Gastrointestinal / Liver Flashcards
1
Q
Define Gastro-oesphageal reflux disease (GORD)
A
Prolonged or recurrent reflux of the gastic contents into the oesphagus.
2
Q
Define Mallory-weiss tear
A
Mucosal lacerations in the upper GI tract
-> bleeding.
3
Q
Define Oesophago-gastric varices
A
Dilated veins at the junction between the portal and systemic venous systems leading to variceal haemorrhage.
4
Q
How does Gastro-oesphageal reflux disease (GORD) clinically present?
A
Heartburn, related to lying down and meals.
Odynophagia (painful swallowing) and regurgitation.
5
Q
How does Mallory-weiss tear clinically present?
A
Bout of retching or vomiting
-> Haemetesis (vomiting blood).
Others: Syncope, light headedness, dizziness.
6
Q
How does Oesophago-gastric varices clinically present?
A
Haematemesis (vomiting blood).
Liver disease.
Pallor.
Shock (low blood pressure / high heart rate).
7
Q
Cause of Gastro-oesphageal reflux disease (GORD)
A
Smoking, alcohol, pregnancy, obesity, big meals.
Complication of a hiatus hernia.
Any reason for inadequate LOS function.
8
Q
Cause of Mallory-weiss tear
A
Trauma from frequent cough, vomit, retching or even hiccuping.
RF: Excessive alcohol consumption.
9
Q
Cause of Oesophago-gastric varices
A
Portal Hypertension.
Majority of patients with oesophageal varices have chronic liver disease.
10
Q
Diagnostic test for Gastro-oesphageal reflux disease (GORD)
A
Endoscopy,
barium swallow.
11
Q
Diagnostic test for Mallory-weiss tear
A
Endoscopy.
12
Q
Diagnostic test for Oesophago-gastric varices
A
Endoscopy.
13
Q
Treatment of Gastro-oesphageal reflux disease (GORD)
A
Lifestyle; weight loss, avoidance of excess alcohol, cessation of smoking.
Antacids (gaviscon, sodium bicarbonate) sufficient for mild.
Severe may require PPI (omeprazole).
H2 receptor antagonist (cimetidine)
14
Q
Treatment of Mallory-weiss tear
A
Resuscitation.
Maintain airway, high flow oxygen, correct fluid losses. Identify comorbidities.
Tear tends to heal rapidly.
15
Q
Treatment of Oesophago-gastric varices
A
Resuscitation.
Maintain airway.
Treat shock.
Vasoactive drugs, endoscopic band ligation and antibiotics (as prophylaxis).
Can obturate with glue like substance.
16
Q
Complications of Gastro-oesphageal reflux disease (GORD)
A
Oesophageal stricture formation: worsening dysphagia.
Barrett’s Oesophagus: abnormal columnar epithelium replaces the squamous epithelium of the distal oesophageus.
Irreversible.
Can develop into oesophageal cancer.
17
Q
Complications of Mallory-weiss tear
A
Hypovolaemic shock (and death).
Rebleeding.
MI.
18
Q
Complications of Oesophago-gastric varices
A
70% chance of rebleeding.
Significant risk of death.
19
Q
Define Peptic ulcer
A
Break in the GI mucosa in or adjacent to acid bearing area.
20
Q
Define Gastritis
A
Inflammation of the gastric mucosa.
21
Q
Define Gastropathy
A
Injury to the gastric mucosa with epithelial cell damage and regeneration.
Little to no inflammation.
22
Q
Types of peptic ulcer
A
Gastric
Duodenal
23
Q
Types of gastritis
A
Acute
Chronic
24
Q
How does a peptic ulcer clinically present?
A
Burning epigastric pain.
Nausea, heartburn, and flatulence.
Occasionally painless haemorrhage.
Differences: Duodenal - more pain when the patient is hungry, and at night.
25
How does gastritis clinically present?
Usually asymptomatic.
Sometimes functional dyspepsia.
26
How does gastropathy clinically present?
Indigestion,
vomiting
and haemorrhage.
27
What is associated with H. pylori?
Peptic ulcers. 80-90% association.
28
Duodenal or gastric ulcer: which has higher prevalence of H. pylori association?
Duodenal associated with 95% of cases.
Gastric associated with 80% of cases.
29
What is acute gastritis associated with?
Associated with neutrophilic infiltration.
30
What is chronic gastritis associated with?
Associated with mononuclear cells
(lymphocytes, plasma cells and macrophages).
31
Causes of peptic ulcers
H. pylori and NSAIDs.
H. pylori: Increased gastric acid secretions.
Disruption of mucous protective layer.
Reduced duodenal bicarbonate production
NSAIDs: Reduced production of prostaglandins which provide mucosal protection in the upper GI.
32
Causes of gastritis
Most commonly: H. pylori infection.
Also possible; autoimmune gastritis (antibodies to parietal cells and intrinsic factor), viruses, duodeno-gastric reflux.
33
Cause of gastropathy
Most commonly: Use of NSAIDs.
Also possible; severe stress, high amounts of alcohol, CMV and herpes simplex infection.
34
Epidemiology of peptic ulcers
50% of all UGIB
Differences: Duodenal 2-3 times more common than gastric.
35
Diagnostic test for peptic ulcers
Testing for H. pylori: Carbon-13 urea breath test or stool antigen test.
Alternatively Endoscopy possible.
36
Diagnostic test for gastritis
Endoscopy: Can appear reddened, or normal.
Histological change; detected through biopsy.
37
Diagnostic test for gastropathy
Endoscopy: Erosions and subepithelial haemorrhage.
38
Treatment of peptic ulcers
Avoid NSAIDs.
Cessation of smoking.
Eradication of H. pylori through antibiotics and PPI (triple therapy: clarithromycin, omeprazole, metronidazole).
39
Treatment of gastritis
Eradication of H. pylori
(triple therapy: clarithromycin, omeprazole, metronidazole).
40
Treatment of gastropathy
PPI with removal of causative agent.
41
Complications of peptic ulcers
Can cause Upper GI bleed.
42
Complications of gastritis
Peptic ulcer.
43
Complications of gastropathy
Peptic ulcer.
44
Sequelae of gastritis
Pernicious anaemia (if due to autoimmune attack of IF).
45
Define Cholangitis
Infection of the biliary tree.
46
Define Primary sclerosing cholangitis.
Chronic inflammation and fibrosis of the bile ducts.
47
How does Cholangitis clinically present?
Charcot's triad:
Fever (with chills),
right upper quadrant pain,
jaundice (dark urine, pale stool, pruritus) in most patients.
48
How does Primary sclerosing cholangitis present.
May be asymptomatic.
Usually incidentally found after LFT.
Charcot's triad:
Fever (with chills),
right upper quadrant pain
and jaundice (dark urine, stool, pruritus).
Hepatomegaly.
49
Primary sclerosing cholangitis - note
75% have association with ulcerative colitis.
50
Cause of Cholangitis
Generally caused by gallstones.
Other causes include infection (usually Klebsiella or E. coli.
Can be due to benign strictures or malignancy of the head of the pancreas.
51
Causes of Primary sclerosing cholangitis
Generally unknown.
Possibly genetic, lymphocyte recruitment, portal bacteraemia and bile salt toxicity.
Secondary: Can be secondary to infection, thrombosis or iatrogenic/trauma
52
Diagnostic tests for Cholangitis
FBC: Raised CRP (and ESR?) LFT: Raised ALP, AST, ALT
Ultrasound: Detect stone/stent/stricture
Blood culture: (if septic)
ERCP: Definitive.
Culturing and can remove blockage.
53
Diagnostic tests for Primary sclerosing cholangitis
Ultrasound: May show bile duct dilatation (not diagnostic)
ERCP: Can help, but invasive.
LFT: elevated ALP or GGT.
Serum transaminase levels can be normal to several times normal.
Serum albumin drops with progression.
54
Treatment of Cholangitis
Fluid resuscitation.
Antibiotic therapy.
Clear obstruction with ERCP.
55
Treatment of Primary sclerosing cholangitis
Usually manage symptoms of liver failure (eventual liver transplant).
ERCP can dilate some extra-hepatic strictures to slow progression.
High dose ursodeoxycholic acid can slow progression.
56
Complications of Cholangitis
Can lead to sepsis.
57
Complications of Primary sclerosing cholangitis
Eventual liver failure.
58
Sequelae of Primary sclerosing cholangitis
15% get cholangiocarcinoma.
59
Define Achalasia
Oesophageal aperistalsis
and failure of LOS to relax impairs oesophageal emptying.
60
Define Systemic Sclerosis (Scleroderma) (SSc)
Multisystem autoimmune disease.
Increased fibroblast activity
-> abnormal growth of connective tissue.
61
Types of Systemic Sclerosis (Scleroderma) (SSc)
Limited cutaneous (CREST syndrome).
Diffuse cutaneous.
62
How does Achalasia clinically present?
Onset at any age.
Long Hx of dysphagia for solids and liquids.
Retrosternal chest pain (not cardiac).
Weight loss.
63
How does limited cutaneous (CREST syndrome) - (type of Systemic Sclerosis (Scleroderma) (SSc)) clinically present?
Raynaud's phenomenon.
Skin hardening in hands or face.
MSK: Joint pain and swelling.
CREST: Calcinosis Raynaud's Esophageal dysmotility Sclerodactyly and Telangiectasia
64
How does Diffuse cutaneous - (type of Systemic Sclerosis (Scleroderma) (SSc)) clinically present?
As above (limited cutaneous (CREST syndrome) but more rapid and widespread onset in diffuse.
GI symptoms: Heartburn, reflux oesophagitis.
Delayed gastric emptying.
Pulmonary: Pulmonary fibrosis.
Pulmonary arterial hypertension.
65
Limited cutaneous (CREST syndrome) - (type of Systemic Sclerosis (Scleroderma) (SSc)) - note
70% of SSc.
Affects face, forearms and lower legs up to the knee.
66
Diffuse cutaneous - (type of Systemic Sclerosis (Scleroderma) (SSc)) - note
30% of SSc.
Also affects upper arms, thighs or trunk.
67
Cause of Achalasia
Unknown.
68
Cause of Systemic Sclerosis (Scleroderma) (SSc)
Uknown.
Likely a genetic component.
69
Diagnostic tests for Achalasia
Barium swallow: Aperistalsis and 'beak deformity' (oesophagus tapering to a point)
Oesophageal manometry: Demonstrates aperistalsis and failure of LOS to relax on swallowing.
70
Diagnostic test for Systemic Sclerosis (Scleroderma) (SSc)
Antinuclear antibodies: Positive in 90% but not specific.
71
Treatment of Achalasia
No cure.
Treat symptoms.
Surgical division of LOS and endoscopic balloon dilatation.
Nitrates where surgery is not an option.
Botox: Best for elderly (who can't do surgery).
72
Treatment of Systemic Sclerosis (Scleroderma) (SSc)
No cure.
Treat symptoms.
73
Complications of Achalasia
Untreated
-> Inhalation of material in oesophagus
-> choking.
74
Complications of Systemic Sclerosis (Scleroderma) (SSc)
Malnutrition due to swallowing problems.
Obstruction in GI tract due to reduced motility.
75
Sequelae of Achalasia
Oesophageal cancer.
76
Define Coeliac disease
Immune mediated inflammatory condition provoked by gluten.
77
Define Ulcerative colitis
Continuous chronic inflammation of only the colon.
78
Define Crohn's disease
Intermittent chronic inflammation of the entire GI tract.
79
How does Coeliac disease clinically present?
Range of possible symptoms, with onset at any age (two peaks; infancy and 5th decade).
Persistent GI symptoms.
Faltering growth.
Prolonged fatigue.
Unexplained weight loss.
Severe mouth ulcers.
Iron, B12 or folate deficiency (anaemia).
IBS.
FH of Coeliac.
80
How does Ulcerative colitis clinically present?
Recurrent diarrhoea, often with blood and mucus.
Some extragastrointestinal manifestations: arthralgia,
fatty liver,
and gall stones.
81
How does Crohn's disease - clinically present?
Symptoms depend on the region affected.
Small bowel: Weight loss, abdominal pain.
Terminal ileum: Right iliac fossa pain mimicking appendicitis.
Colonic: Blood and mucus with diarrhoea, with pain.
82
What does DQ stand for?
DQ: "Dietary query"
83
What aids ulcerative colitis?
Smoking protects.
84
How does smoking impact Crohn's?
Smoking damages.
85
Cause of Coeliac disease
Strong genetic association with HLA DQ2 and DQ8.
Attacks caused by the presence of gluten in the diet.
86
Cause of inflammatory bowel disease - Ulcerative colitis & Crohn's disease
Genetics: Mild genetic link (Strong in Crohn's).
Environmental: Stress and depression -> attacks.
Immune response: Effector T cells predominating over regulatory T cells
-> Pro-inflammatory cytokines (IL12, IL5, IL17 and interferon gamma)
-> Stimulate macrophages to produce Tumour Necrosis Factor Alpha, IL-1 and IL-6.
Neutrophils, mast cells and eosinophils are also activated.
All this causes a wide variety of inflammatory mediators -> Cell damage
87
Diagnostic test for Coeliac disease
Serology: IgA tissue transglutaminase antibodies have a very high sensitivity and specificity for Coeliacs.
Also endomysial antibodies.
Then, Distal Duodenal Biopsy: Histological changes.
88
Diagnostic test for inflammatory bowel disease - Ulcerative colitis & Crohn's disease
Seek to distinguish between the two.
Sigmoidoscopy/rectal biopsy
89
Treatment of Coeliac disease
Gluten free diet.
Nutrituonal supplement as required.
90
Treatment of Ulcerative colitis
5-Aminosalicylic acid (mesalazine) - Drug of choice for remission and relapse prevention.
Surgical resection.
91
Treatment of Crohn's disease
Stop smoking.
Corticosteroids induce remission (but don't prevent relapse).
Thiopurines maintain remission (but have side effects)
Azathioprine.
92
Complications of Coeliac disease
Increased incidence of malignancy, reduced by gluten-free.
93
Complications of Ulcerative colitis
Psychosocial and sexual problems.
Frequent relapse.
94
Complications of Crohn's disease
Bowel obstructions from strictures.
May cause short stature in children.
95
Sequelae of Ulcerative colitis
Colorectal cancer risk doubled.
96
Sequelae of Crohn's disease
Osteoporosis
97
Define Ischaemic colitis
Lack of blood supply to the colon cause inflammation and injury.
98
Define Mesenteric ischaemia
Lack of blood supply to the colon.
99
Types of Mesenteric ischaemia
Acute.
Chronic.
100
How does Ischaemic colitis clinically present?
Abdominal pain and rectal bleeding.
Occasionally shock.
101
How does acute mesenteric ischaemia clinically present?
Moderate-severe- colicky/constant poorly localised pain,
out of proportional to physical findings.
102
How does chronic mesenteric ischaemia clinically present?
Moderate-severe- colicky/constant poorly localised post-prandial pain,
out of proportional to physical findings.
Fear of eating, nausea, vomiting or bowel irreguarity
103
What does mesenteric ischaemia refer to?
Umbrella term,
including embolus/thrombus,
non-occlusive mesenteric ischaemia.
104
Chronic mesenteric ischaemia refers to which arteries?
Can be all three major mesenteric arteries.
105
Cause of Ischaemic colitis
Usually underlying atherosclerosis and vessel occlusion.
106
Causes of Acute mesenteric ischaemia
Arterial thrombosis/embolus,
aortic dissection,
107
Cause of Chronic mesenteric ischaemia
Usually atherosclerosis.
108
Diagnostic test for Ischaemic colitis
Sigmoidoscopy shows normal, with some blood.
109
Diagnostic test for Acute mesenteric ischaemia
Angiography: Shows arterial blockage
110
Diagnostic test for Chronic mesenteric ischaemia
Ultrasound,
arteriography
111
Treatment of Ischaemic colitis
Treat symptoms.
Possible anticoagulants.
Surgery may be required for gangrene, perforation or stricture formation.
112
Treatment of Acute mesenteric ischaemia
Initial resuscitation with IV.
Surgical: Angioplasty, embolectomy.
113
Treatment of Chronic mesenteric ischaemia
Surgical intervention.
Medical: In surgical contraindicated.
Nitrates and anticoagulant.
114
Complications of Ischaemic colitis
Gangrene,
perforation
or stricture formation.
115
Complications of Acute mesenteric ischaemia
Poor outcome;
with treatment 50-80% mortality.
116
Complications of Chronic mesenteric ischaemia
Colitis.
117
Define Haemorrhoids (Piles)
Enlarged vascular mucosal cushions in the anal canal
118
Define Anorectal abscess
Collection of pus in the anal or rectal region.
119
Types of Haemorrhoids (Piles)
Internal: Above dentate line.
External: Below dentate line.
120
How do internal haemorrhoids clinically present?
Painless unless strangulated (upper anal canal has no pain fibres)
1st degree: Do not prolapse.
2nd degree: Prolapse on straining, spontaneous reduction
3rd degree: Prolapse on straining, manual reduction
4th degree: Permanently prolapse, no reduction.
121
How do external haemorrhoids clinically present?
Painful and itchy.
Visible on external examination.
Can coexist with the above.
122
How does an anorectal abscess clinically present?
Painful, hardened tissue in the perianal area,
discharge of pus from the rectum,
a lump or nodule,
tenderness,
fever,
constipation.
123
Cause of Haemorrhoids (Piles)
Unknown.
Risk factors:
Constipation,
prolonged straining,
increased abdominal pressure (ascites),
heavy lifting.
124
Cause of an anorectal abscess
Infection of an anal fissure.
125
Epidemiology of Haemorrhoids (Piles)
Prevalence between 4% and 34%.
126
Diagnostic test for Haemorrhoids (Piles)
DRE: Internal won't be palpable.
Proctoscopy
127
Diagnostic test for an anorectal abscess
DRE.
128
Treatment of Haemorrhoids (Piles)
Increase fluid and fibre.
Pain relief.
Intervention: Rubber band ligation (tie a band around it and necrotise it)
Surgical: Haemorrhoidectomy.
129
Treatment of an anorectal abscess
Surgical drainage.
Pain refief.
130
Complications of Haemorrhoids (Piles)
Skin tags.
If internal strangulated;
ischaemia -> gangrene.
131
Complications of an anorectal abscess
Fistula in ano: Approx. 40% lead to this.
A chronic, abnormal communication between the epithelialised surface of the anal canal and the perianal skin.
132
Define Fissure-in-ano
Tear in the mucosa of the anal canal.
133
Define Pilonidal sinus
Obstruction of natural hair follicles above the anus.
134
Types of Fissure-in-ano
Primary: No apparent cause.
Secondary: Due to underlying condition.
135
How does Fissure-in-ano clinically present?
Pain on defecation.
Bright red bood on defecation.
136
How does Pilonidal sinus clinically present?
Small hole about 6cm above the anus.
Usually no symptoms until infected; then a pus fuilled abscess.
Infection can cause pain, redness and swelling.
137
Cause of Fissure-in-ano
Constipation: A hard stool tears the anal mucosa
IBD: Ulceration as part of inflammation.
Rectal malignancy.
138
Cause of Pilonidal sinus
Congenital.
139
Diagnostic test for Fissure-in-ano
Clinical.
140
Diagnostic test for Pilonidal sinus
Diagnose by observation.
141
Treatment of Fissure-in-ano
Simple pain relief.
Warm baths.
142
Treatment of Pilonidal sinus
Asymptomatic: Keep clean through hygiene.
Shave hair around area
Infected: Consider excision of the sinus tract and closure.
Skin flaps can be used to cover the defect.
143
Complications of Fissure-in-ano
Depends on underlying pathology.
Possible anorectal abscess.
144
Complications of Pilonidal sinus
Infection.
145
Sequelae of Fissue-in-ano
Recurrence.
146
Define irritable bowel syndrome
Relapsing functional bowel disorder associated with a change in bowel habit
-> No organic cause found.
147
Define diverticular disease
Pouches of mucosa extrude through the colonicmuscular wall to form diverticula.
148
Define appendicitis
Inflammation of the appendix.
149
Types of irritable bowel syndrome
Hard,
soft
and mixed stool.
150
How does irritable bowel syndrome clinically present?
Crampy abdominal pain relieved by defecation or wind,
altered bowel habit,
sensation of incomplete evacuation (tenesmus),
abdominal bloating and distension.
151
How does diverticular disease clinically present?
Asymptomatic in 95% of cases.
Symptoms that do occur relate to luminal narrowing;
pain, constipation, bleeding or diverticulitis.
Severe cases; left iliac fossa pain, fever, nausea.
152
How does appendicitis clinically present?
Pain: umbilicus -> right iliac fossa, tender with guarding
General: Nausea, localised tenderness,
diarrhoea/constipation, pyrexia
153
Pathophysiology of irritable bowel syndrome
Broadly unknown.
No organic cause can be found.
154
Cause of irritable bowel syndrome
No structural lesion.
Broadly unknown.
Associated with psychological stress.
155
Cause of diverticular disease
Unknown.
Related to a low fibre diet
-> Increased intracolonic pressure
-> herniation at sites of weakness?
156
Cause of appendicitis
Formation of a faecolith (hard discreet mass of inspissated faeces) that obstructs the lumen of the appendix.
157
Diagnostic test for irritable bowel syndrome
NOT a diagnosis of exclusion.
Coeliac screen.
158
Diagnostic test for diverticular disease
CT scan.
Possibly ultrasound.
159
Diagnostic test for appendicitis
Inflammation markers (CRP, ESR, white cell count) raised but not specific.
CT is gold standard.
160
Treatment of irritable bowel syndrome
Regular meals.
Lots of fluids.
Fibre depends on type; more with diarrhoea less with constipation.
Placebo has strong effect.
161
Treatment of diverticular disease
Antibiotics.
Rarely; surgery for frequent attacks or complications.
162
Treatment of appendicitis
Surgical removal, open or laparoscopically.
Appendix mass can be treated with IV fluids and antibiotics,
and later appendectomy.
163
Complications of diverticular disease
Perforation,
fistula formation with bladder or vagina,
intestinal obstruction.
Bleeding can be massive.
164
Complications of appendicitis
Peritonitis.
Appendix abscess.
165
Sequelae of diverticular disease
Recurrence.
166
Define pancreatitis
Inflammation of the pancreas
167
Types of pancreatitis
Acute
Chronic
168
How does acute pancreatitis clinically present?
Epigastric or upper abdominal pain radiating through to the back.
Nausea and vomiting.
Coma and multiple organ failure are possible, and may delay diagnosis.
Ecchymoses around umbilicus or in flanks suggeset necrotising.
169
How does chronic pancreatitis clinically present?
Severe epigastric abdominal pain radiating through to the back.
Severe weight loss possible.
Diabetes and steatorrhoea (due to insulin and liapse deficiency).
Jaundice possible (due to obstruction of the CBD).
170
How is chronic pancreatitis subtyped?
Subtyped into large and small duct pancreatitis, based on the duct affected.
Small tends not to be associated with calcification.
171
Causes of acute pancreatitis (think acronym!)
Gallbladder disease and excess alcohol consumption.
I GET SMASHED:
Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Autoimmune
Scorpion Stings
Hyperlipidaemia
ERCP (Endoscopic retrograde cholangio pancreatography).
Drugs
172
Causes of chronic pancreatitis
Typically excess alcohol consumption.
Also possibly hereditary,
autoimmune
or as a complication of cystic fibrosis.
173
Diagnostic test for acute pancreatitis
Serum amylase: 3x more than normal.
Lipase levels rising more sensitive.
174
Diagnostic test for chronic pancreatitis
Xray/CT: Displays calcification (not valid in small duct).
Secretin stimulation test: Detects if pancreatic exocrine function is damaged.
175
Treatment of acute pancreatitis
Mild: Pain relief, IV fluids
Severe: IV antibiotics if necrotising, feed with enteral nutrition.
Monitor for complications.
176
Treatment of chronic pancreatitis
Pain relief.
Cessate alcohol.
Replace pancreatic enzymes (aids functionality and pain by down regulating release of pancreatic enzymes)
Surgery: Local resection to aleviate duct dilatation/duct stones.
177
Complications of acute pancreatitis
Pancreatic necrosis.
Pancreatic ascites.
Pancreatic abscess (may require surgery).
178
Complications of chronic pancreatitis
Diabetes.
179
Sequelae of acute pancreatitis
Recurrence.
180
Sequelae of chronic pancreatitis
Pancreatic carcinoma.
181
Define Cholangiocarcinoma
Cancer of the biliary tree (in or out of liver).
182
Define gallstones
Stones block the biliary tract.
183
Types of gallstones
Cholesterol
Pigment
184
How does cholangiocarcinoma clinically present?
Fever,
malaise,
weight loss.
Right upper quadrant pain, jaunce (early).
Hepatomegaly, ascites.
185
How do gallstones clinically present?
70% of stones are asymptomatic at the time of diagnosis.
Of symptomatics, most common is Biliary Colic (Right upper quadrant, sudden, nausea and vomiting),
caused by a gallstone impacting on the cystic duct or the ampulla of vater.
Second most common;
acute cholecystitis,
where distension of the GB -> necrosis and ischaemia.
186
Cause of cholangiocarcinoma
Caused by flukes,
primary sclerosing cholangitis,
HBV,
HCV,
DM,
Caroli's.
187
Cause of cholesterol gallstones
Multifactorial.
Cholesterol supersaturation,
nucleation factors
and reduced gallbladder motility
188
Causes of pigment gallstones
Chronic haemlysis (sphereocytosis and sickle cell),
in which bilirubin production is increased.
Also cirrhosis.
Possible as complication of cholecystectomy and with duct strictures.
189
Diagnostic test for cholangiocarcinoma
Contrast MRI: optimal imaging for diagnosis
ECRP: can obtain samples for biopsy.
190
Diagnostic test for gallstones
Ultrasound.
191
Treatment of cholangiocarcinoma
Complete surgical resection.
Stent (or surgical bypass) to relieve symptoms.
192
Treatment of gallstones
Nonsurgical: Pain relief.
IV antibiotics if necessary
Surgical: Laparoscopic cholecystectomy.
193
Complications of gallstones
Jaundice: if biliary obstruction
Acute cholecystitis: Cystic duct impaction
Pancreatitis: Blocks pancreatic duct
Gallstone ileus: Occludes intestinal lumen
Empyema: Obstructed GB fills with pus
Cholangitis: Inflammation of the gallbladder as a result of bile duct blockage
194
Define hepatitis
Inflammation of the liver as a result of direct viral infection.
195
Types of hepatitis
Hepatitis A, B, C
196
How does Hep A clinically present?
Incubation period of 28 days.
Nausea, anorexia and distaste for cigarettes.
After 2 weeks, jaundice, with dark urine and pale stool.
Sometimes hepatomegaly.
197
How does Hep B clinically present?
Flu-like symptoms.
Fever.
Jaundice in 10% of younger, and 50% of adults.
198
How does Hep C clinically present?
Incubation period of 6-9 weeks.
Often asymptomatic in acute infection.
Chronic infection may present with malaise, weakness and anorexia.
199
How is Hep A spread?
Spread by faecal-oral route.
Associated with shellfish.
200
How is Hep B spread?
Parenteral route.
Infected blood or bodily fluids.
Mostly intercourse, or vertical transmission.
201
How is Hep C spread?
Blood borne.
Mostly transmitted by poorly sterilised instruments/shared needles.
202
Diagnostic test for Hep A
Blood: ALT rises
IgM: Antibody to HAV.
203
Diagnostic test for Hep B
Blood: ALT rises.
HBsAg,
HBcAb,
HBsAb,
IgM HBcAb.
204
Diagnostic test for Hep C
Liver enzymes: rise.
Antibodies to HCV.
205
Treatment of Hep A
Prevention: Vaccine.
Treatment: Treat symptoms.
Avoid alcohol.
206
Treatment of Hep B
Avoid unprotected sex and alcohol.
Treatment: treat symptoms.
Fulminant hepatitis: Antivirals.
207
Treatment of Hep C
Antivirals: Weekly subcut peginterferon alfa-2a and daily oral ribavirin
Information: Advice on not sharing needles
208
Complications of Hep A
Fulminant hepatic failure (rare).
209
Complications of Hep B
Liver failure.
210
Complications of Hep C
Hepatocellular carcinoma (if cirrhosis was found).
211
Define alcoholic liver disease
Chronic liver disease caused by excess of alcohol.
212
Define liver failure
Loss of the liver's ability to regenerate or repair.
213
Types of liver failure
Fulminant hepatic failure.
Late-onset hepatic failure.
Chronic decompensated hepatic failure.
214
How does alcoholic liver disease clinically present?
Fatty liver: Usually no symptoms.
Possible hepatomegaly on examination.
Alcoholic hepatitis: Rapid onset jaundice.
Nauesea, anorexia, enecphalopathy, fever and ascites.
Alcoholic cirrhosis: May be asymptomatic.
Usually present with complications of cirrhosis.
Spider naevei are a classic.
215
How does liver failure clinically present?
Hepatic encephalopathy, abnormal bleeding, ascites, jaundice.
Mental state shows drowsiness and confusion, due to cerebral oedema.
216
When does fulminant hepatic failure occur?
Within 8 weeks of onset of underlying illness.
217
When does late-onset hepatic failure occur?
8-26 week since onset of underlying illness.
218
What is the latent period for chronic dgcompensated hepatic failure?
>6 months
219
What are the 3 main pathological lesions with ALD?
Fatty liver, hepatitis and cirrhosis.
220
Causes of alcoholic liver disease
Excessive consumption of alcohol.
Exact mechanism is unknown, beyond identifying alcohol as a hepatoxin.
Some genetic predisposition.
221
Causes of liver failure
Various.
Toxins: Alcohol, paracetamol poisoning
Infections: Viral hepatitis, Epstein-Barr virus, CMV
Neoplastic: Hepatocellular carcinoma
Metabolic: Wilson's, A1AT deficiency, Haemochromatosis
Others: Acute fatty liver of pregnancy, ischaemia, autoimmune liver disease
222
Epidemiology of alcoholic liver disease
Most common cause of chronic liver disease in western world.
Usually presents in men in 40-50s.
223
Epidemiology of liver failure
(what is the most common cause in acute?)
1/100,000.
Paracetamol poisoning most common cause in acute.
224
Diagnostic test for alcoholic liver disease
Liver biochem: AST and ALT rise (disproportionately AST)
Bloods: Elevated MCV.
225
Diagnostic test for liver failure
Raised bilirubin.
Glucose low (no glucogenesis).
226
Treatment of alcoholic liver disease
Lifelong abstinence from alcohol.
Corticosteroids to control inflammation if there is no renal failure.
227
Treatment of liver failure
Liver transplantation in severe cases.
228
Complications of alcoholic liver disease
Untreated: Liver failure.
229
Complications of liver failure
Infection.
Haemorrhage.
230
Define Hepatocellular carcinoma
Cancer of the hepatocyte.
231
Define Haemochromatosis
Deficiency of the iron regulatory hormone hepcidin
-> Iron overload.
232
Define Wilson's Disease
Disorder of copper metabolism
-> Copper build up in the liver.
233
Types of haemochromatosis
HFE mutations:
C282Y and H63D.
234
How does Hepatocellular carcinoma clinically present?
Fever, malaise, weight loss.
Right upper quadrant pain, jaunce (late).
Hepatomegaly, ascites.
235
How does haemochromatosis clinically present?
Often asymptomatic until later stages.
Usually presents between 40-60.
Fatigue, weakness, arthopathy, heart problems.
Advanced disease: Bronzing of the skin, diabetes, hepatomegaly, arthropathy.
236
How does Wilson's disease clinically present?
Difficult to diagnose.
Onset usually in 20-30s.
Hepatic: Acute liver failure. Chronic hepatitis.
Psychological: Behavioural problems common, might lead to diagnosis.
Eyes: Kayser-Fleischer ring (bronze ring on the cornea), usually on examination with a slit lamp.
Also sunflower cataracts, also with slit lamp.
237
Cause of Hepatocellular carcinoma
Hepatitis B and C,
aflatoxin, alcohol,
haemochromatosis,
cirrhosis and anabolic steroids.
238
Cause of haemochromatosis
Often hereditary in autosomal recessive pattern of HFE gene (responsible for regulating iron uptake).
Can not be genetic or not be associated with HFE, but rarely.
239
Cause of Wilson's Disease
Mutation in ATP7B; over 500 identified.
Autosomal recessive.
240
Diagnostic test for Hepatocellular carcinoma
CT and biopsy.
241
Diagnostic test for haemochromatosis
Screening not advised; penetrance very low.
Consider genetic analysis in unexplained chronic liver disease.
Total Iron Binding capacity reduced, serum iron raised.
LFTs can be normal.
242
Diagnostic test for Wilson's Disease
Slit lamp analysis of eyes to detect Kayser-Fleischer rings.
Low serum caeruloplasmin.
243
Treatment of Hepatocellular carcinoma
Surgery to resect individual tumours.
Liver transplant if multiple.
244
Treatment of haemochromatosis
Phlebotomy; removing 400-500ml of blood every 2 weeks.
Tends to require insulin.
245
Treatment of Wilson's Disease
Avoid alcohol.
Prevent intestinal copper absorption: Chelation agents such as Zinc (lifelong).
Hepatic: About 5% of patients who presented with liver failure will need a transplant.
Neuro: Deep brain stimulation.
246
Complications of haemochromatosis
Liver fibrosis, failure, cirrhosis and hepatocellular carcinoma.
Diabetes in there is deposition in the pancreas.
247
Complications of Wilson's Disease
Cirrhosis -> Liver failure.
Fatal if untreated.
248
Define Alpha-1-antitrypsin deficiency
Deficiency of serine protease inhibitor alpha-1-antitrypsin.
249
Define Volvulus
Complete twisting of a loop of intestine around its mesenteric attachment site.
250
Define Midgut malrotation
Twisting of the entire midgut about the axis of the superior mesenteric artery.
251
Types of volvulus
Stomach,
small intestine,
caecum,
transverse colon
and sigmoid colon.
252
How does Alpha-1-antitrypsin deficiency clinically present?
Lung: presents between 30-50 (smokers earlier).
COPD like symptoms, early onset emphysema.
Liver: Not always present.
Neonates may present jaundice and hepatitis.
Possibly cirrhosis and liver failure.
253
How does Volvulus clinically present?
Rapid onset and bilious vomiting.
Possible palpable abdominal mass.
Ischaemia can lead to acute abdomen pain, abdominal distension and peritonitis.
Blood may pass per rectum.
254
How does Midgut malrotation clinically present?
Can be asymptomatic.
Intermittent intestinal obstruction.
If a volvulus develops, the obstruction will be complete.
Bilious vomiting (green/yellow vomit).
Failure to thrive, anorexia, constipation and bloody stool.
Older children: Recurrent abdominal pain, cyclical vomiting.
255
Cause of Alpha-1-antitrypsin deficiency
Mutation in the SERPINA1 gene.
Autosomal recessive.
Relatively low penetrance.
Many possible mutations.
256
Cause of a Volvulus
Tends to develop in long-standing constipation with large,
elongated, relatively atonic colon (particularly in sigmoid).
257
Cause of Midgut malrotation
Congenital.
At the fourth week of gestation, the GI tract is a straight tube in the abdomen.
In the next 8 weeks, the midgut rotates and becomes fixed to the posterior abdominal wall.
Arrest of development at any stage narrows the mesenteric base and impairs fixation.
This creates high risk of volvulus.
258
Epidemiology of Volvulus
More common in the elderly.
Rare in infants and children (when not associated with a malrotation).
259
Epidemiology of Midgut malrotation
1/500 live births.
90% are diagnosed within the first year of life.
260
Diagnostic test for Alpha-1-antitrypsin deficiency
Serum levels of A1AT.
261
Diagnostic test for Volvulus
Plain abdominal X ray.
262
Diagnostic test for Midgut malrotation
Contrast studies:
Duodenojejunal junction is misplaced; either at or to the right of the midline.
263
Treatment of Alpha-1-antitrypsin deficiency
Lung: As COPD; cessate smoking, corticosteroids, bronchodilators, treat infection.
Liver: Cessate drinking. In liver failure, possibly transplant.
264
Treatment of Voluvulus
(Sigmoid) Decompression: Sigmoidoscope is passed into the loop, and a flatus tube alongside it.
This produces a rush of liquid faeces and flatus and relief.
Surgery: Resection may be required in frequent recurrence.
265
Treatment of Midgut malrotation
Surgery: Volvulus is a devastating complication, so corrected even in asymptomatic.
266
Complications of Alpha-1-antitrypsin deficiency
Variable prognosis.
Untreated -> Liver failure.
267
Complications of Volvulus
Recurrence.
If untreated: Perforation and faecal peritonitis (life-threatening).
268
Complications of Midgut malrotation
Volvulus can develop,
leading to complete bowel obstruction,
and potentially a rupture -> Life-threatening peritonitis.
269
Define Intestinal obstruction
Passage through the intestine is obstructed.
270
Types of Intestinal obstruction
Mechanical.
Functional ('ileus').
271
How does mechanical intestinal obstruction clinically present?
Colicky abdominal pain,
associated with vomiting (earlier with small bowel)
and absolute constipation (earlier with large bowel).
Distension and tinkling bowel sounds.
272
How does functional intestinal obstruction clinically present?
Pain often not present, and bowel sounds reduced.
Constipation and vomiting.
273
How can you subdivide mechanical intestinal obstruction?
Subdivides into small and large bowel obstruction depending on the location of the blockage.
274
Pathophysiology of mechanical intestinal obstruction
Depending on the aetiology,
a physical factor is preventing the movement of contents of the intestine through the tract.
This then causes backing up of the GI tract and an inability to empty
-> vomiting and constipation.
275
Pathophysiology of functional intestinal obstruction
Bowel ceases to function and there is no peristalsis.
This causes impaction since contents no longer move along the intestine.
276
Cause of mechanical intestinal obstruction
Small: Adhesions, strangulated hernia or volvulus.
Possible malignancy.
Most commonly: intra-abdominal adhesions from operations.
Intussusception.
Large: Most often colorectal malignancies.
277
Cause of functional intestinal obstruction
Most often post-operative to peritonitis, or any major abdominal surgery.
Associated with opiate treatment.
Possible; nerves or muscles are damaged.
278
Epidemiology of mechanical intestinal obstruction
Small more common.
279
Diagnostic test for mechanical intestinal obstruction
Abdo X-ray.
280
Diagnostic test for functional intestinal obstruction
Xray: Gas seen throughout the bowel.
281
Treatment of mechanical intestinal obstruction
Conservative; fluid replacement and intestinal decompression.
Surgery: Resection possible, usually done in large bowel.
If as a result of malignancy: Corticosteroids, opioids and anti-emetics.
282
Treatment of functional intestinal obstruction
Conservative; fluid replacement and intestinal decompression.
283
Complications of mechanical intestinal obstruction
Carcinoma that causes obstruction is usually already advanced and metastatic.
284
Define Oesophageal cancer
Cancer of the oesophagus.
285
Define Gastric cancer
Cancer of the stomach.
286
Types of oesophageal cancer
Squamous.
Adenocarcinoma.
287
How does Oesophageal cancer clinically present?
Early: No symptoms
Late: Dysphagia,
weight loss,
heartburn,
haematemesis.
Hoarse voice.
288
How does Gastric cancer clinically present?
Nonspecific: Dyspepsia, weight loss, vomiting, dysphagia and anaemia.
Signs: Epigastric mass, hepatomegaly, jaundice, Troisier's sign (enlarged left supraclavicular node (Virchow's node)).
289
How does Colorectal cancer (CRC) clinically present?
Most are left side of colon: rectal bleeding, increasing symptoms of intestinal obstruction (bowel habit, colicky pain).
Right side + ceacum: iron deficiency anaemia, mass in right iliac fossa.
Non-specific symptoms.
290
Pathophysiology of squamous oesophageal cancer
Tends to be locatated in the proximal 2/3rds of the oesophagus.
Can locally cause pressure recurrent laryngeal nerve.
291
Pathophysiology of adenocarcinoma (oesophageal cancer)
Tends to be located in the distal 1/3rd of the oesophagus.
Can locally cause pressure recurrent laryngeal nerve.
292
Pathophysiology of gastric cancer
90% are adenocarcinomas.
Most involve the pylorus.
293
Pathophysiology of colorectal cancer (CRC)
Adenomatous polyps develop over time, though benign they can become malignant through activation of oncogenes and inactivation of tumour suppressor genes.
>no. of polyps >chance of malignancy.
5% due to genetic syndromes:
HNPCC: accelerated progression of adenoma to CRC, >50% develop CRC after 40.
FAP: APC gene,
>100 polyps develop in teenage years,
100% lifetime risk of CRC.
(Both have increased risk of extracolonic malignancy).
294
Cause of squamous oesophageal cancer
Smoking,
alcohol,
nitrous amines (barbeque food, tobacco).
295
Cause of adenocarcinoma (oesophageal cancer)
Barrett's oesophagus,
obesity.
296
Cause of gastric cancer
H. pylori can double the risk.
Smoking is a risk factor.
Gastritis and pernicious anaemia.
297
Cause of colorectal cancer (CRC)
Age,
family history,
western diet.
298
Epidemiology of adenocarcinoma (oesophageal cancer)
Obese people.
299
Epidemiology of colorectal cancer (CRC)
Mean diagnosis age 60-65.
3rd most common, 2nd biggest killer cancer.
300
Diagnostic test for oesophageal cancers
Oesophagoscopy with biopsy.
CT/MRI to stage cancer.
301
Diagnostic test for gastric cancer
Gastroscopy with biopsy.
CT/MRI to stage cancer.
302
Diagnostic test for colorectal cancer (CRC)
DRE, colonoscopy with biopsy.
Faecal occult blood test for screening only.
303
Treatment of oesophageal cancers
Oesophagectomy with perioperative chemo.
304
Treatment of gastric cancer
Gastrectomy (partial or total) with perioperative chemo.
305
Treatment of colorectal cancer (CRC)
Surgery, ideally with end to end anastomosis, alt. colostomy.
Adjuvant chemo.
Palliation.
306
Complications of colorectal cancer (CRC)
Local invasion and distant metastases, often liver and lung.
