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2A revision > GI and liver > Flashcards

GI and liver Flashcards

1
Q

what is gastrointestinal reflux disease GORD

A

Caused by reflux of stomach contents into the oesophagus

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2
Q

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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3
Q

oesophageal manifestations of GORD

A
  • Heartburn (burning, retrosternal discomfort after meals)
  • Belching
  • Acid brash (acid regurgitation)
  • Waterbrash
  • Odynophagia (swallowing pain)
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4
Q

extra-oesophageal manifestations of GORD

A
  • Nocturnal asthma
  • Chronic cough
  • Laryngitis
  • Sinusitis
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5
Q

investigations for GORD

A
  • Endoscopy if dysphagia
  • 24h oesophageal pH monitoring
  • Manometry help diagnose GORD when endoscopy is normal
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6
Q

management of GORD

A
  • Lifestyle = weight loss, stop smoking, small meals, reduce hot drinks and alcohol, avoid acidic food
  • antacids
  • ranitidine ( H2 receptor antagonist)
  • lansoprazole ( proton pump inhibitor)
  • surgery
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7
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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8
Q

pathology of peptic ulceration

A
  • Inflammation caused by the bacteria H.pylori

- Erosion from stomach acids

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9
Q

clinical manifestations of peptic ulceration

A
  • Epigastric pain often related to hunger, specific foods, or time of day
    -Fullness, Heart burn, Tender epigastrium
    ALARM symptoms (Anaemia, Loss of weight, Anorexia, Recent onset, Melaena/haematemesis)
    -Swallowing difficulty
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10
Q

H.pylori and peptic ulceration

A
  • Test and treat for H.pylori, if positive give appropriate Proton Pump Inhibitor and 2 antibiotic combination.
  • Lansoprazole with clarithromycin and metronidazole
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11
Q

duodenal ulcer

A
  • H.pyori, drugs, increased gastric acid, blood group O
  • epigastric pain and weight loss
  • upper GI endoscopy, test for H.pylori
  • differentials = non-ulcer dyspepsia, duodenal crohn’s
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12
Q

gastric ulcers

A
  • elderly
  • h.pylori, smoking, NSAIDs
  • upper GI endoscopy to exclude malignancy
    proton pump inhibitors
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13
Q

what is oesophago-gastric varices

A
  • Submucosal venous dilatations secondary to high portal pressures.
  • Bleeding can be brisk, particularly if underlying coagulopathy secondary to loss of hepatic synthesis of clotting factors
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14
Q

cause of oesophago-gastric varices

A

Cirrhosis
Thrombosis
Parasitic infection
portal hypertension

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15
Q

causes of portal hypertension

A
  • Pre-hepatic: thrombosis (portal or splenic vein)
  • Intra-hepatic: cirrhosis, schistosomiasis, sarcoid, myeloproliferative diseases, congenital hepatic fibrosis
  • Post-hepatic: Budd-Chiari syndrome, right heart failure, constrictive pericarditis, veno-occlusive disease
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16
Q

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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17
Q

symptoms of OG 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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18
Q

management of OG varices

A

Endoscopic banding or sclerotherapy

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19
Q

upper GI bleeding

A
  • Haematemesis: vomiting of blood. It may be bright red or look like coffee grounds.
  • Melaena: black motions, often like tar, and has a characteristic smell of altered blood
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20
Q

Mallory-Weiss tear

A
  • a tear in the mucous membrane where the oesophagus meets the stomach
  • Persistent vomiting/retching
  • endoscopy (clips, cautery, adrenaline)
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21
Q

what is gastritis

A

Inflammation of the lining of the stomach

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22
Q

causes of gastritis

A
  • excessive alcohol use, chronic vomiting, stress, aspirin.
  • Helicobacter pylori: a bacteria that lives in the mucous lining
  • Bile reflux
  • Infections
  • risk factors = alcohol, h.pylori, NSAIDs, reflux hernia
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23
Q

symptoms of gastritis

A
  • Epigastric pain
  • Vomiting
  • Indigestion (dyspepsia)
  • Abdominal bloating
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24
Q

investigations for gastritis

A
  • upper gi endoscopy
  • test for anaemia and h.pylori
  • test stool for blood
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25
Q

management of gastritis

A
  • H2 receptor antagonists e.g. ranitidine
  • Proton pump inhibitors
  • Avoid hot and spicy foods
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26
Q

what is Coeliac disease

A
  • A disease in which the small intestine is hypersensitive to gluten, leading to difficulty in digesting food
  • Tcell responses to gluten cause villous atrophy and malabsorption
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27
Q

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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28
Q

investigations for coeliac disease

A
  • Low Hb, B12 and ferritin
  • Antibodies: anti-transglutaminase – check IgA levels to exclude subclass deficiency.
  • duodenal biopsy (villous atrophy)
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29
Q

management of coeliac disease

A
  • gluten free diet (some foods prescribeable)

- monitor response with repeat serology

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30
Q

complications of coeliac disease

A
  • Anaemia
  • Dermatitis herpetiformis
  • Osteopenia/ osteoporosis
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31
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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32
Q

causes of malabsorption

A
  • Coeliac disease – reduced surface area
  • Chronic pancreatitis
  • Crohn’s disease
  • Pancreatic insufficiency – poor intraluminal digestion
  • Infection
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33
Q

signs and symptoms of malabsorption

A
  • Diarrhoea
  • Weight loss
  • Lethargy
  • Steatorrhea
  • Bloating
  • anaemia, bleeding disorders (low vit K), oedema, metabolic bone disease
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34
Q

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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35
Q

management of malabsorption

A
  • correct nutritional deficiencies

- treat causative diseases

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36
Q

what 2 conditions does the term inflammatory bowel disease describe

A
  • crohn’s disease (favours ileum but can occur anywhere along tract
  • ulcerative colitis (affects colon only)
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37
Q

what is crohn’s disease

A
  • chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus (especially terminal ileum)
  • patchy distribution with normal gut inbetween = skip lesions
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38
Q

pathology of crohn’s disease

A
  • inappropriate immune response against the gut flora in a genetically susceptible individual.
  • Smoking increases the risk.
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39
Q

symptoms of crohn’s

A
  • Diarrhoea
  • Abdominal pain
  • Weight loss/failure to thrive
  • Systemic symptoms: fatigue, fever, malaise, anorexia
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40
Q

signs of crohn’s

A
  • Bowel ulceration
  • Abdominal tenderness/mass
  • Perianal abscess/fistulae/skin tags
  • Anal strictures
  • Clubbing, skin, joint and eye problems
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41
Q

complications of crohn’s

A
  • Small bowel obstruction
  • Toxic dilatation
  • Abscess formation
  • Fistulae
  • Malnutrition
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42
Q

investigations for crohn’s

A

-Bloods
-Stool: MC&S and CDT to exclude C.difficile, Campylobacter
>Faecal calprotectin is a simple test for GI inflammation.
-Colonoscopy and biopsy

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43
Q

management of mild-moderate crohn’s

A
  • Quit smoking, Optimise nutrition
  • Prednisolone PO, plan maintenance therapy
  • Azathioprine
  • Biologics
  • Surgery
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44
Q

management of severe crohn’s

A
  • Admit for IV hydration/ electrolyte replacement; IV 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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45
Q

what is ulcerative colitis

A
  • A relapsing and remitting inflammatory disorder of the colonic mucosa.
  • affects from the rectum up to the entire colon (only is severe)
  • Inappropriate mucosal immune response to luminal bacteria
  • smoking seems to decrease risk
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46
Q

pathology of ulcerative colitis

A

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

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47
Q

symptoms of ulcerative colitis

A
  • Episodic or chronic diarrhoea
  • Crampy abdominal discomfort
  • Bowel frequency relates to severity
  • Urgency/tenesmus – proctitis
  • Systemic symptoms
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48
Q

signs of ulcerative colitis

A
  • fever, tachycardia, distended abdomen

- clubbing, aphthous oral ulcers, conjunctivitis

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49
Q

investigations for ulcerative colitis

A
  • bloods
  • stools- to exclude campylobacter and c.deff
  • faecal calprotectin (tests for GI inflammation)
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50
Q

complications of ulcerative colitis

A
  • Acute (Toxic dilatation of colon with risk of perforation, Venous thromboembolism)
  • Chronic (Colonic cancer, Neoplasms in mucosa)
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51
Q

management of ulcerative colitis

A
  • mild = mesalamine (induces remission), prednisolone
  • moderate = oral prednisolone
  • severe = rehydrate, electrolyte replacement, monitor bloods, vitals, stools, daily examinations
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52
Q

what is irritable bowel syndrome

A
  • 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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53
Q

clinical manifestations of IBS

A
  • urgency
  • bloating/distension
  • symptoms worse after eating
  • > 6 months
  • exacerbated by stress, menstruation, gastroenteritis
  • general abdominal tenderness
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54
Q

investigations for IBS

A
  • FBC, CRP, ESR, U&E
  • Coeliac screen
  • Faecal calprotectin
  • only diagnose IBS if recurrent abdo pain is associated with relief by defecation, altered stool form, altered frequency
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55
Q

management of IBS

A
  • controlling symptoms, initially using lifestyle/dietary measures, then cognitive therapy or pharmacotherapy
  • for colic/ bloating = oral antispasmodics, probiotics
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56
Q

what is gastroenteritis

A

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

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57
Q

norovirus (gastroenteritis)

A
  • Single-stranded RNA virus. Highly infectious. Transmission by contact with infected people, environment, food
  • most common cause of GE in england
  • presents 12-24h after exposure, lasts 24-72 h
  • acute onset vomiting, watery stools, cramps, nausea
  • treatment= supportive, anti-motility agents
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58
Q

rotavirus (gastroenteritis)

A
  • Double-stranded RNA virus.
  • Commonest cause of gastroenteritis in children.
  • Presentation: incubation 2day. Watery diarrhoea and vomiting for 3-8d, fever, abdominal pain
  • Diagnosis: clinical, antigen in stool
  • Treatment: supportive. Routine vaccination in UK
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59
Q

enterotoxigenic E.coli (gastroenteritis)

A
  • Gram -ve anaerobe
  • Disease due to heat-stable or heat labile toxin which stimulates Na+, Cl- and water efflux into gut lumen
  • Presentation: incubation 1-3days. Watery diarrhoea, cramps lasts 3-4 days
  • Diagnosis: clinical, identification of toxin from stool culture.
  • Treatment: supportive
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60
Q

prevention of traveller’s diarrhoea

A

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

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61
Q

presentations of Traveller’s diarrhoea

A
  • E. coli: watery diarrhoea preceded by cramps and nausea
  • Giardia lamblia: upper GI symptoms e.g. bloating, belching
  • Campylobacter jejuni and Shigella: colitic symptoms, urgency, cramps.
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62
Q

treatment for Traveller’s diarrhoea

A
  • Oral rehydration. Clear fluid or oral rehydration salts.
  • Antimotility agents e.g. loperamide
  • Antibiotics
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63
Q

what is dysentery

A

infectious gastroenteritis with bloody diarrhoea

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64
Q

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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65
Q

campylobacter ( causes dysentery)

A
  • Gram -ve, spiral-shaped rod
  • incubation 1-10d.
  • Bloody diarrhoea, pain, fever, headache.
  • Complications: bacteraemia, hepatitis, pancreatitis, miscarriage, reactive arthritis
  • stool culture and PCR
  • treatment = supportive, Abx if invasive
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66
Q

history for diarrhoea

A
  • acute = viral/bacterial
  • chronic = parasites or non-infectious causes
  • blood/mucus = inflammatory/ invasive infection/ cancer
  • watery = small bowel infection
  • Meat – campylobacter
  • Rice – bacillus cereus
  • Poultry – salmonella
  • Shellfish – norovirus, v.parahaemolyticus
  • Abx = c.diff
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67
Q

diarrhoea red flags

A
  • Dehydration
  • Electrolyte imbalance
  • Renal failure
  • Immune compromise
  • Severe abdominal pain
  • Cancer risk factors (>50, blood, weight loss, chronic diarrhoea)
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68
Q

watery diarrhoea

A
  • non-inflammatory
  • proximal small bowel
  • cholera, e.coli, clostridium perfringens, bacillus cereus, staph.aureus
  • rotavirus, norovirus
  • parasitic = giardia, cryptosporidium
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69
Q

bloody, mucoid diarrhoea

A
  • inflammatory
  • colon
  • shigella, e.coli, salmonella, v.parahaemolyticus, clostridium difficile, campylobacter jejuni
  • parasitic = entamoeba histolytica
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70
Q

clostridium difficile and Abx that cause it

A
  • The cause of pseudomembranous colitis. Gram positive spore forming bacteria.
  • Rule of C’s (Clindamycin, Ciprofloxacin, Co-amoxiclav, Cephalosporins)
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71
Q

signs of clostridium difficile

A
  • Increased temperature
  • Diarrhoea with systemic upset
  • High CRP, WCC and low albumin#
  • rapid screening test followed by specific ELISA for toxins
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72
Q

clinical presentation of oesophageal tumours

A
  • Dysphagia
  • Weight loss
  • Retrosternal chest pain
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73
Q

investigations for oesophageal tumours

A
  • Oesophagoscopy with biopsy
  • Endoscopic ultrasound
  • CT/ MRI for staging
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74
Q

staging of oesophageal tumours

A
  • T1 – invading lamina propria/ submucosa
  • T2 – invading Muscularis propria
  • T3 – invading adventitia
  • T4 – invasion of adjacent structures
  • N0 – no nodal spread
  • N1 – regional node metastases
  • M0 – no distant spread
  • M1 – distal metastases
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75
Q

treatment for oesophageal tumour

A
  • Localised T1/T2 disease – radical curative oesophagectomy may be tried
  • Pre-op chemo – cisplatin
  • Chemoradiotherapy
  • Palliation aims to restore swallowing with chemo/radio
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76
Q

signs and symptoms of gastric carcinoma

A
  • non-specific, dyspepsia, weight loss, vomiting, dysphagia, anaemia
  • epigastric mass, hepatomegaly, jaundice, ascites
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77
Q

investigations for gastric carcinoma

A
  • Gastroscopy and multiple ulcer edge biopsies
  • EUS
  • CT/ MRI for staging
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78
Q

treatment for gastric carcinoma

A
  • partial or total gastrectomy
  • chemo
  • surgical palliation for obstruction or pain
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79
Q

presentation of left-sided colorectal carcinoma

A
  • Bleeding/ mucus PR
  • Altered bowel habit or obstruction
  • Tenesmus
  • PR mass
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80
Q

presentation of right-sided colorectal carcinoma

A
  • Weight-loss
  • Low Hb
  • Abdominal pain
  • Obstruction less likely
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81
Q

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
82
Q

staging of colorectal carcinoma

A
  • TNM system is beginning to be used
  • Dukes’ criteria and 5yr treated survival rate
  • A – limited to Muscularis mucosae
  • B – extension through Muscularis mucosae
  • C – involvement of regional lymph nodes
  • D – distant metastases
83
Q

management of colorectal carcinoma

A
  • surgery
  • radiotherapy (palliation or pre-op)
  • chemo (adjuvant chemo helpful, palliation)
84
Q

symptoms of liver tumours

A
  • Fever
  • Malaise
  • Anorexia
  • Weight loss
  • RUQ pain
85
Q

signs of liver tumours

A
  • Hepatomegaly
  • Signs of chronic liver disease and evidence of decompensation
  • Feel for an abdominal mass
  • Bruit over liver
86
Q

investigation 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
87
Q

Hepatocellular carcinoma (HCC)

A
  • primary hepatocyte neoplasia = 90% of liver tumours
  • fatigue, appetite loss, RUQ pain, weightloss, jaundice, ascites
  • HBV (main cause), hepatitis, cirrhosis, fatty liver
  • 3 phase CT, MRI, biopsy
  • resect tumours, liver transplant, percutaneous ablation
88
Q

cholangiocarcinoma

A
  • biliary tree cancer
  • fever, abdo pain, ascites, malaise, elevated bilirubin
  • cause= Flukes, HBV, HCV, DM
  • most operated on recur
  • can stent obstructed biliary tree
89
Q

benign liver tumours

A
  • haemangioma = incidental finding, no treatment required, avoid biopsy
  • adenoma = from anabolic steroids, oral contraceptives, pregnancy
    >only treat if symptomatic or >5cm
90
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)
91
Q

clinical features of pancreas carcinoma

A
  • at head of pancreas = painless obstructive jaundice
  • 75% in body or tail = epigastric pain radiates to back relieved by sitting forward
  • anorexia, weight loss, diabetes, acute pancreatitis
  • signs = jaundice, palpable gallbladder, epigastric mass, hepato/splenomegaly, lymphadenopathy, ascites
92
Q

investigations for pancreas carcinoma

A
  • Blood: cholestatic jaundice. Ca19-9 elevated

- US or CT show pancreatic mass +/- dilated biliary tree +/- hepatic metastases

93
Q

treatment for pancreas carcinoma

A
  • pancreaticoduodenectomy = post-op mortality high
  • Laparoscopic excision
  • Post-op chemotherapy
  • Endoscopic or percutaneous stent insertion may help jaundice and anorexia
94
Q

what is a volvulus

A

a twist/rotation of segment of bowel

95
Q

what are adhesions (cause bowel obstruction )

A

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

96
Q

causes of small bowel obstruction

A
  • Adhesions (previous surgery)
  • Hernia
  • Rarer; Crohn’s, Malignancy, Volvulus, Intussusception
97
Q

causes of large bowel obstruction

A
  • Colon carcinoma
  • Constipation
  • Diverticular stricture
  • Volvulus - Sigmoid
98
Q

pathology of sigmoid volvulus

A

bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction

99
Q

complications of bowel obstruction

A
  • Infection – peritonitis

- infarction and tissue necrosis

100
Q

investigations for bowel obstruction

A

x-ray

101
Q

management of bowel obstruction

A
  • Immediate action: NGT and IV fluids to rehydrate and correct electrolyte imbalance.
  • Further imaging: CT to establish the cause of obstruction.
  • Surgery: strangulation needs emergency surgery
102
Q

what is a hernia

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
  • irreducible = can’t be pushed back into place
  • incarceration = contents of hernial sac are stuck inside by adhesions
103
Q

clinical manifestations of a hernia

A
  • pain

- lump

104
Q

femoral hernias

A 
-Bowel enters the femoral canal
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)
-women, middle age and elderly
-Irreducible and strangulate
-Treatment – surgical repair
105
Q

incisional hernias

A
  • Follow breakdown of muscle closure after surgery
  • If obese, repair is not easy
  • Mesh repair
106
Q

inguinal hernias

A
  • (indirect)pass through inguinal ring or (direct) directly through the posterior inguinal canal wall
  • men, chronic cough, urinary obstruction, past abdo op
  • indirect can strangulate
  • appear above and medial to pubic tubercle during cough
  • mesh repair (polypropylene mesh)
107
Q

what is ischaemic colitis

A
  • Inflammation and injury of the large intestine resulting from inadequate blood supply.
  • Usually follows low flow in the inferior mesenteric artery territory and it ranges from mild to gangrenous.
108
Q

clinical manifestations of ischaemic colitis

A
  • Lower left-sided abdominal pain

- bloody diarrhoea

109
Q

investigations for ischaemic colitis

A
  • lower GI endoscopy gold standard

- CT

110
Q

management of ischaemic colitis

A
  • conservative = fluid replacement and antibiotics
  • subsequent development of ischaemic strictures is common
  • gangrenous ischaemic colitis (high mortality) needs prompt resuscitation = stoma
111
Q

what is mesenteric ischaemia

A

Injury to the small intestine occurs due to inadequate blood supply

112
Q

what are the causes of acute mesenteric ischaemia

A
  • Superior mesenteric artery thrombosis/embolism
  • Mesenteric vein thrombosis
  • Non-occlusive disease
  • Trauma, vasculitis, radiotherapy or strangulation
113
Q

presentation of acute mesenteric ischaemia

A
  • Acute severe abdominal pain
  • No/minimal abdominal signs
  • Rapid hypovolaemia – shock
  • pain = constant, central/around R iliac fossa
114
Q

investigations for acute mesenteric ischaemia

A
  • high Hb (plasma loss), high WCC, metabolic acidosis, gasless abdomen on X-ray, necrotic bowel (laparotomy)
115
Q

management of acute mesenteric ischaemia

A
  • life threatening complications = septic peritonitis, systemic inflammatory response syndrome leading to organ failure
  • fluid, Abx, LMWH
116
Q

cause of chronic mesenteric ischaemia

A
  • brought about through a combination of a low-flow state with atheroma
  • need CT angiography
117
Q

presentation of chronic mesenteric ischaemia

A
  • Severe, colicky post-prandial abdominal pain
  • Weight loss (painful to eat)
  • Upper abdominal bruit
118
Q

treatment of chronic mesenteric ischaemia

A
  • surgery to prevent acute infarction

- Percutaneous transluminal angioplasty and stent insertion

119
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
  • causes inflamed and painful appendix
120
Q

clinical manifestations of appendicitis

A
  • periumbilical pain moves to R iliac fossa
  • tachycardia, fever
  • percussion tenderness
  • 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.
121
Q

investigations for appendicitis

A
  • bloods = neutrophil leukocytosis, elevated CRP
  • US
  • CT = if US is unclear
122
Q

management of appendicitis

A
  • Prompt appendicectomy

- Antibiotics: piperacillin

123
Q

complications of appendicitis

A
  • perforation
  • appendix mass when inflamed appendix is covered in omentum
  • appendix abscess
124
Q

pathology of gallstones

A
  • Bile contains cholesterol, bile pigments and phospholipids. If concentrations vary, different stones may form.
  • Pigment stones: small, friable and irregular.
  • Cholesterol stones: large, often solitary. Causes – female, age, obesity.
  • Mixed stones: faceted (calcium salts, pigment and cholesterol).
125
Q

clinical manifestations of gallstones

A
  • biliary pain
  • obstructive jaundice
  • cholecystitis (if in gallbladder)
  • cholangitis, pancreatitis (in bile duct)
126
Q

management of gallstones

A
  • Laparoscopic cholecystectomy
  • Bile acid dissolution therapy
  • Bile duct stones: ERCP with sphincterotomy and removal
127
Q

biliary colic

A
  • if stone in cystic duct or common bile duct
  • RUQ pain radiating to back
  • possible jaundice
  • urinalysis, CXR, ECG
  • analgesia, rehydrate, laparoscopic cholecystectomy
128
Q

acute cholecystitis

A
  • 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
  • US = thick walled, shrunked GB, pericholecystic fluid
  • NBM, pain relief, IVI and antibiotics e.g. co-amoxiclav
129
Q

chronic cholecystitis

A
  • chronic inflammation +/- colic
  • flatulent dyspepsia, fat intolerance (causes GB contraction)
  • US, MRCP
  • needs cholecystectomy
130
Q

pathology of acute pancreatitis

A

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

131
Q

causes of acute pancreatitis (GET SMASHED)

A
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion venom
  • Hyperlipidaemia/ hypothermia/ hypercalcaemia
  • ERCP and emboli
  • Drugs
132
Q

symptoms of acute pancreatitis

A
  • Gradual or sudden severe epigastric or central abdominal pain.
  • Vomiting prominent.
  • Pain radiates to back
133
Q

signs of 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
134
Q

investigations for acute pancreatitis

A
  • raised serum amylase – excreted renally so renal failure will increase levels.
  • Serum lipase is more sensitive– rises earlier and falls later.
  • CT
135
Q

management of acute pancreatitis

A
  • nil by mouth
  • analgesia
  • hourly vitals
  • ERCP and gallstone removal
  • repeat imaging
136
Q

pathology of chronic pancreatitis

A
  • chronic inflammation of the pancreas = replacement of functional pancreatic tissue by fibrous scar tissue
  • irreversibly low pancreatic function
137
Q

causes of chronic pancreatitis

A
  • Alcohol
  • Smoking
  • Autoimmune
  • Pancreatic duct obstruction
138
Q

presentation of chronic pancreatitis

A
  • upper abdo pain and weight loss
  • Steatorrhea and diabetes mellitus occur late once most of the gland is destroyed
  • Brittle diabetes
139
Q

investigations for chronic pancreatitis

A
  • US/CT = pancreatic calcifications
140
Q

management of pancreatitis

A
  • analgesia, fat-soluble vitamins
  • diet = no alcohol, low fat
  • pancreatectomy
141
Q

what is liver failure

A
  • Loss of the liver’s ability to regenerate or repair
  • development of coagulopathy and encephalopathy
  • acute= suddenly in previously healthy liver
  • chronic = more common = history of cirrhosis
142
Q

what is fulminant hepatic failure

A

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

143
Q

causes of liver failure

A

Infections: viral hepatitis, yellow fever
Drugs: paracetamol overdose
Toxins: Carbon tetrachloride
Vascular: Budd-Chiari syndrome, veno-occlusive disease
Others: alcoholic fatty liver disease, primary biliary cholangitis, primary sclerosing cholangitis, haemochromatosis, autoimmune hepatitis, metabolic causes, malignancy

144
Q

what is Budd-Chiari syndrome

A

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

145
Q

pathophysiology of liver failure

A
  • destruction of hepatocytes =chronic inflammation = fibrosis
  • destruction of nodule architecture = liver can’t adequately perform functions, repair and regenerate
146
Q

clinical presentation of liver failure

A
  • Abnormal bleeding
  • Ascites
  • Jaundice
  • Hepatic encephalopathy
  • Fetor hepaticus (smells like pear drops)
  • Constructional apraxia
  • Mental state drowsiness and confusion, due to cerebral oedema
147
Q

investigations for liver failure

A
  • Blood: FBC – LFTs, clotting, hepatitis, paracetamol level, ferritin (Raised bilirubin, Glucose low)
  • Microbiology: blood culture, urine culture
  • Radiology: CXR, abdominal US, Doppler flow of portal vein
148
Q

complications of liver failure

A
  • sepsis, hypoglycaemia, GI bleeds/ varices, encephalopathy
149
Q

management of liver failure

A
  • protect airway with intubation
  • urinary and venous catheters
  • treat cause
  • phenytoin for seizures
  • haemofiltration/dialysis
  • avoid sedatives
  • TRANSPLANT
150
Q

what is hepatitis

A

-inflammation of the liver.

Acute <6 months. Chronic >6months.

151
Q

symptoms of acute hepatitis

A
  • General malaise
  • Myalgia
  • GI upset
  • Abdominal pain
  • +/- jaundice (pale stools, dark urine)
  • Tender hepatomegaly
152
Q

causes of hepatitis

A
  • Viral – hepatitis A,B,C,D,E, herpes virus
  • Non-viral (Spirochaetes, Mycobacteria, Parasites, Bacteria)
  • Non-infection (Alcohol, Toxins/poisoning, Autoimmune)
153
Q

clinical manifestations of chronic hepatitis

A
  • signs of chronic liver disease (Dupuytren’s contracture, Spider naevi)
  • compensated = liver function maintained
  • decompensated = jaundice, ascites, low albumin, coagulopathy, encephalopathy
154
Q

Hep A

A
  • RNA virus spread from faeces or shellfish
  • incubation 2-6 weeks
  • fever, malaise, anorexia, nausea, arthralgia
  • AST/ALT rise 22-40 days after exposure
  • IgG detectable for life
  • supportive treatment, monitor liver function
155
Q

hep B

A
  • blood borne, IV drug abusers, sexual, direct contact
  • incubation 1-6 months
  • arthralgia and urticaria common symptoms
  • HBsAg (surface antigen) is present 1-6months after
  • lead to fulminant hepatic failure and cirrhosis
  • treatment = no alcohol, immunise sexual contacts, antivirals, supportive
156
Q

hep C (HCV)

A
  • RNA flavivirus
  • blood transfusion, IV drug abuse, sexual contact
  • Risk factors for progression: male, older, higher viral load, use of alcohol, HIV
  • LFTs and anti-HCV Abs
  • treatment = non-structural viral protein inhibitors, no alcohol, antivirals
  • complications = GN, thyroiditis, autoimmune hepatitis
157
Q

hep D (HDV)

A
  • incomplete RNA virus
  • HBV vaccine prevents HDV
  • blood and bodily fluids
  • cause acute liver failure/cirrhosis
  • anti-HDV Ab
  • treatment = pegylated interferon-alpha or liver transplant
158
Q

hep E (HEV)

A
  • high mortality in pregnancy
  • usually asymptomatic
  • usually self-limiting acute hepatitis
  • risk of chronic infection in immunocompromised
  • anti-HEV IgM/G, nucleic acid amplification test
  • supportive treatment and reverse immunosuppression
159
Q

what is liver cirrhosis

A
  • irreversible liver damage.

- loss of normal hepatic architecture with bridging fibrosis and nodular regeneration

160
Q

causes of cirrhosis

A
  • Most often chronic alcohol abuse, HBV or HCV infection
  • Genetic disorders: haemochromatosis
  • Drugs: amiodarone, methotrexate
161
Q

clinical manifestations of cirrhosis

A
  • Leukonychia: white nails with lunulae undermarcated, from hypoalbuminemia
  • Ectasias
  • Palmar erythema (red palms)
  • Hyperdynamic circulation
  • Hepatomegaly
162
Q

complications of cirrhosis

A
  • hepatic failure

- portal hypertension (ascites, splenomegaly, portosystemic shunt)

163
Q

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
164
Q

management of cirrhosis

A
  • general = good nutrition, alcohol abstinence
  • ascites = fluid restriction, low-salt diet
  • transplant
165
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)
166
Q

pathology of primary biliary cholangitis

A
  • Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis
  • loss of immune tolerance to self-mitochondrial proteins
  • leads to fibrosis, cirrhosis, portal hypertension
167
Q

clinical manifestations of primary biliary cholangitis

A
  • often incidental finding after high ALP
  • Lethargy, sleepiness and pruritus (skin itching)
  • Jaundice
  • Skin pigmentation
  • Hepatosplenomegaly
168
Q

investigations of primary biliary cholangitis

A
  • Blood: high ALP, mildly high AST and ALT. High bilirubin and low albumin
  • Ultrasound; excludes extrahepatic cholestasis
  • Biopsy not usually needed
169
Q

management of primary biliary cholangitis

A
  • cholestyramine for symptoms
  • fat soluble vitamins
  • LFT regularly, US twice yearly
  • liver transplant (end stage)
170
Q

what is alcoholic liver disease

A
  • due to excessive alcohol consumption

- fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis or cirrhosis

171
Q

pathology of alcoholic liver disease

A
  • liver metabolises alcohol causing high levels of NADH = stimulated fatty acid synthesis and production of triglycerides = steatosis
  • oxidative stress = hepatocyte injury and necro-inflammatory activity (ASH- alcoholic steatohepatitis) = liver fibrosis = cirrhosis
  • steatosis - ASH - cirrhosis
172
Q

clinical manifestations of alcoholic liver disease

A
  • severe alcohol hepatitis after binge causes malaise and fever
  • jaundice
  • complications of cirrhosis
173
Q

organs affected by alcoholic liver disease

A
  • liver = cirrhosis
  • CNS: self neglect, decreased memory function, cortical atrophy
  • Gut: obesity, peptic ulcers, varices, pancreatitis, cancer
  • Blood: high MCV, anaemia from marrow depression and GI bleeding
  • Heart: arrhythmias, high BP, cardiomyopathy
  • Reproduction: testicular atrophy
174
Q

investigations for alcoholic liver disease

A

-Alcoholic hepatitis: high WCC, low platelets, high MCV, high urea

175
Q

CAGE questions for alcoholics

A
  • Ever felt you ought to Cut down on your drinking?
  • Annoyed by people criticising your drinking?
  • Guilty about your drinking?
  • Eye-opener in the morning?
176
Q

management of alcoholic liver disease

A
  • alcohol withdrawal

- Acamprosate may help intense anxiety, insomnia and craving

177
Q

what is Wilson’s disease

A

inherited disorder of copper metabolism, leading to the accumulation of toxic levels of copper in the liver and brain (hepatocytes and basal ganglia)

178
Q

clinical manifestations of Wilson’s disease

A
  • present in childhood with chronic liver disease and cirrhosis
  • neuropsychiatric symptoms = tremor, dysarthria, dysphagia, parkinson’s
  • Kayser-Fleischer (KF) rings: copper in iris
179
Q

management of Wilson’s disease

A
  • avoid copper in diet
  • penicillamine for life
  • liver transplant
  • screen siblings
180
Q

what is hereditary haemochromatosis

A
  • inherited disorder characterised by increased intestinal absorption of iron, leading to iron overload in multiple organs, particularly the liver (pancreas, heart, joints, pituitary)
  • deficiency in hepcidin = no inhibition of ferroportin
181
Q

clinical manifestations of hereditary haemochromatosis

A
  • Skin pigmentation (slate-grey)
  • Cirrhosis
  • Hypogonadism
  • Cardiac failure
  • Diabetes mellitus
182
Q

investigations for hereditary haemochromatosis

A
  • high LFT and ferritin
  • X-ray = chondrocalcinosis (stressed joints deteriorate)
  • liver biopsy = PERL’S STAIN for iron loading
183
Q

management of hereditary haemochromatosis

A
  • Venesection (removal of accumulating iron) until ferritin <50mcg/L then needs repeating for life
  • well balanced diet, no alcohol or raw seafood
  • screening for serum ferritin
184
Q

what is alpha1-antitripsin deficiency

A

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

185
Q

clinical manifestations of alpha1-antitripsin deficiency

A
  • Dyspnoea from emphysema
  • Cirrhosis
  • Cholestatic jaundice
186
Q

investigations for alpha1-antitripsin deficiency

A
  • serum antitrypsin low
  • obstructive spirometry
  • liver biopsy = periodic acid schiff
187
Q

diverticular disease definitions

A
  • Diverticulum = outpouching of the gut wall, usually at sites of entry of perforating arteries.
  • Diverticulosis =diverticula are present.
  • Diverticular disease = they are symptomatic.
  • Diverticulitis = inflammation of a diverticulum
188
Q

risk factor for diverticular disease

A

diet low in fibre, high in meat

189
Q

pathology of diverticular disease

A

-Firm stools require higher intraluminal pressures to propel = forces pouches of the colonic mucosa through an anatomical weak point in the muscular layer

190
Q

presentation of diverticular disease

A
  • Intermittent abdominal pain, altered bowel habit, iron deficiency anaemia
  • erosion of blood vessel - rectal bleeding
191
Q

management of diverticular disease

A
  • antispasmodics e.g. mebeverine

- Surgical resection

192
Q

management of diverticulitis

A
  • mild = fluids only and Abx

- complications = abscess formation or perforation

193
Q

what are ascites

A

Effusion and accumulation of serous fluid (protein-containing) in the abdominal cavity
- staged 1-4 (large tense ascites)

194
Q

pathology of ascites caused by portal hypertension

A
  • sodium water imbalance

- neurohormonal agents – renin, aldosterone, sympathetic nervous system, nitric oxide

195
Q

pathology of ascites not caused by portal hypertension or chylous ascites

A
  • Malignancy
  • Cardiac failure
  • Nephrotic syndrome
  • abdominal surgery
196
Q

causes of ascites

A
  • Cirrhosis
  • Malignancy
  • Heart failure
  • TB
  • Pancreatitis
197
Q

signs of ascites

A
  • Flanks fullness
  • Fluid thrill
  • Shifting dullness
198
Q

management of ascites

A
  • treat underlying cause
  • diuretics (spironolactone)
  • salt and fluid restriction
199
Q

what is peritonitis

A
  • Inflammation of the peritoneum.

- Peritonism: tensing muscles to prevent movement of peritoneum

200
Q

causes of peritonitis

A
  • inflamed organ (above), air, pus, faeces, luminal contents and blood
  • cholecystitis, pancreatitis, diverticulitis
  • AEIOU: appendicitis, ectopic pregnancy, infection (TB), obstruction, ulcer.
201
Q

clinical manifestations of peritonitis

A
  • pain, diarrhoea, swelling, shock, abdominal rigidity
  • swinging fever
  • gas under diaphragm on CXR

2A revision (10 decks)

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