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
what are Oesophago-gastric varices
Submucosal venous dilatations secondary to high portal pressures.
26
What is the complication of Oesophago-gastric varices
Bleeding can be brisk, particularly if underlying coagulopathy secondary to loss of hepatic synthesis of clotting factors.
27
What are 3 causes of oesophago-gastric varices
Cirrhosis Thrombosis Parasitic infection
28
What is a pre-hepatic cause of portal hypertension
thrombosis (portal or splenic vein)
29
What are 5 intra-hepatic causes of portal hypertension
cirrhosis, schistosomiasis, sarcoid, myeloproliferative diseases, congenital hepatic fibrosis
30
What are 4 post-hepatic causes of portal hypertension
Budd-Chiari syndrome, right heart failure, constrictive pericarditis, veno-occlusive disease
31
What are 3 Risk factors for variceal bleeds
High portal pressure Variceal size Endoscopic features of the variceal wall and advanced liver disease
32
What are 4 symptoms of oesophago-gastric varices
Only symptomatic if they bleed; Vomiting large amounts of blood Black, tarry or bloody stools Light headedness Loss of consciousness in severe cases
33
What are 3 prevention methods for Oesophago-gastric varices
Don’t drink alcohol Healthy diet and weight Reduce risk of hepatitis – don’t share needles or have unprotected sex
34
What are the 2 management options for Oesophago-gastric varices
Endoscopic banding or sclerotherapy
35
What is haematemesis
vomiting of blood. It may be bright red or look like coffee grounds.
36
What is malaena
black motions, often like tar, and has a characteristic smell of altered blood
37
What are 4 common and 3 rare causes for upper GI bleeds
Peptic ulcers Oesophageal varices Mallory-Weiss tear Gastritis/ oesophagitis Bleeding disorders Portal hypertensive gastropathy Meckel’s diverticulum
38
What is a Mallory- Weiss tear
a tear in the mucous membrane where the oesophagus meets the stomach
39
What is the cause of a Mallory-Weiss tear
Persistent vomiting/retching causes haematemesis via an oesophageal mucosal tear.
40
What is the management of a mallory-weiss tear
Endoscopy to stop the bleeding. Endoscopic haemostasis: 2 of clips, cautery, adrenaline.
41
What is Gastritis
Inflammation of the lining of the stomach.
42
What are 4 causes of gastritis
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
43
what are 4 risk factors for gastritis
Alcohol NSAIDs H.pylori Reflux hernia
44
4 symptoms of gastritis
Epigastric pain Vomiting Indigestion (dyspepsia) Abdominal bloating
45
3 investigations for gastritis
Upper GI endoscopy Blood tests: anaemia and H.pylori infection Faecal occult blood tests – presence of blood in your stool.
46
3 management options for gastritis
H2 receptor antagonists e.g. ranitidine Proton pump inhibitors Avoid hot and spicy foods
47
what is Coeliac disease
A disease in which the small intestine is hypersensitive to gluten, leading to difficulty in digesting food.
48
pathology of coeliac disease
T-cell responses to gluten in the small bowel causes villous atrophy and malabsorption.
49
9 clinical manifestations of coeliac disease
Stinking stools/steatorrhea Diarrhoea Bloating Abdominal pain Nausea and vomiting Aphthous ulcers Angular stomatitis Weight loss, fatigue, weakness Dermatitis herpetiformis
50
3 investigations for coeliac disease
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
51
4 management options for coeliac disease
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.
52
3 complications of coeliac disease
Anaemia Dermatitis herpetiformis Osteopenia/ osteoporosis
53
what is malabsorption
The small intestine can’t absorb enough of certain nutrients and fluids. Malabsorption of protein, fat and carbohydrate leads to weight loss and malnutrition.
54
5 causes of malabsorption
Coeliac disease – reduced surface area Chronic pancreatitis Crohn’s disease Pancreatic insufficiency – poor intraluminal digestion Infection – lymphatic obstruction
55
5 symptoms of malabsorption
Diarrhoea Weight loss Lethargy Steatorrhea Bloating
56
4 signs of malabsorption
Anaemia Bleeding disorders (low vit K) Oedema Metabolic bone disease
57
3 investigations for malabsorption
FBC: low Ca2+, Fe, B12 and folate Lipid profile: coeliac tests Stool: Sudan stain for fat globules
58
2 management steps for malabsorption
Correction of nutritional deficiencies Treatment of causative diseases
59
What is Inflammatory bowel disease
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.
60
What is the main difference between crohns and ulcerative colitis
Crohn’s disease favours the ileum, but can occur anywhere along the intestinal tract. Ulcerative colitis affects the colon (large intestine) only.
61
What is crohns disease
A chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus (especially terminal ileum).
62
What are skip lesions
unaffected bowel between areas of active disease (crohns)
63
pathology of crohns
An inappropriate immune response against the gut flora in a genetically susceptible individual. Smoking increases the risk.
64
4 symptoms of crohns
Diarrhoea Abdominal pain Weight loss/failure to thrive Systemic symptoms: fatigue, fever, malaise, anorexia
65
5 signs of crohns
Bowel ulceration Abdominal tenderness/mass Perianal abscess/fistulae/skin tags Anal strictures Clubbing, skin, joint and eye problems
66
5 complications of crohns
Small bowel obstruction Toxic dilatation Abscess formation Fistulae Malnutrition
67
first line investigations for crohns
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.
68
2 lifestyle management options for crohns
Quit smoking Optimise nutrition
69
management plan for mild-moderate crohns
Prednisolone PO, plan maintenance therapy Azathioprine Biologics Nutrition Surgery
70
management plan for severe crohns
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
71
What is ulcerative colitis
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.
72
Cause of UC
Inappropriate mucosal immune response to luminal bacteria. Smoking appears to decrease the risk of UC.
73
pathology of UC
Hyperaemic/ haemorrhagic colonic mucosa +/- pseudopolyps formed by inflammation.
74
5 symptoms of UC
Episodic or chronic diarrhoea Crampy abdominal discomfort Bowel frequency relates to severity Urgency/tenesmus – proctitis Systemic symptoms: fever, malaise, anorexia, weight loss
75
6 signs of UC
May be none Acute, severe UC – fever, tachycardia, tender distended abdomen Extra-intestinal signs: Clubbing Aphthous oral ulcers Conjunctivitis
76
3 investigations for UC
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.
77
2 complications of acute UC
Toxic dilatation of colon with risk of perforation Venous thromboembolism
78
2 complications of chronic UC
Colonic cancer Neoplasms in mucosa
79
Management of mild UC
Mesalamine is the mainstay for remission-induction/maintenance Prednisolone
80
management of moderate UC
Induce remission oral prednisolone
81
management of severe UC
IV hydration/ electrolyte replacement Monitor pulse, BP, temperature, record stool frequency/character Physical examination daily, and FBC, ESR, CRP, AXR
82
What is IBS
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.
83
5 clinical manifestations of IBS
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
84
3 investigations for IBS
FBC, CRP, ESR, U&E Coeliac screen Faecal calprotectin
85
Diagnosis criteria for IBS
Only diagnose IBS if recurrent abdominal pain associated with at least 2 of: Relief by defecation Altered stool form Altered bowel frequency (constipation/diarrhoea)
86
3 differential diagnoses for IBS
Colonic cancer Inflammatory bowel disease – Crohn’s, UC Coeliac disease
87
What is the overall management plan for IBS
Should focus on controlling symptoms, initially using lifestyle/dietary measures, then cognitive therapy or pharmacotherapy if required
88
treatment of constipation in IBS
ensure adequate water and fibre intake and promote physical activity.
89
treatment of diarrhoea in IBS
avoid sorbitol sweeteners, alcohol and caffeine. Reduce dietary fibre content, encourage patients to identify their own trigger foods.
90
Treatment of Colic/bloating in IBS
oral antispasmodics. Combination probiotics in sufficient doses may help flatulence or bloating. Less alcohol intake.
91
treatment of Psychological symptoms/visceral hypersensitivity for IBS
emphasize the positive. Sinister pathology has been excluded and symptoms tend to improve over time. Consider CBT and hypnosis.
92
What are Gastro-intestinal infections (gastroenteritis)
diarrhoea +/- vomiting due to enteric infection with viruses, bacteria or parasites.
93
What is Norovirus
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.
94
4 symptoms of norovirus
Acute-onset vomiting, watery diarrhoea, cramps, nausea.
95
2 investigations for norovirus
clinical, stool sample reverse transcriptase PCR
96
3 treatments for norovirus
supportive, anti-motility agents, usually self-limiting.
97
What is rotavirus
Double-stranded RNA virus. Commonest cause of gastroenteritis in children.
98
Presentation of rotavirus
incubation 2day. Watery diarrhoea and vomiting for 3-8d, fever, abdominal pain
99
2 investigations for rotavirus
clinical, antigen in stool
100
2 treatments for rotavirus
supportive. Routine vaccination in UK
101
What is Enterotoxigenic E.coli
Gram -ve anaerobe Disease due to heat-stable or heat labile toxin which stimulates Na+, Cl- and water efflux into gut lumen
102
presentation of Enterotoxigenic E.coli
incubation 1-3days. Watery diarrhoea, cramps lasts 3-4 days
103
2 investigations for Enterotoxigenic E.coli
clinical, identification of toxin from stool culture.
104
treatment for Enterotoxigenic E.coli
supportive, self-limiting
105
Prevention of travellers diarrhoea
boil water, cool thoroughly, peel fruit and vegetables. Avoid ice, salads, shellfish. Drink with a straw.
106
presentation of E.coli
watery diarrhoea preceded by cramps and nausea
107
presentation of giardia lamblia
upper GI symptoms e.g. bloating, belching
108
presentation of Campylobacter jejuni and Shigella
colitic symptoms, urgency, cramps.
109
Diagnosis criteria for travellers diarrhoea
3 or more unformed stools per day plus one of the following: Abdominal pain Cramps Nausea Vomiting Dysentery
110
3 treatment steps for travellers diarrhoea
Oral rehydration. Clear fluid or oral rehydration salts. Antimotility agents e.g. loperamide Antibiotics
111
define Acute diarrhoea
3 episodes partially formed or watery stool/day for <14d
112
define dysentry
infectious gastroenteritis with bloody diarrhoea
113
define Persistent diarrhoea
acutely starting diarrhoea lasting >14d
114
define Traveller’s diarrhoea
Traveller’s diarrhoea: starting during, or shortly after, foreign travel
115
define Food poisoning
disease caused by consumption of food/wate
115
What is campylobacter
Gram -ve, spiral-shaped rod
115
7 infective causes of diarrhoea
Rotavirus/norovirus most common in the UK Campylobacter Shigella Salmonella S.aureus E.coli C.diff
116
presentation of campylobacter
incubation 1-10d. Bloody diarrhoea, pain, fever, headache.
117
5 complications of camylobacter
bacteraemia, hepatitis, pancreatitis, miscarriage, reactive arthritis
118
2 investigations for campylobacter
stool culture. PCR/enzyme immunoassay.
119
treatment plan for campylobacter
supportive. Antibiotics only in invasive cases, refer to local sensitivities.
120
6 key points of history for diarrhoea
Onset/duration Characteristics of stool Food/drink Travel Fresh water/ swimming Medications
121
how does onset/duration change diagnosis of diarrhoea
Acute – viral/bacterial Chronic – parasites and non-infectious causes
122
how does Characteristics of stool change diagnosis of diarrhoea
Floating: fat content – malabsorption, coeliac Blood or mucus: inflammatory/invasive infection/ cancer Watery: small bowel infection
123
how does food/drink affect diagnosis of diarrhoea
Meat – campylobacter Rice – bacillus cereus Poultry – salmonella Shellfish – norovirus, v.parahaemolyticus
124
how does travel history change diarrhoea diagnosis
No cholera in the UK – traveller’s diarrhoea
125
how does fresh water/swimming change diarrhoea diagnosis
crypto, giardia, aeromonas
126
how does medication history change diarrhoea diagnosis
Recent antibiotics – C.diff or side effects
127
128
4 cancer risk factors with diarrhoea
Over 50 Chronic diarrhoea Weight loss Blood in stool
129
what are 3 investigations for diarrhoea
Stool tests Blood tests Lower GI endoscopy
130
what is looked at in stool tests for diarrhoea
Microscopy Culture Ova, cysts and parasites Toxin detection
131
what is looked at in blood tests for diarrhoea
Blood culture Inflammatory markers ESR/ CRP
132
mechanism of watery diarrhoea
non-inflammatory (enterotoxin or superficial adherence/invasion)
133
mechanism of bloody/mucoid diarrhoea
inflammatory (invasion/cytotoxin)
134
location of watery diarrhoea
proximal small bowel
135
location of bloody/mucoid diarrhoea
colon
136
bacterial causes of watery diarrhoea
vibrio cholerae e.coli (ETEC) c.diff bacillus cereus s.aureus
137
bacterial causes of bloody/mucoid diarhoea
shigella e.coli (EIEC,EHEC) Salmomella enteritidis v.parahaemolyticus c.diff campylobacter jejuni
138
viral causes of watery diarrhoea
rotavirus norovirus
139
parasitic causes of watery diarrhoea
giardia cryptosporidium
140
parasitic cause of bloody, mucoid diarrhoea
entamoeba histolytica
141
management of diarrhoea
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.
142
What is Clostridium difficile
The cause of pseudomembranous colitis. Gram positive spore forming bacteria.
143
What are 4 antibiotics that cause clostridium difficile
rule of Cs Clindamycin Ciprofloxacin Co-amoxiclav Cephalosporins
144
3 signs of C.diff
Increased temperature Diarrhoea with systemic upset High CRP, WCC and low albumin
145
3 steps of detection of C.diff
Urgent testing of suspicious stool (characteristic smell) Two-stage process with rapid screening test for C.diff protein followed by specific ELISA for toxins.
146
treatment of C.diff
Stop causative antibiotic. Barrier nursing
147
clinical presentation of oesophageal tumour
Dysphagia Weight loss Retrosternal chest pain
148
3 investigations for oesophageal tumours
Oesophagoscopy with biopsy Endoscopic ultrasound CT/ MRI for staging
149
describe the t1-4 stages of oesophageal cancer
T1 – invading lamina propria/ submucosa T2 – invading Muscularis propria T3 – invading adventitia T4 – invasion of adjacent structures
150
describe the N and M stages of oesophageal cancers
N0 – no nodal spread N1 – regional node metastases M0 – no distant metastases spread M1 – distal metastases
151
4 treatment options for oesophageal cancer
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
152
6 symptoms of gastric carcinoma
Often non-specific Dyspepsia Weight loss Vomiting Dysphagia Anaemia
153
4 signs of gastric carcinoma
Epigastric mass Hepatomegaly Jaundice Ascites
154
3 investigations for gastric carcinoma
Gastroscopy and multiple ulcer edge biopsies EUS (endoscopic ultrasound) CT/ MRI for staging
155
4 treatment options for gastric carcinoma
Partial gastrectomy for distal tumours Total gastrectomy if more proximal Combination chemo Surgical palliation for obstruction, pain or haemorrhage
156
4 presentations of left sided colorectal carcinoma
Bleeding/ mucus PR Altered bowel habit or obstruction Tenesmus PR mass
157
4 presentations of right sided colorectal carcinoma
Weight-loss Low Hb Abdominal pain Obstruction less likely
158
4 presentations in both left and right sided colorectal carcinoma
Abdominal mass Perforation Haemorrhage Fistula
159
4 urgent referral criteria for colorectal carcinoma
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
160
5 investigations for colorectal carcinoma
FBC – microcytic anaemia Faecal occult blood – used for UK screening programme Sigmoidoscopy Barium enema or colonoscopy – or CT Liver USS
161
surgical management of colorectal carcinoma
Aims to cure and increases survival by up to 50% Different types of surgery done for different sites of cancer
162
radiotherapy for colorectal cancer
Used in palliation for colonic cancer Occasionally used pre-op to allow resection
163
chemotherapy for colorectal cancer
Adjuvant chemo helpful Chemo is also used in palliation of metastatic disease
164
5 symptoms of liver tumours
Fever Malaise Anorexia Weight loss RUQ pain
165
4 signs of liver tumours
Hepatomegaly Signs of chronic liver disease and evidence of decompensation Feel for an abdominal mass Bruit over liver
166
3 investigations for liver tumours
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
what is hepatocellular carcinoma (HCC)
Primary hepatocyte neoplasia accounts for 90% of primary liver tumours
168
6 clinical features of HCC
Fatigue Appetite loss RUQ pain Weight loss Jaundice Ascites
169
4 causes of HCC
HBV – main cause Autoimmune hepatitis Cirrhosis – alcohol, hemochromatosis, PBC Non-alcoholic fatty liver
170
3 investigations for HCC
3 phase CT MRI Biopsy
171
3 treatments of HCC
Resecting solitary tumours Liver transplant Percutaneous ablation
172
What is Cholangiocarcinoma
Biliary tree cancer.
173
4 clinical presentations of cholangiocarcinoma
Fever Abdominal pain and ascites Malaise Elevated bilirubin
174
175
3 treatment options for cholangiocarcinoma
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
features of haemangiomas
collection of small blood vessels incidental finding on US or CT No treatment required Avoid biopsy
177
causes of adenomas
anabolic steroids, oral contraceptives, pregnancy
178
when to treat adenomas
Only treat if symptomatic or >5cm.
179
Pathology of pancreas carcinoma
Mostly ductal adenocarcinoma – metastasise early, present late A few arise in ampulla of Vater or pancreatic islet cells (insulinoma, gastrinoma, glucagonomas, somatostinomas, VIPomas
180
2 clinical features of pancreas carcinoma
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
4 complications of pancreas carcinoma
anorexia, weight loss, diabetes, acute pancreatitis
182
6 signs of pancreas carcinoma
Jaundice + palpable gallbladder Epigastric mass Hepatomegaly Splenomegaly Lymphadenopathy Ascites
183
2 investigations for pancreatic carcinoma
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
6 management options for pancreas carcinoma
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
what is intestinal obstruction
Blockage to the lumen of the gut. Commonly refers to blockage of intra-abdominal part of the intestine.
186
What is a volvulus
a twist/rotation of segment of bowel
187
what are bowel adhesions
sticking together (abdominal structures to one another, bowel loops or omentum, other solid organs, abdominal wall)
188
3 classes of mechanical classification of bowel obstruction
Mechanical (intraluminal)/ true (extraluminal) Paralytic (pseudo obstruction)
189
4 classes of bowel obstruction according to pathology
Simple Closed loop Strangulation Intussusception
190
2 common and 4 rare causes of small bowel obstruction
Adhesions (previous surgery) Hernia Rarer; Crohn’s, Malignancy, Volvulus, Intussusception
191
what is intussesception
the inversion of one portion of the intestine within another.
192
4 causes of large bowel obstruction
Colon carcinoma Constipation Diverticular stricture Volvulus - Sigmoid
193
what is sigmoid volvulus
occurs when the bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction.
194
6 clinical manifestations of intestinal obstruction
Anorexia Nausea Vomiting: Nature – forceful/ regurgitation Content – bilious, feculent Distension Abdominal pain Altered bowel habits: Constipation Obstipation
195
2 complications of intestinal obstruction
Tissue death – blood supply can be cut off to part of the intestine Infection – peritonitis.
196
first line investigation for intestinal obstruction
X-ray
197
general principals of intestinal obstruction management
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
immediate management of intestinal obstruction
NGT and IV fluids to rehydrate and correct electrolyte imbalance.
199
what further imaging is used for intestinal obstruction management
CT to establish the cause of obstruction.
200
which type of bowel obstruction requires emergency surgery
strangulation needs emergency surgery.
201
What are hernias
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
What is an irreducible hernia
contents cannot be pushed back into place
203
what is an obstructed hernia
bowel contents cannot pass – features of intestinal obstruction
204
What is a strangulated hernia
ischaemia occurs – the patient requires urgent surgery
205
What is an incarceration hernia
contents of the hernial sac are stuck inside by adhesions
206
what is the usual presentation of a hernia
Usually presents as lump and pain
207
pathology of femoral hernias
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
epideimiology and features of femoral hernias
Occur more often in women, middle age and elderly Irreducible and strangulate
209
treatment of femoral hernias
surgical repair
210
What are incisional hernias and their repair
Follow breakdown of muscle closure after surgery If obese, repair is not easy Mesh repair – less recurrence but more infections compared to sutures
211
what are inguinal hernias
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
4 predisposing conditions for inguinal hernias
Male sex Chronic cough Urinary obstruction Past abdominal surgery
213
2 examinations for inguinal hernias
Is lump visible? Ensure it is not a scrotal lump Ask patient to cough – should appear above and medial to pubic tubercle
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Do direct or indirect inguinal hernias strangulate
Indirect hernias
215
repair of inguinal hernias
Lose weight and stop smoking pre-op Hernias may recur Mesh techniques – polypropylene mesh reinforces posterior wall
216
what is ischaemic colitis
Inflammation and injury of the large intestine resulting from inadequate blood supply.
217
pathology of ischaemic colitis
Usually follows low flow in the inferior mesenteric artery territory and it ranges from mild to gangrenous.
218
2 clinical manifestations of Ischaemic colitis
Lower left-sided abdominal pain May have bloody diarrhoea
219
2 investigations for ischaemic colitis
CT may be helpful but lower GI colonoscopy is gold-standard.
220
management of ischaemic colitis
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
what is mesenteric ischaemia
Injury to the small intestine occurs due to inadequate blood supply.
222
7 causes of acute mesenteric ischaemia
Superior mesenteric artery thrombosis/embolism Mesenteric vein thrombosis Non-occlusive disease Trauma, vasculitis, radiotherapy strangulation.
223
what is the classical clinical presentation triad for acute mesenteric ischaemia
Acute severe abdominal pain No/minimal abdominal signs Rapid hypovolaemia – shock
224
pain picture for acute mesenteric ischaemia
tends to be constant, central or around the right iliac fossa (RIF)
225
5 investigations for acute mesenteric ischaemia
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
2 main life-threatening complications secondary to acute mesenteric ischaemia
Septic peritonitis Progression of a systemic inflammatory response syndrome to multi-organ failure.
227
management of acute mesenteric ischaemia
Resuscitation with fluid, antibiotics and LMW heparin are required. If arteriography is done, thrombolytics may be attempted on potentially viable bowel.
228
cause of chronic mesenteric ischaemia
Typically brought about through a combination of a low-flow state with atheroma.
229
3 clinical presentations of chronic mesenteric ischaemia
Severe, colicky post-prandial abdominal pain Weight loss (painful to eat) Upper abdominal bruit may be present
230
2 investigations for chronic mesenteric ischaemia
CT angiography and contrast-enhanced MR angiography
231
treatment of chronic mesenteric ischaemia
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
what is appendicitis
Inflamed and painful appendix. It is the most common surgical emergency.
233
pathology of appendicitis
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
5 clinical manifestations of appendicitis
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
3 specific signs for appendicitis
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
5 differential diagnoses for appendicitis
UTI Mesenteric adenitis Diverticulitis/ cholecystitis/ cystitis Food poisoning Crohn’s disease
237
3 investigations for appendicitis
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
management for appendicitis
Prompt appendicectomy Antibiotics: piperacillin Laparoscopy: diagnostic and therapeutic advantages. Not recommended with suspected gangrenous perforation – rate of abscess formation is higher.
239
3 complications of appendicitis
Perforation Appendix mass – occurs when inflamed appendix becomes covered with omentum Appendix abscess – if an appendix mass enlarges.
240
pathology of gallstones
Bile contains cholesterol, bile pigments and phospholipids. If concentrations vary, different stones may form.
241
features of pigment gallstones
small, friable and irregular.
242
features of cholesterol stones
large, often solitary.
243
features of mixed stones
faceted (calcium salts, pigment and cholesterol).
244
5 Fs for gallstones
Fair Forty Fertile Fat Female
245
clinical manifestations for gall stones in the gall bladder
Biliary pain Cholecystitis maybe Obstructive jaundice
246
clinical manifestations for gall stones in the bile duct
Biliary pain Obstructive jaundice Cholangitis Pancreatitis
247
management options for gallstones
Laparoscopic cholecystectomy Bile acid dissolution therapy Bile duct stones: ERCP with sphincterotomy and removal (balloon)/ crushing (laser)/ stent placement Surgery (large stones)
248
5 complications for gallstones in the gall bladder and cystic duct
Biliary colic Acute and chronic cholecystitis Carcinoma Mirizzi’s syndrome
249
3 complications for gallstones in the bile ducts
Obstructive jaundice Cholangitis Pancreatitis
250
what is gallstone ileus
when a gallstone erodes through the gallbladder into the ileum, causing complications
251
what is biliary colic
Gallstones are symptomatic with cystic duct obstruction or if passed into the common bile duct. RUQ pain radiating to the back Possible jaundice
252
investigations for biliary colic
urinalysis, CXR and ECG
253
treatment for biliary colic
analgesia, rehydrate. Elective laparoscopic cholecystectomy
254
What is acute cholecystitis
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
3 investigations for acute cholecystitis
high WCC ultrasound – thick-walled, shrunken GB, pericholecystic fluid. Plain AXR only shows 10% of gallstones.
256
treatment of acute cholecystitis
- NBM, pain relief, IVI and antibiotics e.g. co-amoxiclav.
257
what is flatulent dyspepsia
Vague abdominal discomfort Distension Nausea Flatulence Fat intolerance (fat stimulates cholecystokinin release and GB contraction)
258
investigations for chronic cholecystitis
Ultrasound to image stones and assess CBD diameter. MRCP is used to find CBD stones.
259
treatment of chronic choleystitis
cholecystectomy.
260
pathology of acute pancreatitis
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
GET SMASHED causes for acute pancreatitis
Gallstones Ethanol Trauma Steroids Mumps Autoimmune Scorpion venom Hyperlipidaemia/ hypothermia/ hypercalcaemia ERCP and emboli Drugs
262
symptoms of acute pancreatitis
Gradual or sudden severe epigastric or central abdominal pain. Vomiting prominent. Pain radiates to back, sitting forward may relieve.
263
6 signs for acute pancreatitis
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
3 investigations for acute pancreatitis
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
management of acute pancreatitis
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
3 early complications of acute pancreatitis
Shock Renal failure Sepsis
267
3 late complications of acute pancreatitis
Pancreatic necrosis and pseudocyst Bleeding from elastase eroding a major vessel Thrombosis may occur in splenic arteries causing bowel necrosis
268
what is chronic pancreatitis
A chronic inflammatory process of the pancreas, leading to irreversibly low pancreatic function.
269
pathology of acute pancreatitis
Chronic inflammation in the pancreas leads to the replacement of functional pancreatic tissue by fibrous scar tissue.
270
4 causes of chronic pancreatitis
Alcohol Smoking Autoimmune Pancreatic duct obstruction
271
3 clinical presentations of chronic pancreatitis
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
4 investigations for chronic pancreatitis
Ultrasound and CT scan: pancreatic calcifications confirm the diagnosis. MRCP, AXR – speckled calcification
273
3 management options for chronic pancreatitis
Drugs: give analgesia and fat-soluble vitamins Diet: no alcohol, low fat may help Surgery: e.g. pancreatectomy for unremitting pain/ weight loss
274
4 complications of chronic pancreatitis
Diabetes Biliary obstruction Local arterial aneurysm Gastric varices
275
features of liver failure
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
what is fulminant hepatic failure
a clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function.
277
3 infection causes of liver failure
viral hepatitis, yellow fever, leptospirosis
278
3 drug causes of liver failure
paracetamol overdose, halothane, isoniazid
279
2 toxin causes of liver failure
Carbon tetrachloride, Amanita phalloides mushroom
280
2 vascular causes of liver failure
Budd-Chiari syndrome, veno-occlusive disease
281
7 misc. causes of liver failure
alcoholic fatty liver disease, primary biliary cholangitis, primary sclerosing cholangitis, haemochromatosis, autoimmune hepatitis, metabolic causes, malignancy.
282
what is Budd-Chiari syndrome
hepatic vein obstruction by thrombosis or tumour causes congestive ischaemia and hepatocyte damage.
283
pathophysiology of liver failure
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
7 clinical presentations of liver failure
Abnormal bleeding Ascites Jaundice Hepatic encephalopathy Fetor hepaticus (sweet and musty breath) Constructional apraxia Mental state drowsiness and confusion, due to cerebral oedema
285
3 investigations of liver failure
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
8 management steps of liver failure
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
4 complications of liver failure
Cerebral oedema, bleeding, encephalopathy, ascites
288
7 symptoms of acute hepatitis
Can be asymptomatic General malaise Myalgia GI upset Abdominal pain +/- jaundice (pale stools, dark urine) Tender hepatomegaly
289
6 viral causes of hepatitis
hepatitis A,B,C,D,E, herpes virus
290
4 non-viral causes of hepatitis
Spirochaetes Mycobacteria Parasites Bacteria
291
3 non-infection causes of hepatitis
Alcohol Toxins/poisoning Autoimmune
292
4 signs of compensated chronic hepatitis
Dupuytren’s contracture Spider naevi LFTs can be normal Compensated – liver function maintained
293
8 signs of decompensated chronic hepatitis
Dupuytren’s contracture Spider naevi LFTs can be normal jaundice ascites low albumin coagulopathy encephalopathy
294
how is hepatitis A spread
faecal-oral or shellfish
295
incubation time of hep.A
2-6weeks
296
5 symptoms of hep.A
Fever Malaise Anorexia Nausea Arthralgia
297
3 investigations for hep.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
treatment for Hep.A
Supportive Monitor liver function Fulminant hepatitis failure/ acute liver failure
299
how does hep.B spread
blood borne, IV drug abusers, sexual, direct contact
300
5 risk groups for hep.B
IV drug abusers and their sexual partners/carers, health workers, haemophiliacs, sexually promiscuous
301
incubation period of Hep.B
Incubation: 1-6 months
302
Signs for hep.B
Resemble hepatitis A but arthralgia and urticaria are commoner
303
2 investigations for hep.B
HBsAg (surface antigen) is present 1-6months after exposure Antibodies imply past infection
304
how is vaccinations used for hep.b
high risk groups vaccinated passive immunisation may be given to non-immune contacts after high-risk exposure also prevents HDV
305
3 complications of hep.b
Fulminant hepatic failure Cirrhosis Membranous nephropathy
306
4 treatment steps for hep.b
Avoid alcohol Immunise sexual contacts Antivirals Supportive
307
spread of hepatitis C (HCV)
blood transfusion, IV drug abuse, sexual contact
308
risk factors for progression of HCV
male, older, higher viral load, use of alcohol, HIV
309
2 investigations for HCV
LFTs Anti-HCV antibodies confirms exposure
310
3 treatments for HCV
Non-structural viral protein inhibitors. Quit alcohol Directly acting antivirals
311
3 complications for HCV
Glomerulonephritis Thyroiditis Autoimmune hepatitis
312
spread of HDV
via blood and bodily fluids.
313
test for HDV
anti-HDV antibody
314
treatment of HDV
pegylated interferon-alpha. If limited success – liver transplant.
315
transmission of HEV
via faecal-oral route (food, contaminated water, undercooked seafood and pork)
316
5 acute presentations of HEV
Fever, malaise, nausea + vomiting, jaundice, hepatomegaly
317
investigations for HEV
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
Management of HEV
1st line – no treatment. Very mild illness which is self-limiting within a month. It is a notifiable disease. No vaccine available.
319
4 complications of HEV
Complications Chronic hepatitis, liver failure (especially in pregnant women), cirrhosis, hepatocellular carcinoma
320
what is liver cirrhosis
Cirrhosis implies irreversible liver damage. Histologically, there is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration.
321
7 causes of Cirrhosis
Most common: Alcoholic liver disease, non-alcoholic fatty liver disease, hepatitis B, hepatitis C Rarer: haemochromatosis, Wilson’s disease, alpha 1 trypsin deficiency
322
5 clinical manifestations of cirrhosis
Leukonychia: white nails with lunulae undermarcated, from hypoalbuminemia Ectasias Palmar erythema (red palms) Hyperdynamic circulation Hepatomegaly
323
5 complications of cirrhosis leading to liver failure
Coagulopathy (failure of hepatic synthesis of clotting factors) Encephalopathy Hypoalbuminaemia Sepsis Spontaneous bacterial peritonitis
324
3 complications of cirrhosis leading to portal hypertension
Ascites Splenomegaly Portosystemic shunt including oesophageal varices
325
3 investigations for cirrhosis
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
management of cirrhosis
General: Good nutrition is vital Alcohol abstinence Ascites: Fluid restriction, low-salt diet Transplant
327
what is primary biliary cholangitis
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
Pathology of Primary biliary cholangitis
Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis (may lead to fibrosis, cirrhosis and portal hypertension).
329
cause of primary biliary cholangitis
Unknown environmental triggers (possibly pollutants, xenobiotics) and a genetic predisposition leading to loss of immune tolerance to self-mitochondrial proteins.
330
5 clinical manifestations of primary biliary cholangitis
Often asymptomatic and diagnosed after incidental finding high ALP. Lethargy, sleepiness and pruritus (skin itching) may precede jaundice. Jaundice Skin pigmentation Hepatosplenomegaly
331
3 investigations for primary biliarycholangitis
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
management of primary biliary cholangitis
For symptomatic patients try cholestyramine. Fat-soluble vitamin prophylaxis Monitoring: regular LFT and ultrasound twice yearly Liver transplantation: end-stage disease
333
What is alcholic liver disease
Liver disease due to excessive alcohol consumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis or cirrhosis.
334
pathology of alcoholic liver disease
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
4 clinical manifestations of alcoholic liver disease
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
how does alcohol affect the liver
Fatty liver – acute/reversible, but can progress to cirrhosis Alcoholic hepatitis – can progress to cirrhosis Cirrhosis – irreversible liver damage
337
How does alcohol affect the CNS
self neglect, decreased memory function, cortical atrophy
338
how does alcohol affect the gut
obesity, peptic ulcers, varices, pancreatitis, cancer
339
how does alcohol affect blood
high MCV, anaemia from marrow depression and GI bleeding
340
how does alcohol affect the heart
arrhythmias, high BP, cardiomyopathy
341
how does alcohol affect reproductive system
testicular atrophy
342
investigation for alcohol hepatitis
Blood: high WCC, low platelets, high MCV, high urea
343
management of alcoholic liver disease
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
CAGE questions for alcohol
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
What is wilsons disease
An inherited disorder of copper metabolism, leading to the accumulation of toxic levels of copper in the liver and brain.
346
Pathology of wilsons disease
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
5 clinical manifestations of wilsons
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
4 CNS signs of wilson's
Tremor Dysarthria (unclear articulation of speech) Dysphagia Parkinson’s
349
6 investigations for wilsons
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
management of wilsons
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
5 side effects of penicillamine
nausea, rash, low WCC, Hb and platelets
352
What is hereditary haemochromatosis
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
pathology of Hereditary haemochromatosis
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
6 clinical manifestations of haemochomatosis
Early symptoms are non-specific e.g. fatigue and arthropathy Later symptoms; Skin pigmentation (slate-grey) Cirrhosis Hypogonadism Cardiac failure Diabetes mellitus
355
3 investigations for haemochromatosis
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
3 management options for haemochromatosis
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
what is α1-antitrypsin deficiency
An inherited disorder affecting the lungs (emphysema) and the liver (cirrhosis).
358
pathology of α1-antitrypsin deficiency
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
clinical manifestations of α1-antitrypsin deficiency
Symptomatic patients usually have the PiZZ genotype ( both parents carriers): Dyspnoea from emphysema Cirrhosis Cholestatic jaundice
360
4 investigations for α1-antitrypsin deficiency
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
4 management options for α1-antitrypsin deficiency
Smoking cessation Prompt treatment/ preventative vaccination for lung infections. Liver transplanted – needed in decompensated cirrhosis Lung transplant – improves survival
362
What is Ascites
Effusion and accumulation of serous fluid (protein-containing) in the abdominal cavity.
363
Classification of ascites
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
What is the pathology of portal hypertension ascites
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
pathology of non-portal hypertensive ascites
Malignancy Cardiac failure Nephrotic syndrome
366
pathology of Chylous ascites
Abdominal surgery/ trauma, malignancy, radiation, congenital
367
5 causes of ascites
Cirrhosis Malignancy Heart failure TB Pancreatitis
368
4 symptoms of ascites
Abdominal distension – clothes getting tighter Nausea, loss of appetite Constipation Weight loss
369
3 signs of ascites
Flanks fullness Fluid thrill Shifting dullness
370
3 investigations for ascites
Naked eye assessment – swollen stomach Chemistry: proteins and amylase Ultrasound scan and abdominal CT
371
management of ascites
Treat underlying cause Diuretics – spironolactone, metolazone Salt and fluid restriction
372
complication of ascites
Can lead to spontaneous bacterial peritonitis.
373
What is peritonitis
Inflammation of the peritoneum.
374
what is peritonism
tensing muscles to prevent movement of peritoneum.
375
5 causes of peritonitis
Cholecystitis Pancreatitis Appendicitis Diverticulitis AEIOU
376
AEIOU causes for peritonitis
appendicitis, ectopic pregnancy, infection (TB), obstruction, ulcer.
377
6 inflammatory agents for peritonitis
inflamed organs, air, pus, faeces, luminal contents and blood.
378
pathology of 4 causes of peritonitis
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
8 clinical manifestations of peritonitis
Abdominal pain Diarrhoea Swelling Swinging fever Prostration Shock Tenderness + rebound/percussion pain Board-like abdominal rigidity
380
2 differential diagnoses for peritonitis
Appendicitis Angioedema
381
3 investigations for peritonitis
Ultrasound/ CT scan Ascitic tap: Raised WCC (neutropil) Erect CXR may show gas under diaphragm
382
5 complications of peritonitis
Sepsis Multi-organ failure CV events (MI, stroke) Respiratory complications (pneumonia, pulmonary embolus) Surgical complications
383
4 surgical management options for peritonitis
Laparotomy Laparoscopy Treat problem – patch hole, remove organ/cause Wash out infection
384
4 management options for peritonitis
Surgery Intensive care Support of kidneys Physio/early mobilisation
385
what is a Diverticulum
an outpouching of the gut wall, usually at sites of entry of perforating arteries.
386
what is diverticulitis
refers to inflammation of a diverticulum.
387
what is diverticular disease
symptomatic diverticula
388
cause of diverticular disease
A diet low in fibre and high in meat is the strongest risk factor.
389
pathology of diverticular disease
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
presentation of diverticular disease
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
4 investigations for diverticular disease
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
management of diverticular disease
Try antispasmodics e.g. mebeverine Surgical resection occasionally needed
393
management of diverticulitis
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
What are haemorrhoids
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
what are complications of haemorrhoids
Cause bright red rectal bleeding and discomfort
396
what are anal tags
Polypoid projections of the anal mucosa and submucosa
397
histology of haemorrhoids
Excised haemorrhoids examined microscopically contain large dilated blood vessels, which may show evidence of thrombosis, with an overlying hyperplastic squamous epithelium.
398
histology of anal tags
Microscopically composed of a fibrovascular core covered by squamous epithelium. The fibrovascular core lacks the typically ecstatic vessels of haemorrhoids
399
What is an anal fissure
A tear in the mucosa of the lower anal canal which is most always located posteriorly in the midline
400
cause of anal fissures
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
what is an anorectal abscess
A collection of pus within deep perianal tissue A complication of infection within a deep anal gland
402
presentation of anorectal abscess
perianal erythema, swelling and pain
403
What is an anorectal fistula
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
What causes anal cancer
Uncommon and invariably associated with HPV infection
405
what type of cancer are the majority of anal cancers
Vast majority are squamous cell carcinomas which arise from areas of squamous dysplasia known as anal intraepithelial neoplasia which is graded 1-3.
406
Gold standard investigations for chrons
Colonoscopy and biopsy (granulomatous transmural inflammation. Skip lesions, cobblestone appearance. Strictures “string sign”)