Gastroenterology Flashcards
(401 cards)
1
Q
What characterises ischaemic hepatitis?
A
- Marked elevation in AST and ALT, peaks 1-3 days after insult (usually 1000s).
- Rise in lactate dehydrogenase.
2
Q
What are differentials of AST and ALT values >1000?
A
Ischaemic heptatitis
Acute viral hepatitis
Drug-induced hepatitis
3
Q
How can one differentiate between autoimmune and ischaemic hepatitis from LFTs?
A
AST and ALT elevation are not as elevated (<250U/L) in autoimmune hepatitis.
4
Q
How does ischaemic hepatitis occur?
A
Following instances of acute hepatic hypoperfusion (fall in blood flow from both hepatic artery and portal venous system).
5
Q
What are the vessels responsible for hepatic oxygenation
A
Hepatic artery
Portal venous system
6
Q
When should acute hepatitis B infection be suspected?
A
If risk factors present: IV drug use, history of risky sexual practices, jaundice
7
Q
Are peripheries warm or cold in sepsis and septic shock?
A
Sepsis = warm
Septic shock = cold
8
Q
What does workup of acute liver injury include following LFTs?
A
Additional bloods (viral serology included)
Paracetamol levels
Autoantibodies
9
Q
When should hepatocellular carcinoma be suspected?
A
Mild-moderate AST or ALT derangement (<250U/L), if obstructing the intra/extrahepatic biliary tree or if preceded by cirrhosis
10
Q
What is ischaemic hepatitis (‘shock liver’)?
A
Diffuse hepatic injury from acute hypoperfusion
NOT INFLAMMATORY
11
Q
How is ischaemic hepatitis diagnosed?
A
In the presence of an inciting event and marked increases in aminotransferase levels (50x upper limit ofo normal)
12
Q
What doe ischaemic hepatitis present with?
A
AKI (tubular necrosis) or other end-organ dysfunction
13
Q
Is ischaemic hepatitis an inflammatory process?
A
No
14
Q
What is the pattern of acute travellers diarrhoea?
A
Diarrhoea, abdominal cramps, nausea following recent travel
15
Q
What is the most probable organism causing acute travellers diarrhoea?
A
Enterotoxigenic E. coli
16
Q
What are chronic causes of diarrhoea?
A
Irritable bowel syndrome (EXTREMELY COMMON CAUSE)
Crohn’s disease
Ulcerative colitis
Colorectal cancer
Coeliac disease
17
Q
What symptoms are associated with Campylobacter jejuni infection?
A
Bloody stools
Abdominal pain
18
Q
What presentation is typical of Clostridium difficile infection?
A
Profuse diarrhoea
Typically follows hospital stay or course of antibiotics
19
Q
What is the WHO definition of diarrhoea?
A
> 3 loose or watery stools per day
20
Q
What is the WHO classification of acute vs. chronic diarrhoea?
A
Acute: <14 days
Chronic: >14 days
21
Q
What are acute causes of diarrhoea?
A
Gastroenteritis
Diverticulitis
Antibiotic therapy
Constipation causing overflow
22
Q
What are other conditions associated with diarrhoea?
A
Thyrotoxicosis
Laxative abuse
Appendicitis
Radiation enteritis
23
Q
What are the features of IBS?
A
Most consistent:
- Abdominal pain
- Bloating
- Change in bowel habits
Additional: lethargy, nausea, backache, bladder symptoms
24
Q
How can patients with IBS be divided?
A
Diarrhoea-predominant IBS
Constipiation-predominant IBS
25
What are features of ulcerative colitis?
Following insidious and intermittent symptoms:
- Bloody diarrhoea
- Crampy abdominal pain
- Weight loss
Additional: faecal urgency, tenesmus
26
What are features of Crohn's disease?
Crampy abdominal pain
Diarrhoea
Additional: malabsorption, mouth ulcers, perianal disease, intestinal obstruction
27
Is bloody diarrhoea more common in Crohn's disease or ulcerative colitis?
More common in Crohn's disease
28
What are features of colorectal cancer?
Symptoms depend on site of lesion
Include diarrhoea, rectal bleeding, anaemia, constitutional symptoms (weight loss, anorexia)
29
What are features of coeliac disease in children?
Failure to thrive, diarrhoea, abdominal distension
30
What are features of coeliac disease in adults?
Lethargy, anaemia, diarrhoea, weight loss
Other autoimmune conditions may coexist
31
What is the appropriate course of action for a patient over 16 with suspected upper GI bleed?
Book endoscopy within 24 hours of hospital admission
32
What is the appropriate course of action for an unstable patient over 16 with severe upper GI bleed?
Immediate endoscopy after resuscitation
33
What are causes of acute upper GI bleeding?
Various conditions, but commonly either oesophageal varices or peptic ulcer disease
34
What are clinical features of acute upper GI bleeding?
Haematemesis - most common
Melena
Raise urea
Features associated with diagnosis
35
How does haematemesis commonly present in acute upper GI bleeding?
Often bright red, but sometimes 'coffee ground'
36
What is melena and how does it commonly present in acute upper GI bleeding?
Passage of altered blood per rectum
Typically black and 'tarry'
37
Why is raised urea sometimes seen in acute upper GI bleeding?
High urea levels can indicate an upper GI bleed versus a lower GI bleed.
This is because when upper GI bleeding occurs, the blood is digested into proteins. These proteins are transported to the liver via the portal vein and metabolized to urea in the urea cycle.
38
What can be used to diffrentiate between upper vs. lower GI bleeding?
Raised urea is sometimes seen in acute upper GI bleeding
39
What are the three broad categories of causes of upper GI bleeds?
Oesophageal
Gastric
Duodenal
40
What are oesophageal causes of upper GI bleeds?
Oesophageal varices
Oesophagitis
Cancer
Mallory-Weiss tear
41
What are gastric causes of upper GI bleeds?
Gastric ulcer
Gastric cancer
Dieulafoy lesion
Diffuse erosive gastritis
42
What are duodenal causes of upper GI bleeds?
Duodenal ulcer
Aorto-enteric fistula
43
What are the presenting features of an upper GI bleed caused by oesophageal varices?
Large volume of fresh blood
Swallowed blood may cause melena
Often assoc. with haemodynamic compromise
May stop spontaneously but re-bleeds are common until managed
44
What are presenting features of an upper GI bleed caused by oesophagitis?
Small volume of fresh blood, often streaking vomit
Melena rare
Often ceases spontaneously
Hx of antecedent GORD type symptoms
45
What are presenting features of an upper GI bleed caused by cancer?
Small volume of blood, except as a preterminal event with erosion of major vessels
Assoc. with dysphagia and constitutional symptoms (weight loss)
May recur until malignancy managed
46
What are presenting features of an upper GI bleed caused by a Mallory-Weiss tear?
Brisk small-moderate volume of bright red blood following a bout of repeated vomiting
Melena rare
Usually ceases spontaneously
47
What are presenting features of an upper GI bleed caused by a gastric ulcer?
Small low volume bleed - tend to present as iron deficiency anaemia
Erosion into significant vessel can produce haemorrhage and haematemesis
48
What are presenting features of an upper GI bleed caused by gastric cancer?
Frank haematemesis or altered blood mixed with vomit
Prodromal features of dyspepsia and maybe constitutional symptoms
Bleeding amount variable, but erosion of major vessel can produce haemorrhage
49
What are presenting features of an upper GI bleed caused by a Dieulafoy lesion?
No prodromal features before haematemesis and melena but maybe considerable haemorrhage and possibly difficult to detect endoscopically
50
What are presenting features of an upper GI bleed caused by diffuse erosive gastritis?
Usually haematemesis and epigastric discomfort
Underlying cause common (e.g. NSAID)
Large volume haemorrhage possible with considerable haemodynamic compromise
51
What are presenting features of an upper GI bleed caused by duodenal ulcer?
Usually posteriorly sited
May erode the gastroduodenal artery
Present with haematemesis, melena, epigastric discomfort
52
How is the pain of a duodenal ulcer different to that of a gastric ulcer?
Often occurs several hours after eating
53
What are presenting features of an upper GI bleed caused by an aorto-enteric fistula?
Rare, but cause of major haemorrhage with high mortality
In patients with previous AAA surgery
54
What are the risk assessments for upper GI bleeds?
Glasgow-Blatchford score
Rockall score
55
What is the Glasgow-Blatchford score used for?
Used at first assesment
Helps clinicians decide whether patients can be managed as outpatients or not
56
What is the Rockall score used for?
Used after endoscopy
Provides % risk of rebleeding and mortality
57
What features are included in the Rockall score?
Age, features of shock, comorbidities, aetiology of bleeding, endoscopic stigmata of recent haemorrhage
58
Patients with a Blatchford score of 0 can be considered for?
Early discharge
59
What are the guidelines for resuscitation in patients with acute upper GI bleeds?
- ABC, wide-bore IV access*2
- Platelet transfusion if actively bleeding platelet count of <50x10^9/L
-FFP if fibrinogen <1g/L
-FFP if PT or APTT > 1.5x normal
- Prothrombin complex concentrate if taking warfarin + active bleeding
60
How are non-variceal bleeds managed?
PPI NOT RECOMMENDED BEFORE ENDOSCOPY
But PPI given to those with non-variceal upper GI bleed and stigmata of recent haemorrhage at endoscopy
If further bleeding, options: repeat endoscopy, interventional radiology, surgery
61
How are variceal bleeds managed?
Terlipressin and prophylactic antibiotics at presentation, before endoscopy
Band ligation used for oesophageal varices
N-butyl-2-cyanoacrylate injection used for gastric varices
Transjugular intrahepatic portosystemic shunts offered if bleed not controlled with boave
62
How are acute flares of ulcerative colitis categorised?
Truelove-Witt index: mild, moderate, severe
- Mild: <4 stools daily, small amt of blood
-Moderate: 4-6 stools daily, varying blood levels, no systemic upset
-Severe: >6 bloody stools daily, systemic upset
63
What are features of a severe flare of ulcerative colitis?
Bowels open >6x/day with blood
Tachycardic, febrile, anaemic, raised inflammatory markers
64
What are features of a severe flare of ulcerative colitis (Truelove and Witts')?
Bowels open >6x/day with blood
Tachycardic (90+bpm), febrile (37.8+), anaemic (<105), ESR > 30mm/h, raised inflammatory markers
65
What is temperature of febrile?
>37.5ºC
66
What is Hb level of anaemia?
Hb <105
67
What levels are inflammatory marker levels are considered 'raised'?
CRP >30
68
How is acute severe ulcerative colitis treated to induce remission?
LIFE-THREATENING, NEEDS IMMEDIATE HOSPITAL ADMISSION
First-line: IV corticosteroids (hydrocortisone or methylprednisolone)
If above contraindicated/declined/intolerated, then IV ciclosporine
If no improvement within 72, consider adding cicloscporin or surgical management
69
What can be used to treat acute severe ulcerative colitis if ciclosporin is contraindicated?
Infliximab
70
What are features of systemic upset?
Pyrexia
Tachycardia
Anaemia
Raised inflammatory markers
71
How often are patients with acute severe ulcerative colitis assessed?
Daily
72
What are the three categories of mild-to-moderate ulcerative colitis?
Proctitis
Proctosigmoidits and left-sided ulcerative colitis
Extensive disease
73
How are patients with mild-to-moderate UC caused by proctitis treated to induce remission?
Topical rectal aminosalicylate (e.g. mesalazine
If no remission within 4 weeks, add oral aminosalicylate
If still no remission, add topical/oral corticosteroid
74
How are patients with mild-to-moderate UC flare caused by proctosigmoiditis and left-sided UC treated to induce remission?
Topical rectal aminosalicylate
If no remission within 4 weeks, add high-dose oral aminosalicylate and topical corticosteroid
If still no remission, stop topical treatments and give oral aminosalicylate and corticosteroid
75
How are patients with mild-to-moderate UC flare caused by extensive disease treated to induce remission?
Topical rectal aminosalicylate and high-dose oral aminosalicylate
If no remission within 4 weeks, stop topical treatments and give high-dose oral aminosalicylate and oral corticosteroid
76
How is remission maintained in patients with mild-to-moderate UC flare caused by proctitis and proctosigmoiditis?
Topical (rectal) aminosalicylate alone (daily or intermittent)
OR
Oral aminosalicylate + topical (rectal) aminosalicylate (daily or intermittent)
OR
Oral aminosalicylate by itself: may not be effective as other 2 options
77
How is remission maintained in patients with mild-to-moderate UC flare caused by left-sided and extensive UC?
Low maintenance dose of oral aminosalicylate
78
How is remission maintained in patients following a severe relapse or 2 or more exacerbations in the past year?
Oral azathioprine OR oral mercaptopurine
79
Is methotrexate used in management of UC?
Not recommended (in contrast to Crohn's)
80
Where are probiotics used in treatment of UC?
In patients with mild to moderate disease - may prevent relapse
81
What is the recommendation for oral steroids in maintaining remission of UC?
Not routinely permitted
BUT are recommended for UC flares
82
What is the recommendation for anti-motility drugs, like loperamide, in treating UC flareups?
Not recommended as may increase risk of toxic megacolon
83
What is the recommendation for oral NSAIDs in treating UC flareups?
Not recommended as they can worsen colitis symptoms
Paracetamol considered instead
84
What is the first marker to appear in hepatitis B serology?
Surface antigen (HBsAg)
Causes production of anti-HBS
85
What does HBsAg imply?
Active infection
86
What does HbsAg present for <6 months and >6 months imply?
Acute disease
Chronic disease (i.e. infective)
87
What is anti-HBs?
Antibodies produced in response to HBsAg
88
What does positive anti-HBs without HBsAg imply?
Clearance of antibodies and resolution of infection - i.e. immunity
EITHER exposure or immunisation immunity
89
What is HBeAg and what is it used for?
Marker of active infectivity and replication in both chronic or acute infection
Used to distinguish between active or inactive chronic infection
90
What does positive/reactive anti-HBc imply?
Previous or current infection
91
What is another term for anti-HBc?
What is another term for anti-HBs?
HBcAb
HBsAb
92
What do IgM and IgG anti-HBc suggest?
IgM - acute or recent infection, present for ~6 months
IgG - chronic or resolved infection (gradually replaces IgM)
93
What would be the results of HBV serology of someone with previous immunisation?
Anti-HBs positive
All others negative (anti-HBc IgM, anti-HBe, HBeAg, HBsAg)
94
What would be the results of HBV serology of someone with previous infection (>6 months) who is not a carrier?
Anti-HBc positive
HBsAg negative
95
What would be the results of HBV serology of someone with previous infection who is now a carrier?
Anti-HBc positive
HBsAg positive
96
What is a typical presentation of someone with acute hepatitis B infection?
Jaundice
RUQ pain
Nausea
Anorexia
Constitutional symptoms (weight loss, fever, fatigue)
Up to 50% = subclinical/anicteric hepatitis (no associated jaundice)
97
What does positive HBeAg imply?
Acute and active chronic infection
98
What does positive anti-HBe imply?
Progression from active to inactive infection
Remains positive for life - specifically indicates immunity from previous infection
99
Interpret:
HBsAg positive, anti-HBs negative, HBeAg positive, anti-HBe negative, IgM anti-HBc negative
Chronic infection (inactive carrier)
100
Interpret:
HBsAg positive, anti-HBs negative, HBeAg negative, anti-HBe positive, IgM anti-HBc negative
Chronic infection (active carrier)
101
Interpret:
HbsAg negative, anti-HBs positive, HBeAg negative, anti-HBe positive, IgM anti-HBc negative
Immunity (following previous infection)
102
What is hepatitis B?
Infection of the liver caused by HBV
103
What does HBV serological testing involve?
Measurement of different HBV-specific antigens and antibodies
Differentiates: infection (acute/chronic) and immunity (vaccination/cleared infection)
104
How is HBV transmitted?
Parenteral routes - either infected blood or bodily fluids
Typically - blood-blood contact, sexual intercourse, vertical transmission (mother to infact)
105
What is the typical presentation of someone with chronic HBV infection?
No physical signs unless complications of chronic infection arise
May show signs of chronic liver disease or hepatocellular carcinoma
106
What is the window period between first exposure to HBV and detection of HBsAg in the serum?
Average: 75 days
Range: 45-200 days
107
What is HBsAg seroconversion?
Development of anti-HBs
108
How long do anti-HBs and anti-HBe remain in the serum for?
For life
109
What is HBcAg?
Hepatitis B core antigen - part of the HBV nucleocapsid
Not routinely measured in clinical practice, but anti-HBc is relevant
110
What is HBeAg?
Hepatitis B envelope antigen - found between core and lipid envelope of HBV
111
What does positive anti-HBe imply?
Marks transition from active disease to inactive carrier state
112
What does anti-HbE imply?
Immunity from a previous infection only
113
What is a high HBV DNA viral load associated with?
Increased risk of progression to cirrhosis and hepatocellular carcinoma
Expected in patients with chronic infection
114
Likelihood of progression from acute to chronic infection depends on?
Numerous factors, including the duration of infection and immunocompetency
115
What family is HBV part of?
HBV is a member of the Hepadnavirus family
116
What is HBV?
A circular, partially double-stranded DNA virus
117
What are the levels of transaminases in someone with acute HBV infection?
Elevated
118
What are the levels of transaminases in someone with chronic active HBV infection?
Elevated
119
What are the levels of transaminases in someone with chronic inactive HBV infection?
Normal
120
What are the levels of transaminases in someone with immunity following acute HBV infection?
Elevated or normal
121
What are the levels of transaminases in someone with immunity following HBV vaccination?
Normal
122
What does the HBV vaccine contain?
Inactivated HBsAg prepared from yeast cells using recombinant DNA technology
123
By which mechanism does loperamide act through to slow down bowel movements?
Stimulates mu-opioid receptors in the submucosal neural plexus of the intestinal wall
This reduces intestinal peristalsis
124
Does loperamide have systemic effects
Does not have systemic effects as it is not absorbed through the gut
125
What is loperamide?
Mu-opioid receptor agonist
126
Name two antidiarrhoeal agents which are mu-opioid receptor agonists?
Loperamide
Diphenoxylate
127
What is dyspepsia?
Indigestion
128
What can be used to control dyspepsia
Lansoprazole
129
What is dysphagia?
Difficulty in swallowing
130
What is Barrett's oesophagus?
Metaplasia of the lower oesophageal mucosa, with usual squamous epithelium being replaced by columnar epithelium
131
What does Barrett's oesophageus increase risk of?
Oesophageal adenocarcinoma (50-100x)
132
Are there screening programs for Barrett's?
No
Usually identified when patients have endoscopye for upper GI symptoms (e.g. dyspepsia)
133
How can Barrett's be subvdivided?
Short (<3cm)
Long (>3cm)
134
What does length of the affected segment in Barrett's correlate with?
Chances of identifying metaplasia
135
What is the prevalence of Barrett's oesophagus?
~1 in 20
Identified in up to 12% of people undergoing endoscopy for reflux
136
What are histological features of Barrett's oesophagus?
Columnar epithelium resembling either cardiac region of stomach or that of the small intestine
137
What are the three anatomical regions of the stomach?
Cardiac
Fundus
Pyloric
138
What does the cardiac region contain?
Mucous secreting glands (i.e. cardiac glands)
Closest to the oesophagus
139
What does the fundus contain?
Gastric glands (i.e. fundic glands)
140
What does the pyloric region contain?
Cells which secrete two types of mucus and gastrin
141
Where does the pyloric region end?
Pyloric sphincter
142
When does the pyloric sphincter relax?
When the formation of chyme is complete and is expelled into the duodenum
143
What are risk factors for Barrett's oesophagus?
GORD - STRONGEST RF
Male gender (1:7)
Smoking
Central obesity
144
Is alcohol an independent risk factor for Barrett's?
No
But is associated with both GORD and oesophageal cancer
145
Is Barrett's oesophagus symptomatic?
No
But, will often have coexisting GORD symptoms
146
How is Barrett's oesophagus managed?
Endoscopic surveillance with biopsies
High-dose PPI
147
Do high-dose PPIs limit progression to dyspepsia or induce regression of the lesion in Barrett's?
Evidence is limited
148
How frequently is endoscopy recommended in patients with metaplasia, but not dysplasia?
Every 3-5 years
149
If dysplasia of any grade is identified in Barrett's, what is the next course of action?
Endoscopic intervention.
Options:
- Endoscopic mucosal resection
- Radiofrequency ablation
150
An isolated rise in bilirubin in response to physiological stress (e.g. fasting) is typical of?
Gilbert's syndrome
151
Does Gilbert's syndrome require treatment or regular monitoring?
No
152
Can Gilbert's syndrome progress/cause chronic liver disease?
No
153
What is Gilbert's syndrome?
Autosomal recessive condition of defective bilirubin conjugation due to UDP glucoronosyltransferase
154
Prevalence of Gilbert's?
1-2%
155
What are features of Gilbert's syndrome?
Unconjugated hyperbilirubinaemia
Jaundice only during intercurrent illness/exercise/fasting
156
New-onset dysphagia is a red flag symptom of oesophageal cancer that requires?
Urgent endoscopy, regardless of age or other symptoms
Oesophagogastroduodenoscopy is needed within 2 weeks
157
What are conditions requiring an urgent oesophagogastroduodenoscopy?
>55 patient with weight loss and either upper abdo pain, dyspepsia or reflux
New-onset dysphagia
158
When would non-urgent upper GI endoscopy be appropriate?
Patients who don't meet referral criteria for urgent suspected cancer OGD, but still have signs/symptoms suggestive of oesophageal cancer
E.g. >55 with treatment-resistant dyspepsia, upper abdo pain with low Hb or raised platelet count with N&V, reflux, dyspepsia, weight loss, or upper abdo pain
159
When would same-day assessment in the MAU be used?
Patients acutely unwell with signs of haemodynamic instability OR
Patients with suspected conditions needing same-day investigations or treatments
160
What is peritonitis?
Inflammation of the peritoneum
161
What is spontaneous bacterial peritonitis?
Form of peritonitis typically seen in patients with ascites secondary to liver cirrhosis
162
What is ascites?
Abnormal fluid build-up in the abdomen
163
What are features of spontaneous bacterial peritonitis?
Ascites
Abdominal pain
Fever
N&V
General malaise
164
How is spontaneous bacterial peritonitis diagnosed?
Paracentesis - neutrophil > 250 cells/ul
165
What is the most common organism found on ascitic fluid culture in spontaneous bacterial peritonitis?
E. coli
166
What is the management of spontaneous bacterial peritonitis?
IV cefotaxime
167
When should antibiotic prophylaxis be given to patients with ascites?
- Pt with episode of SBP
- Pt with fluid protein < 15g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
168
Which antibiotic is given as prophylaxis to patients with ascites?
Oral ciprofloxacin or norfloxacin
169
What is a marker of poor prognosis in SBP?
Alcoholic liver disease
170
What is a liver flap?
Negative myoclonus of irregular lapses of posutre in different body parts
171
What is another term for a liver flap?
Asterixis
172
Patients with SBP may develop?
Hepatic encephalopathy
173
What is used as a prophylaxis for oesophageal variceal bleeding?
Non-selective beta-blocker (e.g. propranolol)
Endoscopic sclerotherapy = limited role
174
What is oesophageal varices?
Abnormal, enlarged veins on the oesophagus
175
What is the acute treatment of variceal haemorrhage?
- ABC
- Correct clotting (FFP, vit. K)
- Vasoactive agents (terlipressin, otherwise octreotide)
- Prophylactic IV antibiotics
- Endoscopy
- Sengstaken-Blakemore tube if uncontrolled haemorrhage
- Transjugular Intrahepatic Portosystemic Shunt if above fail
176
What prophylactic IV antibiotics are used in acute treatment of variceal haemorrhage?
Quinolones typically
177
When should terlipressin and antibiotics be given in treatment of suspected variceal haemorrhage?
Before endoscopy
178
Which endoscopic prcedure is superior in treatment of variceal haemorrhage?
Endoscopic variceal band ligation > endoscopic sclerotherapy
179
What is a transjugular intrahepatic portosystemic shunt?
Connects hepatic vein to the portal vein
So blood from portal system bypasses liver to enter systemic circulation without metabolism of waste products
180
What is a common complication of TIPSS?
Exacerbation of hepatic encephalopathy (e.g. inadequate metabolism of nitrogenous waste products by liver -> build-up in circulation -> increased ammonia can cross the BBB)
181
What is the prophylaxis of variceal haemorrhage?
Propranolol - reduces rebleeding and mortality
Endoscopic variceal band ligation at 2-weekly intervals until all varices eradicated
PPI cover given to prevent EVBL induced ulceration
182
What is the most common acute abdominal condition requiring surgery?
Acute appendicitis
183
When is acute appendicitis most common?
10-20 years
184
What is the pathogenesis of acute appendicitis?
1. Lymphoid hyperplasia or faecolith
2. Obstruction of appendiceal lumen
3. Gut organisms invading appendix wall
4. Oedema, ischaemia, ± performation
185
What are the presenting features of appendicitis?
Abdominal pain
Vomiting 1-2x
Mild pyrexia (37.5-38)
Anorexia - very common (unusual for pt to be hungry)
186
What is the pattern of pain in appendicitis?
Periumbilical abdominal pain
Migration from centre to RIF
Pain is worse on coughing or going over speed bumps
187
Is diarrhoea common or rare in appendicitis?
Rare, but pelvic appendicitis can cause local rectal iritatioin of some loose stools
Pelvic abscess can also cause diarrhoea
188
Temperatures higher than 37.5-38 in patients with appendicitis-like symptoms are typical of?
Mesenteric adenitis
189
Around 50% of appendicitis patients have symptoms of?
Anorexia, peri-umbilical pain, nausea
Followed by localised RLQ pain
190
What features appear on examination in appendicitis?
Generalised peritonitis or localised peritonism
Retrocaecal appendicitis = few signs
Digital rectal exam may show boggy sensation if pelvic abscess present or right-sided tenderness with pelvic appendix
Classical signs = Rovsing's sign and psoas sign
191
What is Rovsing's sign?
Palpatioin in LIF causes pain in RIF
Now of limited value
192
What is the psoas sign?
Pain on extending hip if retrocaecal appendix
193
What justifies appendicectomy?
Raised inflammatory markers + compatible history and exam findings
194
How is appendicitis diagnosed?
Neutrophil-predominant leucocytosis
Urinalysis - excludes pregnancy, renal colic, UTI
Imaging - no definite rules
195
When is ultrasound useful in appendicitis?
In females where pelvic organ pathology suspected - presence of free fluid should raise suspicion
196
When are CT scans useful in appendicitis?
Not used much in the UK, but very common in US
197
Thin male patients with a high likelihood of appendicitis can be diagnosed...?
Clinically
198
What is the management of appendicitis?
Appendicectomy - either open or laparoscopic
Prophylactic IV antibiotics (reduce wound infection)
If perforated appendicitis, need lots of abdominal lavage
199
How common is perforated appendicitis?
15-20% of appendicitis patients
200
What should be given to patients without peritonitis with an appendix mass?
Broad-spectrum antibiotics and consdieration of interval appendicectomy
201
When are prophylactic antibiotics given in appendicitis management?
Before appendicectomy
202
Patients with ascites and protein concentration <= 15g/L should be given?
Oral ciprofloxacin or norfloxacin as prophylaxis against SBP
203
What are features specific to ulcerative colitis over Crohn's disease?
Bloody diarrhoea is more common in UC
Abdominal pain in LLQ
Tenesmus
204
What are features specific to Crohn's disease over ulcerative colitis?
Non-bloody diarrhoea is more common in CD
Weight loss more prominent
Upper GI symptoms, mouth ulcers, perianal disease
Palpable abdominal mass in RIF
205
What are extraintestinal features specific to ulcerative colitis over Crohn's disease?
PSC more common in UC
206
What are extraintestinal features specific to Crohn's disease over ulcerative colitis?
Gallstones are more common secondary to reduced bile acid reabsorption
Oxalate renal stones
207
What are complications specific to ulcerative colitis over Crohn's disease?
Risk of colorectal cancer higher in UC
208
What are complications specific to Crohn's disease over ulcerative colitis?
Obstruction
Fistula
Colorectal cancer
209
Differentiate between the pathology of Crohn's disease and ulcerative colitis?
Crohn's: lesions anywhere from mouth to anus, skip lesions possible
UC: inflammation always starts at the rectum and never spread beyond the ileocaecal valve, continuous disease
210
What is the histology of Crohn's disease?
Inflammation in all layers from mucosa to serosa
Increased goblet cells
Granulomas
211
What is the histology of ulcerative colitis?
No inflammation beyond submucosa unless fulminant disease
Neutrophils migrate through gland walls to form crypt abscesses
Depletion of goblet cells and mucin from glandular epithlium
Infrequent granulomas
Inflammatory cells in lamina propria
212
What is seen on endoscopy iin Crohn's disease?
Deep ulcers, skip lesions (cobblestone appearance)
213
What is seen on endoscopy in ulcerative colitis?
- Widespread ulceration
- Preservation of adjacent mucosa which has appearance of polyps ('pseudopolyps)
- Red, raw mucosa - bleeds easily
214
What is seen on radiology in Crohn's disease?
Small bowl enema
- Strictures (Kantor's string sign)
- Proximal bowel dilation
- Rose thorn ulcers
- Fistulae
215
What is seen on radiology in ulcerative colitis?
Barium enema
- Loss of haustrations ('lead pipe colon')
- Superficial ulceration (pseudopolyps)
- If long-standing disease, colon is narrow and short (drainpipe colon)
216
What is Peutz-Jeghers syndrome?
Autosomal dominant condition
217
What does the gene responsible for Peutz-Jeghers syndrome encode?
Encodes serine threonine kinase LKB1 or STK11
218
Do the polyps in Peutz-Jeghers syndrome have malignant potential?
No
But ~50% of patients die from another GIT cancer by 60
219
What are features of Peutz-Jeghers syndrome?
Hamartomatous polyps in GIT (mainly small intestine) -- SBO common presenting complaint due to intussusception usually + GIT bleed
Pigmented lesions on lips, oral mucosa, face, palms, soles
220
What is the management of Peutz-Jeghers syndrome?
Conservative unless complications develop
221
What are causes of vitamin B12 deficiency?
Pernicious anaemia (most common)
Gastritis
Gastrectomy
Malnutrition
222
What is pernicious anaemia
Autoimmune disorder affecting gastric mucosa --> vitamin B12 deficiency
223
What is the pathophysiology of pernicious anaemia?
Antibodies to intrinsic factor ± gastric parietal cells
- antibodies to IF bind to IF and block the vitamin B12 binding site
- antibodies to gastric parietal cells reduce acid production and promote atrophic gastritis --> reduced IF production --> reduced vitamin B12 absorption
224
Why is pernicious anaemia megaloblastic? *check this
Vitamin B12 needed for RBC production and myelination --> megaloblastic anaemia and neuropathy
225
What is the most serious complication that occurs secondary to pernicious anaemia?
Gastric carcinoma
226
Why can upper GI bleeds result in melaena?
May occur as blood gets digested through the lower GI tract
227
What is a distended abdomen associated with?
Both large and small bowel obstructions (due to accumulation of digestive materials and gases in GIT)
228
What is the demarcation between the upper and lower GI tract?
Duodenojejunal junction (ligament of Treitz)
229
Can epigastric pain differentiate between upper and lower GI bleeding?
No, can be caused by any midgut structure (which is made up of the distal 2nd+3rd+4th part of duodenum, jejunum, ileum, caecum, appendix, ascending colon, hepatic flexure, and proximal 2/3 of transverse colum)
230
What is haematochezia?
Passage of fresh blood per anus, usually in or with stools
Typically a feature of lower GI bleeding as blood is undigestive BUT can occur with massive upper GI bleeding
231
Long-term PPI therapy can cause?
Hypomagnesaemia, which can cause muscle weakness
Most commonly seen after 1 year, but can be after 3 months
232
How do PPIs work?
Irreversible blockage of H+/K+ ATPase of gastric parietal cells
233
Examples of PPIs?
Omeprazole
Lansoprazole
234
Side effects of PPIs?
Hyponatraemia, hypomagnaseamia
Osteoporosis
Microscopic colitis
Increased risk of C. difficile infection
235
When should PPIs be stopped before an upper GI endoscopy? Why?
2 weeks before
So that pathology can be identified
236
What are indications for upper GI endoscopy?
Age > 55 years
Symptoms > 4 weeks or persistent symptoms despite treatment
Dysphagia
Relapsing symptoms
Weight loss
237
What is Courvoisier's law?
Gallstones unlikely in a patient with painless, enlarged gallbladder and mild jaundice
More likely to be a malignancy of the pancreas or biliary tree
238
What are the presenting features of PSC?
Mild hepatomegaly
Pruritus
Fatigue
239
What is primary sclerosing cholangitis?
Disease of unknown aetiology
Characterised by inflammation fibrosis and stricturing of mdium-large ducts in the intra and/or extrahepatic biliary tree
240
How many patients with ulcerative colitis devellop PSC and how many people with PSC also have ulcerative colitis?
5%
90%
241
What is mild, non-tender hepatomegaly a common clinical manifestation of?
Cholestatic liver disease, like PBC or PSC
242
How is PSC diagnosed?
Cholangiogram via ERCP or MRCP
243
Which is the gold-standard in PSC diagnosis: ERCP or MRCP?
ERCP
244
Which is performed first in PSC diagnosis: ERCP or MRCP?
MRCP as it is noninvasive, visualises the liver and avoids 10% risk of hospitalisation from ERCP
245
What are the MRCP findings of PSC?
Beaded build duct appearance
246
What is an appropriate investigation for widespread pruritus?
Skin biopsy - but more useful when a discrete lesion is present
247
Beneftis and limitation osf CT abdomen in PSC investigations?
- Can assess gross liver morphology
- Cannot visualise the intra and/or extrahepatic biliary tree to confirm PSCQ diagnosis
248
What diseases are associated with PSC?
Ulcerative colitis
Crohn's
HIV
249
What are features of PSC?
Choelstasis - jaundice, pruritis, raised bilirubin + ALP
- RUQ pain
- Fatigue
250
What are complications of PSC?
Cholangiocarcinoma (10%)
Increased risk of colectal cancer
251
What does ERCP stand for?
Endoscopic retrograde cholangiopancreatography
252
What does MRCP stand for?
Magnetic resonance cholangiopancreatography
253
What might p-ANCA be in PSC?
Positive
254
Is liver biopsy helpful in PSC investigations?
Limited role
May show fibrous, obliterative cholangitis ('onion skin')
255
What is the peak incidence of ulcerative colitis?
15-25
55-65
256
Why should colonoscopy be avoided in patients with severe colitis?
risk of perforation
Flexible sigmoidoscopy is preferred
257
What are extraintestinal sympsoms common to both Crohn's disease and ulcerative colitis related to disease activity?
Arthritis - pauciarticular, asymmetric (MOST COMMON)
Erythema nodosum
Episcleritis (CD >)
Osteoporosis
258
What are extraintestinal sympsoms common to both Crohn's disease and ulcerative colitis unrelated to disease activity?
Arthritis - polyarticular, symmetric
Uveitis (UC >)
Pyoderma gangrenosum
Clubbing
PSC (UC >>>>)
259
What is the appropriate first-line investigation for IBD?
Faecal calprotectin
260
When is gastrectomy indicated?
Some cases of ruptured ulcer or malignancy
261
Can TXA be used in GI bleed management?
HALT-IT trial shows that it worsens outcomes due to increased risk of thrombosis in upper GI haemorrhage
262
Where are vasopressin receptor antagonists used?
Management of SIADH
263
What is the schilling test?
Administering radiolabeled B12 - but no longer needed because artificial B12 replacement is widely available
264
What is TTG a first-line blood test for?
Coeliac disease investigation
265
Acute bleeding into the peritoneal cavity would cause signs of?
Peritonism - e.g. rebound tenderness, guarding
266
What does C. difficile antigen positivity in isolation ndicate?
Bowel is colonised with C.difficile, but not necessarily causing diarrhoea
267
What are risk factors for developing C. difficile diarrhoea?
Recent use of broad-spectrum antibiotics
PPI
268
What tests are used to test for C. difficile?
Antigen
Toxin
269
What does C. difficile toxin positivity indicate?
Bacteria is actively replicating and it is the likely cause of diarrhoea
270
C. difficile produces an exotoxin which causes...
intestinal damage, leading to a syndrome called pseudomembranous colitis
271
How do broad-spectrum anitbiotics lead to C. difficile development?
They suppress normal gut flora
272
Which antibiotics are the leading causes of C. difficile?
Historically, clindamycin
Now, second and third gen cephalosporins
273
What are features of C. difficile?
Diarrhoea
Abdominal pain
Raised WCC
If severe: toxic megacolon
274
What type of microbe is C. difficile?
Gram positive rod
275
How is a diagnosis of C. difficile made?
Detecting C. difficile toxin in stool
276
What is mild C. difficile?
Normal WCC
277
What is moderate C. difficile?
Elevated WCC
3-5 loose stools per day
278
What is severe C. difficile?
Elevated WCC or acutely high creatinine or temp over 38.5 or evidence of sever colitis
279
What is life-threatening C. difficile?
Hypotension
Partial or complete ileus
Toxic megacolon or CT evidence of severe disease
280
What is the management of C. difficile?
First episode of infection
first-line: oral vancomycin, 10 days
Second-line: oral fiaxomicin
Third-line: oral vancomycin ± IV metronidazole
281
What is the management of C. difficile on recurrent episode?
Within 12 weeks of symptom resolution: oral fidaxomicin
After 12 weeks of symptoms resolution: oral vancomycin OR fidaxomicin
282
What is the management of life-threatening C. difficile infection?
Oral vancomycin AND IV metronidazole
Specialist advice - surgery may be considered
283
What are other therapies of C. difficile?
Bezlotoxumab - mAb targeting C. difficile toxin B (NICE don't support use to prevent recurrences)
Faecal microbiota transplant (considered for patients with 2 or more previous episodes)
284
What are radiological signs of C. difficile?
Loss of bowel wall architecture and thumb-printing
Oedamatous colon with enhancing walls but normal calibre
285
What is spontaneous bacterial peritonitis?
Ascitic fluid infection without evident treatable intraabdominal source
286
SBP occurs almost always in...
patients with known cirrhosis and ascities, commonly because of ALD, hepatitis b, hepatitis C, and NAFLD
287
What is secondary peritonitis?
Peritoneal infection secondary to another infection (e.g. diverticulitis, appendicitis)
288
What is used as secondary prophylaxis of hepatic encephalopathy?
Lactulose (first-line) and rifaximin
289
What is thought to cause hepatic encephalopathy?
Excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut
290
What are features of hepatic encephalopathy?
Confusion
Altered consciousness
Asterixis
Triphasic slow waves on EEG
291
How does lactulose work?
Promotes excretion of ammonia and increases metabolism of ammonia by gut bacteria
292
How does rifaximin work?
Modulate gut flora, decreasing ammonia production
293
What are spironolactone and furosemide used to manage in cirrhosis?
ascites and oedema in patients with hypoalbuminemia secondary to cirrhosis
294
What is the ligament of Treitz also known as?
Suspensory muscle of the duodenum
295
Where is the ligament of Treitz found?
Duodenojejunal flexure
296
What does the ligament of Treitz mark?
Boundary between the first and second parts of the small intestine
297
Where is the ligament of Treitz clinically relevant in children?
When malrotation of the gut is suspected
298
What is the ampulla of Vater?
Site where common bile duct opens onto duodenum
299
What does the ileocaecal valve delineate?
Large intestine and small intestine
300
ALP vs ALT higher in cholestatic liver injruy?
ALP >>> ALT
301
Co-amoxiclav is known to cause
Cholestatic liver injury
302
How to distinguish biliary sepsis from ischaemic hepatitis
Abdominal pain seen in biliary sepsis
303
A lemon tinge to the skin is associated with
pernicious anaemia
304
Three symptoms of anaemia
Dyspnoea
Fatigue
Lethargy
305
Loss of vibration sense, lemon tinge to the skin are associated with
pernicious anaemia
306
Why does lemon tinge to skin occur in pernicious anaemmia
Combination fo pallor due to anaemia and mild jaundice caused by haemolysis
307
Why does loss of vibration sense occur in pernicious anaemia, and reflex loss and weakness?
Low b12 levels
308
What factors are linked to UC flares?
Stress
Medications - NSAIDs and antibiotics
Cessation of smoking
309
Vit A is teratogenic in high doses - pregnant women shouldn't excceed daily intake of?
10,000 IU
310
What is vitamin A?
Fat soluble vitamin
311
Functions of vitamin A?
Converted into retinal - a visual pigment
Epithelial cell differentiation
Antioxidant
312
Consequences of vitamin A deficiency?
Night blindness
313
The double duct sign on MRCP is indicative of
pancreatic cancer
and ampullary tumours
to a far lesser extent, acute pancreatitis
314
What ist he double duct sign
Dilatation of both the common bile duct and pancreatic duct
315
Triad for ascending cholangitis?
RUQ pain
Jaundice
Fever
Charcot triad
316
What is the most common affected site in ulcerative colitis?
Rectum
317
What is carcinoid syndrome?
Usually when metastases present in liver and release serotonin into systemic circulation
318
Carcinoid syndrome may also occur with
Lung carcinoid as mediators aren't 'cleared' by the liver
319
What are features of carcinoid tumours
Flushing - earliest symptom often
Diarrhoea
Bronchospasm
Hypotension
Right heart valvular stenosis
Pellagra cna rarely develope
320
Why does right heart valvular stenosis occur in carrcinoid tumours
Left heart affected in bronchial carcinoid
321
How can carcinoid tumours result in Cushing's
Other molecules like ACTH and GHRH may be secreted
322
Investigations for carcinoid tumours?
Urinary 5-HIAA (as tumour will secrete serotonin)
Plasma chromogranin A y
323
Management of carcinoid tumours?
Somatostatin analogues (e.g. octreotide)
Diarrhoea (cyproheptadine)
324
What kind of pattern of damage does paracetamol overdose cause
Hepatocellular pattern of drug-induced liver injury
325
What kind of pattern of damage does alcohol cause
Heptocellular pattern of drug-induced liver injury
AST level check - if AST/ALT ratio is 2.0 or higher = alcohol-related liver disease
326
What kind of pattern of damage does atorvastatin cause
Hepatocellular pattern of drug-induced liver injury
ALT >>>> ALP
Isolated cases of raised ALT = worth checking CK as muscle injury can also cause this
327
What kind of pattern of damage does oral contraceptive pill cause
Cholestatic derangement on LFT
328
What kind of pattern of damage does nitrofurantoin cause
Hepatocellular pattern of drug-induced liver injury
ALT > ALP
329
Management for people with asymptomatic incidental gallbladder stones?
Reassurance - unless the stones are within the common bile duct
330
What is the intervention fro people with symptomatic gallstones or stones found in the common bile duct
Surgical at time of laparocsopic cholecystectomy
With ERCP before or at the time of laparoscopic cholecystectomy
331
What does Crohn's commonly affect
Terminal ileum
Colon
332
What is the gold-standard investigation for perianal fistulae in Crohn's patients
MRI pelvis - visualise course of tract and plan surgical management
333
When is colonoscopy used in Crohn's
General assessment of Crohn's disease
334
What is ESR?
Non-specific test for inflammation
Measures time taken for coagulated RBCs to settle in the bottom of a tube
335
Why may ESR be used in Crohn's
Assess disease activity
336
Why may stool culture be uesd in Crohn's
Patients with Crohn's treated with antibiotics to rule out C. difficile infection
337
Why would wound swab be used in Crohn's
It patient getting recurrent abscesses without fistula being identified or if they had a risk factor for one of the rare causes of anorectal abscesses like HIV
Wound swabbed to rule out TB or actinomycosis infection
338
What is a perianal fistula
Inflammatory tract or connectioin between anal canal and perianal skin
339
Why is MRI used in investigating suspected perianal fistulae
Determine if there is an abscess and fistula is simple - low fistula- or complex - high fistula that passes through or above muscle layers
340
How is vitamin B12 deficiency managed
Intramuscular
Loading regime followed by 2-3 monthly injections
341
Which is first: vitamin b12 replacement o folate
B12
Folate replacement prior can precipitate subacute combined degeneration of spinal cord
342
Why do people with coeliac's disease need regular immunisations
Often have degree of functional hyposplenism
So offered pneumococcal vaccine - booster every 5 years is recommended
Influenza vaccine on individual basis
343
Courvoisier's law states that
in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
and is likely to be malignancy, particularly pancreatic
344
presentation of a painless, palpable mass in combination with anorexia and fatigue makes
malignancy a likely diagnosis
345
What's the most common inheritable form of colorectal cancer
HNPCC - Lynch syndrome
Accounts for 5% of all colorectal cancer cases and is also assoc with endometrial cancer
346
What's the secon dmost common cause of colorectal cancer
FAP
347
What is Gardner syndrome
Variant of FAP
Often with cutanoues signs
348
What's Von Hippel-Lindau disease
Rare autosomal dominant disease associated with CNS cancers and retinal cancers
349
Features of Gardner syndrome
osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin
350
Grading of hepatic encephalopathy
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
351
Kayser-Fleischer rings are seen in
eyes of patients with Wilson's diseaes
352
What is Wilson's disease
Inherited condition where too much copper is deposited in the tissues and causes liver and neurological problems
353
What is the primary treatment for Wilson's diseas
Penicillamine - metal chelating agent
Trientine also a chelating agent for patients wintolerant to penicillamine
354
What is ursodeoxycholic acid used to manage
biliary conditions, like gallstones
355
Which mutations are associated with HNPCC?
MSH2/MLH1 gene
356
Which mutations are associated with FAP?
APC gene
357
Alcoholic ketoacidosis is managed with
Infusion of 0.9% saline and thiamine
358
What happens in alcoholic ketoacidosis
Body is starved and needs to breakdown fats to produce energy, producing ketones as a by-product in the presence of normal blood glucose
359
Why is thiamine given in management of alcoholic ketoacidosis?
Patients with history of alcohol excess often deficient in thiamine - can cause Wernicke's encephalopathy
360
What is Wernicke's encephalopathy
Neuropsychiatric condition causing ataxia, confusion, nystagmus, opthalmoplegai
361
Classic presentation of vit C deficiency
Lethargy
Arthralgia
Easy bruising
Bleeding gums
362
What's haemophilia A
Congenital deficiency in clotting factor 8
Typically in childhood with bleeding into joints
363
What's haemophilia B
Deficiency in clotting facot 9
Congenital
More common in infancy
Presents with mucosal bleeding
364
Time course for acute lymphoblastic leukaemia for symptom onset
Period of days to weeks
365
What is Budd-Chiari syndrome?
Hepatic vein thrombosis
Usually seen in context of underlying haematological disease or another procoagulant condition
366
Features of Budd-Chiari syndrome
Abdominal pain - sudden onset, severe
Ascites -> abdominal distension
Tender hepatomegaly
367
Investigations for Budd-Chiairi syndrome
USS with doppler flow studies - very sensitive
368
Causes of Budd-Chiari syndrome
polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases
369
Presentation of pharyngeal pouch
Dysphagia
Regurgitation
Halitosis
370
Age typical of pharyngeal pouch
> 70
371
Treatment of pharyngeal pouch
Surgical repair
372
CCB used for
Oesophageal spasm
373
PPI used for
GORD
374
What should be done if on full-dose PPI and dyspepsia symptoms not resolved
Test and treat for H. pylori
375
Patients with ascites secondary to liver cirrhosis should be given ?
an aldosterone antagonist
376
Why is furosemide not given to patients with ascites secondary to liver cirrhosis?
Ineffective at blocking aldosterone and its sodium retaining effects in the distal tubule and collecting duct
377
Increased goblet cells where
Crohn's disease
378
Crypt hypertrophy where
Coeliac disease
379
Subepithelial fibrosis where
Asthma
380
Villous atrophy where
Coeliac disease
381
Crypt abscesses where
Ulcerative colitis
382
History of ulcerative colitis coupled with new clinical signs of hepatobiliary disease should make you think of
PSC
383
Anti-dsDNA assoc with
SLE
384
Anti-CCP assoc with
RA
385
Anti-GBM assoc with
Goodpasture's syndrome
386
ANCA antibodies assoc with
Small vessel vasculitides
387
c-ANCA assoc with
Granulomatosis with polyangitis and eosinophilic granulmatosis with polyangitis
388
p-ANCA assoc with
Broad range of conditions, including PSC, autoimmune hepatitis, UC
389
Referral to upper GI surgeons for oesophagectomy is reserved for
T1b cancer
390
Dysplasia on biopsy in Barrett's oesophagus requires
Endoscopic intervention
391
Hallmarks of refeeding syndrome
deranged electrolytes (low potassium, low magnesium and low phosphate) and fluid shifts
392
Deranged electrolytes can lead to
Arrhythmias
393
AKI more commonly causes hyper or hypokalaemia
Hyperkalaemia
394
First-line in maintaining remission in UC patients with proctitis and proctosigmoidits
Topical (rectal) aminosalicylate - e.g. mesalazine
395
Prominent symptoms of Crohn's in adults vs children
Adults - (bloody) diarrhoea
Children - abdominal pain
396
Zollinger-Ellison syndrome
Epigastric pain
Diarrhoea
MEN-1 in a third of patients --> hyperparathyroidism
397
MEN-1
parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
pituitary (70%)
pancreas (50%, e.g. Insulinoma, gastrinoma)
also: adrenal and thyroid
398
Early signs of haemochromatosis
Fatigue
erectile dysfunction
arthralgia
399
Fetor hepaticus, sweet and fecal breath, is a sign of
liver failure
400
Diverticulitis classically causes pain in the
llq
401
Netabolic acidosis is highly suggestive of
metabolic acidosis
