Q

4 cancer risk factors with diarrhoea

A

Over 50
Chronic diarrhoea
Weight loss
Blood in stool

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129
Q

what are 3 investigations for diarrhoea

A

Stool tests
Blood tests
Lower GI endoscopy

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130
Q

what is looked at in stool tests for diarrhoea

A

Microscopy
Culture
Ova, cysts and parasites
Toxin detection

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131
Q

what is looked at in blood tests for diarrhoea

A

Blood culture
Inflammatory markers
ESR/ CRP

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132
Q

mechanism of watery diarrhoea

A

non-inflammatory
(enterotoxin or superficial adherence/invasion)

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133
Q

mechanism of bloody/mucoid diarrhoea

A

inflammatory
(invasion/cytotoxin)

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134
Q

location of watery diarrhoea

A

proximal small bowel

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135
Q

location of bloody/mucoid diarrhoea

A

colon

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136
Q

bacterial causes of watery diarrhoea

A

vibrio cholerae
e.coli (ETEC)
c.diff
bacillus cereus
s.aureus

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137
Q

bacterial causes of bloody/mucoid diarhoea

A

shigella
e.coli (EIEC,EHEC)
Salmomella enteritidis
v.parahaemolyticus
c.diff
campylobacter jejuni

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138
Q

viral causes of watery diarrhoea

A

rotavirus
norovirus

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139
Q

parasitic causes of watery diarrhoea

A

giardia
cryptosporidium

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140
Q

parasitic cause of bloody, mucoid diarrhoea

A

entamoeba histolytica

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141
Q

management of diarrhoea

A

Treat cause.
Food handlers – no work until stool samples are -ve. If a hospital outbreak, wards may need closing
Oral rehydration is better than IV, but if sustained diarrhoea/vomiting then IV fluids with electrolytes may be needed.
Avoid antibiotics unless infective diarrhoea is causing systemic upset.

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142
Q

What is Clostridium difficile

A

The cause of pseudomembranous colitis. Gram positive spore forming bacteria.

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143
Q

What are 4 antibiotics that cause clostridium difficile

A

rule of Cs
Clindamycin
Ciprofloxacin
Co-amoxiclav
Cephalosporins

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144
Q

3 signs of C.diff

A

Increased temperature
Diarrhoea with systemic upset
High CRP, WCC and low albumin

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145
Q

3 steps of detection of C.diff

A

Urgent testing of suspicious stool (characteristic smell)
Two-stage process with rapid screening test for C.diff protein followed by specific ELISA for toxins.

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146
Q

treatment of C.diff

A

Stop causative antibiotic.
Barrier nursing

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147
Q

clinical presentation of oesophageal tumour

A

Dysphagia
Weight loss
Retrosternal chest pain

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148
Q

3 investigations for oesophageal tumours

A

Oesophagoscopy with biopsy
Endoscopic ultrasound
CT/ MRI for staging

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149
Q

describe the t1-4 stages of oesophageal cancer

A

T1 – invading lamina propria/ submucosa
T2 – invading Muscularis propria
T3 – invading adventitia
T4 – invasion of adjacent structures

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150
Q

describe the N and M stages of oesophageal cancers

A

N0 – no nodal spread
N1 – regional node metastases
M0 – no distant metastases spread
M1 – distal metastases

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151
Q

4 treatment options for oesophageal cancer

A

Localised T1/T2 disease – radical curative oesophagectomy may be tried
Pre-op chemo – cisplatin
Chemoradiotherapy
Palliation aims to restore swallowing with chemo/radiotherapy, stenting and laser use

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152
Q

6 symptoms of gastric carcinoma

A

Often non-specific
Dyspepsia
Weight loss
Vomiting
Dysphagia
Anaemia

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153
Q

4 signs of gastric carcinoma

A

Epigastric mass
Hepatomegaly
Jaundice
Ascites

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154
Q

3 investigations for gastric carcinoma

A

Gastroscopy and multiple ulcer edge biopsies
EUS (endoscopic ultrasound)
CT/ MRI for staging

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155
Q

4 treatment options for gastric carcinoma

A

Partial gastrectomy for distal tumours
Total gastrectomy if more proximal
Combination chemo
Surgical palliation for obstruction, pain or haemorrhage

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156
Q

4 presentations of left sided colorectal carcinoma

A

Bleeding/ mucus PR
Altered bowel habit or obstruction
Tenesmus
PR mass

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157
Q

4 presentations of right sided colorectal carcinoma

A

Weight-loss
Low Hb
Abdominal pain
Obstruction less likely

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158
Q

4 presentations in both left and right sided colorectal carcinoma

A

Abdominal mass
Perforation
Haemorrhage
Fistula

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159
Q

4 urgent referral criteria for colorectal carcinoma

A

Over 40 with PR bleeding and bowel habit change
Any age with right lower abdominal mass
Palpable rectal mass
Men/non-menstruating women with unexplained iron-deficiency anaemia

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160
Q

5 investigations for colorectal carcinoma

A

FBC – microcytic anaemia
Faecal occult blood – used for UK screening programme
Sigmoidoscopy
Barium enema or colonoscopy – or CT
Liver USS

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161
Q

surgical management of colorectal carcinoma

A

Aims to cure and increases survival by up to 50%
Different types of surgery done for different sites of cancer

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162
Q

radiotherapy for colorectal cancer

A

Used in palliation for colonic cancer
Occasionally used pre-op to allow resection

163
Q

chemotherapy for colorectal cancer

A

Adjuvant chemo helpful
Chemo is also used in palliation of metastatic disease

164
Q

5 symptoms of liver tumours

A

Fever
Malaise
Anorexia
Weight loss
RUQ pain

165
Q

4 signs of liver tumours

A

Hepatomegaly
Signs of chronic liver disease and evidence of decompensation
Feel for an abdominal mass
Bruit over liver

166
Q

3 investigations for liver tumours

A

Blood: FBC, clotting, LFT, hepatitis serology, α-fetoprotein
Imaging: US/ CT to identify lesions. MRI distinguishes malignant and benign lesions
Biopsy: find primary e.g. CXR, endoscopy

167
Q

what is hepatocellular carcinoma (HCC)

A

Primary hepatocyte neoplasia accounts for 90% of primary liver tumours

168
Q

6 clinical features of HCC

A

Fatigue
Appetite loss
RUQ pain
Weight loss
Jaundice
Ascites

169
Q

4 causes of HCC

A

HBV – main cause
Autoimmune hepatitis
Cirrhosis – alcohol, hemochromatosis, PBC
Non-alcoholic fatty liver

170
Q

3 investigations for HCC

A

3 phase CT
MRI
Biopsy

171
Q

3 treatments of HCC

A

Resecting solitary tumours
Liver transplant
Percutaneous ablation

172
Q

What is Cholangiocarcinoma

A

Biliary tree cancer.

173
Q

4 clinical presentations of cholangiocarcinoma

A

Fever
Abdominal pain and ascites
Malaise
Elevated bilirubin

174
Q
A
175
Q

3 treatment options for cholangiocarcinoma

A

Most tumours are inoperable at presentation. Most operated on recur.
Post-op complications include liver failure, bile leak and GI bleeds
Stenting of an obstructed extrahepatic biliary tree, percutaneously or via ERCP

176
Q

features of haemangiomas

A

collection of small blood vessels
incidental finding on US or CT
No treatment required
Avoid biopsy

177
Q

causes of adenomas

A

anabolic steroids, oral contraceptives, pregnancy

178
Q

when to treat adenomas

A

Only treat if symptomatic or >5cm.

179
Q

Pathology of pancreas carcinoma

A

Mostly ductal adenocarcinoma – metastasise early, present late
A few arise in ampulla of Vater or pancreatic islet cells (insulinoma, gastrinoma, glucagonomas, somatostinomas, VIPomas

180
Q

2 clinical features of pancreas carcinoma

A

Tumours in the head of the pancreas present with painless obstructive jaundice
75% of tumours in the body and tail present with epigastric pain – radiates to back, relieved by sitting forward

181
Q

4 complications of pancreas carcinoma

A

anorexia, weight loss, diabetes, acute pancreatitis

182
Q

6 signs of pancreas carcinoma

A

Jaundice + palpable gallbladder
Epigastric mass
Hepatomegaly
Splenomegaly
Lymphadenopathy
Ascites

183
Q

2 investigations for pancreatic carcinoma

A

Blood: cholestatic jaundice. Ca19-9 elevated – non-specific, but helps assess prognosis
Imaging
US or CT show pancreatic mass +/- dilated biliary tree +/- hepatic metastases
Guide biopsy and help staging prior to surgery

184
Q

6 management options for pancreas carcinoma

A

Surgery – considering pancreaticoduodenectomy if fit and with no metastases
Post-op morbidity is high
Laparoscopic excision
Post-op chemotherapy to delay disease progression
Palliation of jaundice
Endoscopic or percutaneous stent insertion may help jaundice and anorexia
Pain – opiates or radiotherapy

185
Q

what is intestinal obstruction

A

Blockage to the lumen of the gut. Commonly refers to blockage of intra-abdominal part of the intestine.

186
Q

What is a volvulus

A

a twist/rotation of segment of bowel

187
Q

what are bowel adhesions

A

sticking together (abdominal structures to one another, bowel loops or omentum, other solid organs, abdominal wall)

188
Q

3 classes of mechanical classification of bowel obstruction

A

Mechanical (intraluminal)/ true (extraluminal)
Paralytic (pseudo obstruction)

189
Q

4 classes of bowel obstruction according to pathology

A

Simple
Closed loop
Strangulation
Intussusception

190
Q

2 common and 4 rare causes of small bowel obstruction

A

Adhesions (previous surgery)
Hernia
Rarer; Crohn’s, Malignancy, Volvulus, Intussusception

191
Q

what is intussesception

A

the inversion of one portion of the intestine within another.

192
Q

4 causes of large bowel obstruction

A

Colon carcinoma
Constipation
Diverticular stricture
Volvulus - Sigmoid

193
Q

what is sigmoid volvulus

A

occurs when the bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction.

194
Q

6 clinical manifestations of intestinal obstruction

A

Anorexia
Nausea
Vomiting:

Nature – forceful/ regurgitation
Content – bilious, feculent

Distension
Abdominal pain
Altered bowel habits:

Constipation
Obstipation

195
Q

2 complications of intestinal obstruction

A

Tissue death – blood supply can be cut off to part of the intestine
Infection – peritonitis.

196
Q

first line investigation for intestinal obstruction

A

X-ray

197
Q

general principals of intestinal obstruction management

A

cause, site, speed of onset, and completeness of obstruction determine definitive therapy. Strangulation and large bowel obstruction require surgery; ileus and conservatively, at least initially.

198
Q

immediate management of intestinal obstruction

A

NGT and IV fluids to rehydrate and correct electrolyte imbalance.

199
Q

what further imaging is used for intestinal obstruction management

A

CT to establish the cause of obstruction.

200
Q

which type of bowel obstruction requires emergency surgery

A

strangulation needs emergency surgery.

201
Q

What are hernias

A

the protrusion of a viscus part or part of a viscus through a defect of the walls of its containing cavity into an abnormal position.

202
Q

What is an irreducible hernia

A

contents cannot be pushed back into place

203
Q

what is an obstructed hernia

A

bowel contents cannot pass – features of intestinal obstruction

204
Q

What is a strangulated hernia

A

ischaemia occurs – the patient requires urgent surgery

205
Q

What is an incarceration hernia

A

contents of the hernial sac are stuck inside by adhesions

206
Q

what is the usual presentation of a hernia

A

Usually presents as lump and pain

207
Q

pathology of femoral hernias

A

Bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin.

208
Q

epideimiology and features of femoral hernias

A

Occur more often in women, middle age and elderly
Irreducible and strangulate

209
Q

treatment of femoral hernias

A

surgical repair

210
Q

What are incisional hernias and their repair

A

Follow breakdown of muscle closure after surgery
If obese, repair is not easy
Mesh repair – less recurrence but more infections compared to sutures

211
Q

what are inguinal hernias

A

Indirect hernias pass through the internal inguinal ring and out through the external inguinal ring
Direct hernias push their way directly forward through the posterior wall of the inguinal canal, into a defect in the abdominal wall

212
Q

4 predisposing conditions for inguinal hernias

A

Male sex
Chronic cough
Urinary obstruction
Past abdominal surgery

213
Q

2 examinations for inguinal hernias

A

Is lump visible? Ensure it is not a scrotal lump
Ask patient to cough – should appear above and medial to pubic tubercle

214
Q

Do direct or indirect inguinal hernias strangulate

A

Indirect hernias

215
Q

repair of inguinal hernias

A

Lose weight and stop smoking pre-op
Hernias may recur
Mesh techniques – polypropylene mesh reinforces posterior wall

216
Q

what is ischaemic colitis

A

Inflammation and injury of the large intestine resulting from inadequate blood supply.

217
Q

pathology of ischaemic colitis

A

Usually follows low flow in the inferior mesenteric artery territory and it ranges from mild to gangrenous.

218
Q

2 clinical manifestations of Ischaemic colitis

A

Lower left-sided abdominal pain
May have bloody diarrhoea

219
Q

2 investigations for ischaemic colitis

A

CT may be helpful but lower GI colonoscopy is gold-standard.

220
Q

management of ischaemic colitis

A

Treatment – usually conservative with fluid replacement and antibiotics
Most recover but subsequent development of ischaemic strictures is common
Gangrenous ischaemic colitis requires prompt resuscitation followed by resection of the affected bowel and stoma formation. Mortality is high.

221
Q

what is mesenteric ischaemia

A

Injury to the small intestine occurs due to inadequate blood supply.

222
Q

7 causes of acute mesenteric ischaemia

A

Superior mesenteric artery thrombosis/embolism
Mesenteric vein thrombosis
Non-occlusive disease
Trauma,
vasculitis,
radiotherapy
strangulation.

223
Q

what is the classical clinical presentation triad for acute mesenteric ischaemia

A

Acute severe abdominal pain
No/minimal abdominal signs
Rapid hypovolaemia – shock

224
Q

pain picture for acute mesenteric ischaemia

A

tends to be constant, central or around the right iliac fossa (RIF)

225
Q

5 investigations for acute mesenteric ischaemia

A

High Hb due to plasma loss
High WCC, modestly raised plasma amylase
Persistent metabolic acidosis
Abdominal X-ray shows a gasless abdomen
Laparotomy – nasty, necrotic bowel

226
Q

2 main life-threatening complications secondary to acute mesenteric ischaemia

A

Septic peritonitis
Progression of a systemic inflammatory response syndrome to multi-organ failure.

227
Q

management of acute mesenteric ischaemia

A

Resuscitation with fluid, antibiotics and LMW heparin are required.
If arteriography is done, thrombolytics may be attempted on potentially viable bowel.

228
Q

cause of chronic mesenteric ischaemia

A

Typically brought about through a combination of a low-flow state with atheroma.

229
Q

3 clinical presentations of chronic mesenteric ischaemia

A

Severe, colicky post-prandial abdominal pain
Weight loss (painful to eat)
Upper abdominal bruit may be present

230
Q

2 investigations for chronic mesenteric ischaemia

A

CT angiography and contrast-enhanced MR angiography

231
Q

treatment of chronic mesenteric ischaemia

A

Once diagnosis is confirmed, surgery should be considered due to the ongoing risk of acute infarction.
Percutaneous transluminal angioplasty and stent insertion has replaced open revascularisation

232
Q

what is appendicitis

A

Inflamed and painful appendix. It is the most common surgical emergency.

233
Q

pathology of appendicitis

A

Gut organisms invade the appendix wall after lumen obstruction by lymphoid hyperplasia, faecolith or filarial worms. This leads to oedema, ischaemic necrosis and perforation.

234
Q

5 clinical manifestations of appendicitis

A

Classic periumbilical pain that moves to the right iliac fossa.
Tachycardia
Fever
Percussion tenderness in RIF
Pain on the right during PR examination suggests an inflamed, low lying pelvic appendix

235
Q

3 specific signs for appendicitis

A

Rovsing’s sign: greater pain in the RIF than the LIF when the LIF is pressed
Psoas sign: pain on extending hip if retrocaecal appendix.
Cope sign: pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus.

236
Q

5 differential diagnoses for appendicitis

A

UTI
Mesenteric adenitis
Diverticulitis/ cholecystitis/ cystitis
Food poisoning
Crohn’s disease

237
Q

3 investigations for appendicitis

A

Blood tests may reveal neutrophil leucocytosis and elevated CRP
Ultrasound may help, but appendix not always visualised
CT has high diagnosis accuracy and is useful if diagnosis is unclear

238
Q

management for appendicitis

A

Prompt appendicectomy
Antibiotics: piperacillin
Laparoscopy: diagnostic and therapeutic advantages. Not recommended with suspected gangrenous perforation – rate of abscess formation is higher.

239
Q

3 complications of appendicitis

A

Perforation
Appendix mass – occurs when inflamed appendix becomes covered with omentum
Appendix abscess – if an appendix mass enlarges.

240
Q

pathology of gallstones

A

Bile contains cholesterol, bile pigments and phospholipids. If concentrations vary, different stones may form.

241
Q

features of pigment gallstones

A

small, friable and irregular.

242
Q

features of cholesterol stones

A

large, often solitary.

243
Q

features of mixed stones

A

faceted (calcium salts, pigment and cholesterol).

244
Q

5 Fs for gallstones

A

Fair
Forty
Fertile
Fat
Female

245
Q

clinical manifestations for gall stones in the gall bladder

A

Biliary pain
Cholecystitis
maybe Obstructive jaundice

246
Q

clinical manifestations for gall stones in the bile duct

A

Biliary pain
Obstructive jaundice
Cholangitis
Pancreatitis

247
Q

management options for gallstones

A

Laparoscopic cholecystectomy
Bile acid dissolution therapy
Bile duct stones:
ERCP with sphincterotomy and removal (balloon)/ crushing (laser)/ stent placement
Surgery (large stones)

248
Q

5 complications for gallstones in the gall bladder and cystic duct

A

Biliary colic
Acute and chronic cholecystitis
Carcinoma
Mirizzi’s syndrome

249
Q

3 complications for gallstones in the bile ducts

A

Obstructive jaundice
Cholangitis
Pancreatitis

250
Q

what is gallstone ileus

A

when a gallstone erodes through the gallbladder into the ileum, causing complications

251
Q

what is biliary colic

A

Gallstones are symptomatic with cystic duct obstruction or if passed into the common bile duct.
RUQ pain radiating to the back
Possible jaundice

252
Q

investigations for biliary colic

A

urinalysis, CXR and ECG

253
Q

treatment for biliary colic

A

analgesia, rehydrate. Elective laparoscopic cholecystectomy

254
Q

What is acute cholecystitis

A

inflammation of gallbladder
Follows stone or sludge impaction in the neck of the gallbladder, which may cause continuous epigastric or RUQ pain, vomiting, fever, local peritonism or a GB mass.
High WCC (differs it from biliary colic)
If the stone moves to the CBD, obstructive jaundice and cholangitis may occur.

255
Q

3 investigations for acute cholecystitis

A

high WCC
ultrasound – thick-walled, shrunken GB, pericholecystic fluid.
Plain AXR only shows 10% of gallstones.

256
Q

treatment of acute cholecystitis

A
  • NBM, pain relief, IVI and antibiotics e.g. co-amoxiclav.
257
Q

what is flatulent dyspepsia

A

Vague abdominal discomfort
Distension
Nausea
Flatulence
Fat intolerance (fat stimulates cholecystokinin release and GB contraction)

258
Q

investigations for chronic cholecystitis

A

Ultrasound to image stones and assess CBD diameter. MRCP is used to find CBD stones.

259
Q

treatment of chronic choleystitis

A

cholecystectomy.

260
Q

pathology of acute pancreatitis

A

Pancreatitis is characterised by self-perpetuating pancreatic enzyme-mediated autodigestion; oedema and fluid shifts cause hypovolaemia, as extracellular fluid is trapped in the gut, peritoneum and retroperitoneum.

261
Q

GET SMASHED causes for acute pancreatitis

A

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia/ hypothermia/ hypercalcaemia
ERCP and emboli
Drugs

262
Q

symptoms of acute pancreatitis

A

Gradual or sudden severe epigastric or central abdominal pain. Vomiting prominent.
Pain radiates to back, sitting forward may relieve.

263
Q

6 signs for acute pancreatitis

A

High heart rate
Fever
Jaundice
Shock
Rigid abdomen with local/general tenderness
Periumbilical bruising (Cullen’s) or flanks (Grey Turner’s) from blood vessel autodigestion

264
Q

3 investigations for acute pancreatitis

A

Raised serum amylase – excreted renally so renal failure will increase levels.
Serum lipase is more sensitive and specific for pancreatitis – rises earlier and falls later.
CT: assess severity and complications

265
Q

management of acute pancreatitis

A

Nil by mouth
Analgesia
Hourly pulse, BP and urine output: daily FBC, U&E, Ca2+, glucose, amylase
ERCP and gallstone removal
Repeat imaging is performed to monitor progress

266
Q

3 early complications of acute pancreatitis

A

Shock
Renal failure
Sepsis

267
Q

3 late complications of acute pancreatitis

A

Pancreatic necrosis and pseudocyst
Bleeding from elastase eroding a major vessel
Thrombosis may occur in splenic arteries causing bowel necrosis

268
Q

what is chronic pancreatitis

A

A chronic inflammatory process of the pancreas, leading to irreversibly low pancreatic function.

269
Q

pathology of acute pancreatitis

A

Chronic inflammation in the pancreas leads to the replacement of functional pancreatic tissue by fibrous scar tissue.

270
Q

4 causes of chronic pancreatitis

A

Alcohol
Smoking
Autoimmune
Pancreatic duct obstruction

271
Q

3 clinical presentations of chronic pancreatitis

A

Persistent upper abdominal pain and weight loss
Radiates to the back and is relieved by sitting forward or hot water bottles on epigastrium/back
Steatorrhea and diabetes mellitus occur late once most of the gland is destroyed
Brittle diabetes

272
Q

4 investigations for chronic pancreatitis

A

Ultrasound and CT scan: pancreatic calcifications confirm the diagnosis.
MRCP, AXR – speckled calcification

273
Q

3 management options for chronic pancreatitis

A

Drugs: give analgesia and fat-soluble vitamins
Diet: no alcohol, low fat may help
Surgery: e.g. pancreatectomy for unremitting pain/ weight loss

274
Q

4 complications of chronic pancreatitis

A

Diabetes
Biliary obstruction
Local arterial aneurysm
Gastric varices

275
Q

features of liver failure

A

Loss of the liver’s ability to regenerate or repair.

Liver failure may be recognised by the development of coagulopathy and encephalopathy. This may occur suddenly in the previously healthy liver (acute liver failure), but it more often occurs on a background of cirrhosis (chronic liver failure).

276
Q

what is fulminant hepatic failure

A

a clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function.

277
Q

3 infection causes of liver failure

A

viral hepatitis, yellow fever, leptospirosis

278
Q

3 drug causes of liver failure

A

paracetamol overdose, halothane, isoniazid

279
Q

2 toxin causes of liver failure

A

Carbon tetrachloride, Amanita phalloides mushroom

280
Q

2 vascular causes of liver failure

A

Budd-Chiari syndrome, veno-occlusive disease

281
Q

7 misc. causes of liver failure

A

alcoholic fatty liver disease, primary biliary cholangitis, primary sclerosing cholangitis, haemochromatosis, autoimmune hepatitis, metabolic causes, malignancy.

282
Q

what is Budd-Chiari syndrome

A

hepatic vein obstruction by thrombosis or tumour causes congestive ischaemia and hepatocyte damage.

283
Q

pathophysiology of liver failure

A

Destruction of hepatocytes
Development of fibrosis in response to chronic inflammation
Destruction of the architecture of the nodules of the liver removes the ability of the liver to adequately perform functions, repair and regenerate

284
Q

7 clinical presentations of liver failure

A

Abnormal bleeding
Ascites
Jaundice
Hepatic encephalopathy
Fetor hepaticus (sweet and musty breath)
Constructional apraxia
Mental state drowsiness and confusion, due to cerebral oedema

285
Q

3 investigations of liver failure

A

Blood: FBC – LFTs, clotting, hepatitis, paracetamol level, ferritin
Raised bilirubin
Glucose low – no glycogenesis
Microbiology: blood culture, urine culture, neutrophils >250/mm3 indicates spontaneous bacterial peritonitis
Radiology: CXR, abdominal US, Doppler flow studies of the portal vein

286
Q

8 management steps of liver failure

A

Beware of sepsis, hypoglycaemia, GI bleeds/ varices, encephalopathy.
Protect airway with intubation and insert a tube to avoid aspiration and remove any blood from the stomach
Insert urinary and central venous catheters to help assess fluid status
Treat the cause
Treat seizures with phenytoin
Hemofiltration/ haemodialysis
Avoid sedatives/ other drugs with hepatic metabolism
LIVER TRANSPLANT

287
Q

4 complications of liver failure

A

Cerebral oedema, bleeding, encephalopathy, ascites

288
Q

7 symptoms of acute hepatitis

A

Can be asymptomatic
General malaise
Myalgia
GI upset
Abdominal pain
+/- jaundice (pale stools, dark urine)
Tender hepatomegaly

289
Q

6 viral causes of hepatitis

A

hepatitis A,B,C,D,E, herpes virus

290
Q

4 non-viral causes of hepatitis

A

Spirochaetes
Mycobacteria
Parasites
Bacteria

291
Q

3 non-infection causes of hepatitis

A

Alcohol
Toxins/poisoning
Autoimmune

292
Q

4 signs of compensated chronic hepatitis

A

Dupuytren’s contracture
Spider naevi
LFTs can be normal
Compensated – liver function maintained

293
Q

8 signs of decompensated chronic hepatitis

A

Dupuytren’s contracture
Spider naevi
LFTs can be normal
jaundice
ascites
low albumin
coagulopathy
encephalopathy

294
Q

how is hepatitis A spread

A

faecal-oral or shellfish

295
Q

incubation time of hep.A

A

2-6weeks

296
Q

5 symptoms of hep.A

A

Fever
Malaise
Anorexia
Nausea
Arthralgia

297
Q

3 investigations for hep.A

A

AST and ALT rise 22-40d after exposure, returning to normal over 5-20wks
IgM rises due to recent infection
IgG is detectable for life

298
Q

treatment for Hep.A

A

Supportive
Monitor liver function
Fulminant hepatitis failure/ acute liver failure

299
Q

how does hep.B spread

A

blood borne, IV drug abusers, sexual, direct contact

300
Q

5 risk groups for hep.B

A

IV drug abusers and their sexual partners/carers, health workers, haemophiliacs, sexually promiscuous

301
Q

incubation period of Hep.B

A

Incubation: 1-6 months

302
Q

Signs for hep.B

A

Resemble hepatitis A but arthralgia and urticaria are commoner

303
Q

2 investigations for hep.B

A

HBsAg (surface antigen) is present 1-6months after exposure
Antibodies imply past infection

304
Q

how is vaccinations used for hep.b

A

high risk groups vaccinated
passive immunisation may be given to non-immune contacts after high-risk exposure
also prevents HDV

305
Q

3 complications of hep.b

A

Fulminant hepatic failure
Cirrhosis
Membranous nephropathy

306
Q

4 treatment steps for hep.b

A

Avoid alcohol
Immunise sexual contacts
Antivirals
Supportive

307
Q

spread of hepatitis C (HCV)

A

blood transfusion, IV drug abuse, sexual contact

308
Q

risk factors for progression of HCV

A

male, older, higher viral load, use of alcohol, HIV

309
Q

2 investigations for HCV

A

LFTs
Anti-HCV antibodies confirms exposure

310
Q

3 treatments for HCV

A

Non-structural viral protein inhibitors.
Quit alcohol
Directly acting antivirals

311
Q

3 complications for HCV

A

Glomerulonephritis
Thyroiditis
Autoimmune hepatitis

312
Q

spread of HDV

A

via blood and bodily fluids.

313
Q

test for HDV

A

anti-HDV antibody

314
Q

treatment of HDV

A

pegylated interferon-alpha. If limited success – liver transplant.

315
Q

transmission of HEV

A

via faecal-oral route (food, contaminated water, undercooked seafood and pork)

316
Q

5 acute presentations of HEV

A

Fever, malaise, nausea + vomiting, jaundice, hepatomegaly

317
Q

investigations for HEV

A

Serum ALT and AST raised, bilirubin raised, ESR raised
HEV serology: HEV IgM antibodies = active infection. HEV IgG antibodies = recovery. HEV RNA = current infection

318
Q

Management of HEV

A

1st line – no treatment. Very mild illness which is self-limiting within a month. It is a notifiable disease. No vaccine available.

319
Q

4 complications of HEV

A

Complications Chronic hepatitis, liver failure (especially in pregnant women), cirrhosis, hepatocellular carcinoma

320
Q

what is liver cirrhosis

A

Cirrhosis implies irreversible liver damage. Histologically, there is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration.

321
Q

7 causes of Cirrhosis

A

Most common: Alcoholic liver disease, non-alcoholic fatty liver disease, hepatitis B, hepatitis C
Rarer: haemochromatosis, Wilson’s disease, alpha 1 trypsin deficiency

322
Q

5 clinical manifestations of cirrhosis

A

Leukonychia: white nails with lunulae undermarcated, from hypoalbuminemia
Ectasias
Palmar erythema (red palms)
Hyperdynamic circulation
Hepatomegaly

323
Q

5 complications of cirrhosis leading to liver failure

A

Coagulopathy (failure of hepatic synthesis of clotting factors)
Encephalopathy
Hypoalbuminaemia
Sepsis
Spontaneous bacterial peritonitis

324
Q

3 complications of cirrhosis leading to portal hypertension

A

Ascites
Splenomegaly
Portosystemic shunt including oesophageal varices

325
Q

3 investigations for cirrhosis

A

Blood: LFT – increased bilirubin, AST, ALT, ALP
Low albumin
Low WCC and platelets indicate hypersplenism
Liver ultrasound – may show a small liver or hepatomegaly, splenomegaly
MRI – increased caudate lobe size

326
Q

management of cirrhosis

A

General:
Good nutrition is vital
Alcohol abstinence
Ascites:
Fluid restriction, low-salt diet
Transplant

327
Q

what is primary biliary cholangitis

A

Autoimmune disease of the liver. Results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver (cholestasis).

328
Q

Pathology of Primary biliary cholangitis

A

Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis (may lead to fibrosis, cirrhosis and portal hypertension).

329
Q

cause of primary biliary cholangitis

A

Unknown environmental triggers (possibly pollutants, xenobiotics) and a genetic predisposition leading to loss of immune tolerance to self-mitochondrial proteins.

330
Q

5 clinical manifestations of primary biliary cholangitis

A

Often asymptomatic and diagnosed after incidental finding high ALP.
Lethargy, sleepiness and pruritus (skin itching) may precede jaundice.
Jaundice
Skin pigmentation
Hepatosplenomegaly

331
Q

3 investigations for primary biliarycholangitis

A

Blood: high ALP, mildly high AST and ALT. High bilirubin and low albumin
Ultrasound; excludes extrahepatic cholestasis
Biopsy: not usually needed but can be used to look for granulomas around bile ducts.

332
Q

management of primary biliary cholangitis

A

For symptomatic patients try cholestyramine.
Fat-soluble vitamin prophylaxis
Monitoring: regular LFT and ultrasound twice yearly
Liver transplantation: end-stage disease

333
Q

What is alcholic liver disease

A

Liver disease due to excessive alcohol consumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis or cirrhosis.

334
Q

pathology of alcoholic liver disease

A

Alcohol metabolism in the liver generates high levels of NADH which stimulates fatty acid synthesis and production of triglycerides, leading to steatosis.
Oxidative stress from metabolism of alcohol leads to hepatocyte injury and necro-inflammatory activity (ASH – alcoholic steatohepatitis). Ongoing, this causes liver fibrosis which may progress to cirrhosis

335
Q

4 clinical manifestations of alcoholic liver disease

A

Steatosis (fatty liver cells which disturbs metabolism) and mild ASH are usually asymptomatic but are a common cause of mildly abnormal LFTs.
Severe alcohol hepatitis following binge drinking causes malaise and fever.
Jaundice
Complications of cirrhosis e.g. ascites or ruptured oesophageal varices

336
Q

how does alcohol affect the liver

A

Fatty liver – acute/reversible, but can progress to cirrhosis
Alcoholic hepatitis – can progress to cirrhosis
Cirrhosis – irreversible liver damage

337
Q

How does alcohol affect the CNS

A

self neglect, decreased memory function, cortical atrophy

338
Q

how does alcohol affect the gut

A

obesity, peptic ulcers, varices, pancreatitis, cancer

339
Q

how does alcohol affect blood

A

high MCV, anaemia from marrow depression and GI bleeding

340
Q

how does alcohol affect the heart

A

arrhythmias, high BP, cardiomyopathy

341
Q

how does alcohol affect reproductive system

A

testicular atrophy

342
Q

investigation for alcohol hepatitis

A

Blood: high WCC, low platelets, high MCV, high urea

343
Q

management of alcoholic liver disease

A

PREVENTION – CAGE questions
ALCOHOL WITHDRAWAL – alcohol free beers may be helpful to patients with addiction to alcohol
Acamprosate may help intense anxiety, insomnia and craving after alcohol withdrawal.

344
Q

CAGE questions for alcohol

A

Ever felt you ought to Cut down on your drinking?
Have people Annoyed you by criticising your drinking?
Ever felt Guilty about your drinking?
Ever had an Eye-opener in the morning?

345
Q

What is wilsons disease

A

An inherited disorder of copper metabolism, leading to the accumulation of toxic levels of copper in the liver and brain.

346
Q

Pathology of wilsons disease

A

Possession of two mutated ATP7B alleles on chromosome 13 causes disruption of normal copper transport and accumulation of toxic levels of copper in hepatocytes and basal ganglia.

347
Q

5 clinical manifestations of wilsons

A

Most present in childhood or early adulthood with chronic liver disease or cirrhosis.
A small proportion of patients present in hepatic failure
About half of patients also develop neuropsychiatric symptoms due to copper accumulation in the brain
CNS signs
Kayser-Fleischer (KF) rings: copper in iris

348
Q

4 CNS signs of wilson’s

A

Tremor
Dysarthria (unclear articulation of speech)
Dysphagia
Parkinson’s

349
Q

6 investigations for wilsons

A

Urine: 24h copper excretion is high (>100mcg, normal is <40mcg)
High LFT
Serum copper - <11μmol/L
Molecular genetic testing can confirm the diagnosis
Slit lamp exam: KF rings seen in iris
Liver biopsy: raised hepatic copper

350
Q

management of wilsons

A

Diet: avoid foods with high copper content e.g. chocolate, nuts, mushrooms.
Drugs: lifelong penicillamine
Liver transplant in severe liver failure
Screen siblings – asymptomatic homozygotes need treating.

351
Q

5 side effects of penicillamine

A

nausea, rash, low WCC, Hb and platelets

352
Q

What is hereditary haemochromatosis

A

An inherited disorder characterised by increased intestinal absorption of iron, leading to iron overload in multiple organs, particularly the liver and sometimes leading to organ damage

353
Q

pathology of Hereditary haemochromatosis

A

Hepcidin controls plasma iron concentrations by inhibiting iron export by ferroportin from duodenal enterocytes and macrophages.
Deficiency of hepcidin results in raised plasma iron concentrations and accumulation in multiple organs, including the liver, pancreas, heart, joints and pituitary.

354
Q

6 clinical manifestations of haemochomatosis

A

Early symptoms are non-specific e.g. fatigue and arthropathy
Later symptoms;
Skin pigmentation (slate-grey)
Cirrhosis
Hypogonadism
Cardiac failure
Diabetes mellitus

355
Q

3 investigations for haemochromatosis

A

Blood: high LFT and ferritin levels are raised
Images: chondrocalcinosis (haemochromatosis causes stressed joints to deteriorate faster than resting joints, and this is visible on X-rays).
Liver and cardiac MRI
Liver biopsy: Perl’s stain quantifies iron loading and assesses severity of disease

356
Q

3 management options for haemochromatosis

A

Venesection (removal of accumulating iron) until ferritin <50mcg/L. Iron will continue to accumulate, so maintenance venesection will be needed for life.
Diet: a well-balanced diet should be encouraged, avoiding alcohol but no need to avoid iron-rich foods. Avoid uncooked seafood.
Screening: serum ferritin, transferrin saturation.

357
Q

what is α1-antitrypsin deficiency

A

An inherited disorder affecting the lungs (emphysema) and the liver (cirrhosis).

358
Q

pathology of α1-antitrypsin deficiency

A

Lung A1At protects against tissue damage from neutrophil elastase. Deficiency means there is no protection and leads to emphysema in adults and liver disease in children.
It is also one of a family of serine protease inhibitors made in the liver, that control inflammatory cascades.

359
Q

clinical manifestations of α1-antitrypsin deficiency

A

Symptomatic patients usually have the PiZZ genotype ( both parents carriers):
Dyspnoea from emphysema
Cirrhosis
Cholestatic jaundice

360
Q

4 investigations for α1-antitrypsin deficiency

A

Serum α1-antitrypsin levels low
Lung function testing: reductions in FEV1 with obstructive pattern
Liver biopsy: periodic acid Schiff (PAS)
Phenotyping: distinguish between SZ and ZZ phenotypes

361
Q

4 management options for α1-antitrypsin deficiency

A

Smoking cessation
Prompt treatment/ preventative vaccination for lung infections.
Liver transplanted – needed in decompensated cirrhosis
Lung transplant – improves survival

362
Q

What is Ascites

A

Effusion and accumulation of serous fluid (protein-containing) in the abdominal cavity.

363
Q

Classification of ascites

A

Stage 1 detectable only after careful examination/ ultrasound scan (mild)
Stage 2 easily detectable but of relatively small volume
Stage 3 obvious, not tense ascites (moderate)
Stage 4 tense ascites (large)

364
Q

What is the pathology of portal hypertension ascites

A

A state of sodium water imbalance
Interplay of various neurohormonal agents – renin, aldosterone, sympathetic nervous system, nitric oxide
Over filling – inappropriate Na + H2O retention – no volume depletion – hypervolemia

365
Q

pathology of non-portal hypertensive ascites

A

Malignancy
Cardiac failure
Nephrotic syndrome

366
Q

pathology of Chylous ascites

A

Abdominal surgery/ trauma, malignancy, radiation, congenital

367
Q

5 causes of ascites

A

Cirrhosis
Malignancy
Heart failure
TB
Pancreatitis

368
Q

4 symptoms of ascites

A

Abdominal distension – clothes getting tighter
Nausea, loss of appetite
Constipation
Weight loss

369
Q

3 signs of ascites

A

Flanks fullness
Fluid thrill
Shifting dullness

370
Q

3 investigations for ascites

A

Naked eye assessment – swollen stomach
Chemistry: proteins and amylase
Ultrasound scan and abdominal CT

371
Q

management of ascites

A

Treat underlying cause
Diuretics – spironolactone, metolazone
Salt and fluid restriction

372
Q

complication of ascites

A

Can lead to spontaneous bacterial peritonitis.

373
Q

What is peritonitis

A

Inflammation of the peritoneum.

374
Q

what is peritonism

A

tensing muscles to prevent movement of peritoneum.

375
Q

5 causes of peritonitis

A

Cholecystitis
Pancreatitis
Appendicitis
Diverticulitis
AEIOU

376
Q

AEIOU causes for peritonitis

A

appendicitis, ectopic pregnancy, infection (TB), obstruction, ulcer.

377
Q

6 inflammatory agents for peritonitis

A

inflamed organs, air, pus, faeces, luminal contents and blood.

378
Q

pathology of 4 causes of peritonitis

A

Medical causes – spontaneous bacterial peritonitis, pelvic inflammatory disease, dialysis related, TB
Surgical causes – perforation of GIT e.g. trauma, appendicitis, cancer
Sterile – pancreatitis, familial Mediterranean fever
Perforation of peptic/duodenal ulcer

379
Q

8 clinical manifestations of peritonitis

A

Abdominal pain
Diarrhoea
Swelling
Swinging fever
Prostration
Shock
Tenderness + rebound/percussion pain
Board-like abdominal rigidity

380
Q

2 differential diagnoses for peritonitis

A

Appendicitis
Angioedema

381
Q

3 investigations for peritonitis

A

Ultrasound/ CT scan
Ascitic tap: Raised WCC (neutropil)
Erect CXR may show gas under diaphragm

382
Q

5 complications of peritonitis

A

Sepsis
Multi-organ failure
CV events (MI, stroke)
Respiratory complications (pneumonia, pulmonary embolus)
Surgical complications

383
Q

4 surgical management options for peritonitis

A

Laparotomy
Laparoscopy
Treat problem – patch hole, remove organ/cause
Wash out infection

384
Q

4 management options for peritonitis

A

Surgery
Intensive care
Support of kidneys
Physio/early mobilisation

385
Q

what is a Diverticulum

A

an outpouching of the gut wall, usually at sites of entry of perforating arteries.

386
Q

what is diverticulitis

A

refers to inflammation of a diverticulum.

387
Q

what is diverticular disease

A

symptomatic diverticula

388
Q

cause of diverticular disease

A

A diet low in fibre and high in meat is the strongest risk factor.

389
Q

pathology of diverticular disease

A

Firm stools require higher intraluminal pressures to propel
High intraluminal pressure forces pouches of the colonic mucosa through an anatomical weak point in the muscular layer where blood vessels pass through to supply the mucosal layer.

390
Q

presentation of diverticular disease

A

Intermittent abdominal pain, altered bowel habit, iron deficiency anaemia
Acute inflammation in a diverticulum presents with severe left iliac fossa pain
Occasionally, erosion of a large submucosal vessel can cause severe rectal bleeding.

391
Q

4 investigations for diverticular disease

A

Diverticula are a common incidental finding at colonoscopy
CT abdomen is best to confirm acute diverticulitis and can identify extent of disease and any complications
Colonoscopy risk perforation in acute setting
AXR may identify obstruction or free air

392
Q

management of diverticular disease

A

Try antispasmodics e.g. mebeverine
Surgical resection occasionally needed

393
Q

management of diverticulitis

A

Mild attacks can be treated at home with bowel rest (fluids only) and antibiotics
Most attacks settle but complications include abscess formation or perforation.

394
Q

What are haemorrhoids

A

Abnormally dilated and prolapsed anal cushions
Extremely common
Thought to be due to disruption of the normal suspensory mechanisms caused by chronic straining at stool

395
Q

what are complications of haemorrhoids

A

Cause bright red rectal bleeding and discomfort

396
Q

what are anal tags

A

Polypoid projections of the anal mucosa and submucosa

397
Q

histology of haemorrhoids

A

Excised haemorrhoids examined microscopically contain large dilated blood vessels, which may show evidence of thrombosis, with an overlying hyperplastic squamous epithelium.

398
Q

histology of anal tags

A

Microscopically composed of a fibrovascular core covered by squamous epithelium. The fibrovascular core lacks the typically ecstatic vessels of haemorrhoids

399
Q

What is an anal fissure

A

A tear in the mucosa of the lower anal canal which is most always located posteriorly in the midline

400
Q

cause of anal fissures

A

Cause is unclear, but chronic infection may lead to loss of the normal elasticity of the mucosa, such that passage of hard faeces may precipitate the tear

401
Q

what is an anorectal abscess

A

A collection of pus within deep perianal tissue
A complication of infection within a deep anal gland

402
Q

presentation of anorectal abscess

A

perianal erythema, swelling and pain

403
Q

What is an anorectal fistula

A

An abnormal epithelial-line tract connecting the anal canal to the perianal skin
Usually the result of infection in an anal gland tracking to the skin surface

404
Q

What causes anal cancer

A

Uncommon and invariably associated with HPV infection

405
Q

what type of cancer are the majority of anal cancers

A

Vast majority are squamous cell carcinomas which arise from areas of squamous dysplasia known as anal intraepithelial neoplasia which is graded 1-3.

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Q

Gold standard investigations for chrons

A

Colonoscopy and biopsy (granulomatous transmural inflammation. Skip lesions, cobblestone appearance. Strictures “string sign”)

Phase 2a Medicine (10 decks)

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