Gastrointestinal Flashcards
(75 cards)
1
Q
What is Admirand’s triangle?
A
- Low lecithin
- Low bile salts
- High cholesterol
Increases risk of gallstones
2
Q
Define acute cholecystitis.
A
Acute cholecystitis is an inflammation of the gallbladder.
3
Q
What causes cholecystitis?
A
- Gallstones in 90-95% of cases
- Obstruction of the gallbladder neck or cystic duct by a gallstone causes bile to become trapped in the gallbladder, resulting in irritation and increased pressure in the gallbladder.
- Acalculous cholecystitis (without gallstones)
- Cystic duct obstruction is often present and is associated with bile stasis or thickening.
4
Q
What is the different between biliary colic and acute cholecystitis?
A
- If the obstruction is partial and of short duration, the person experiences biliary colic, characterized by severe pain and tenderness of the right side of the abdomen and/or back). Acute cholecystitis occurs when the obstruction is complete and prolonged (usually several hours).
5
Q
What are the RFs for acute cholecystitis?
A
- Increasing age
- Female
- Obesity
- Low fibre diet
6
Q
What are the signs and symptoms of acute cholecystitis?
A
- Sudden-onset, constant, severe pain in the upper right quadrant, lasting several hours.
- Tenderness, with or without guarding, in the right upper quadrant.
- Murphy’s sign on examination: inspiratory arrest upon palpation of the right upper quadrant
- Fever
7
Q
What are the investigations for acute cholecystitis?
A
- Abdominal ultrasound
- If the diagnosis remains unclear then cholescintigraphy (HIDA scan) may be used
- technetium-labelled HIDA (hepatobiliary iminodiacetic acid) is injected IV and taken up selectively by hepatocytes and excreted into bile
- in acute cholecystitis there is cystic duct obstruction (secondary to odema associated with inflammation or an obstructing stone) and hence the gallbladder will not be visualised
- Blood tests
- white blood cell count - may be raised
- C-reactive protein - raised
- serum amylase- might be high
- ALT/AST - Normal
- ALP - little high
8
Q
What is Mirizzi syndrome?
A
Mirizzi syndrome is defined as common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder
- Deranged LFTs may indicate Mirizzi syndrome
9
Q
What is the management of acute cholecystitis?
A
A-E Management
- NBM
- IV Abx
- Analgesia
- Fluids
- Laparoscopic cholecystectomy within 1 week of diagnosis
10
Q
What are the complications of acute cholecystitis?
A
- Sepsis
- Gallbladder empyema
- Gangrenous gallbladder
- Perforation
11
Q
Define ascending cholangitis.
A
Ascending cholangitis is a bacterial infection (typically E. coli) of the biliary tree.
12
Q
What commonly causes ascending cholangitis?
A
Gallstones
13
Q
What organisms commonly cause ascending cholangitis?
A
- Escherichia coli
- Klebsiella species
- Enterococcus species
14
Q
What are the signs and symptoms of ascending cholangitis?
A
Acute cholangitis presents with Charcot’s triad:
- Right upper quadrant pain
- Fever
- Jaundice (raised bilirubin)
Reynold’s pentad = + hypotension, confusion
15
Q
How do you investigate ascending cholangitis?
A
- Endoscopic US
- MRCP
- CT scan
- Abdo ultrasound - usually done first if suspected
16
Q
How do you manage ascending cholangitis?
A
A-E Assessment
- NBM
- IV Fluids
- Blood cultures
- intravenous antibiotics
- endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction
17
Q
Describe ERCPs
A
An endoscopic retrograde cholangio-pancreatography (ERCP) is required to remove stones blocking the bile duct. It involves inserting an endoscope down the oesophagus, past the stomach, to the duodenum and the opening of the common bile duct (the sphincter of Oddi).
- Cholangio-pancreatography: retrograde injection of contrast into the duct through the sphincter of Oddi and x-ray images to visualise biliary system
- Sphincterotomy: making a cut in the sphincter to dilate it and allow stone removal
- Stone removal: a basket can be inserted and pulled through the common bile duct to remove stones
- Balloon dilatation: a balloon can be inserted and inflated to treat strictures
- Biliary stenting: a stent can be inserted to maintain a patent bile duct (for strictures or tumours)
- Biopsy: a small biopsy can be taken to diagnose obstructing lesions
18
Q
What is a PTC?
A
Percutaneous transhepatic cholangiogram (PTC) involves radiologically guided insertion of a drain through the skin and liver, into the bile ducts. The drain relieves the immediate obstruction.
A stent can be inserted to give longer-lasting relief of obstruction.
This is an option for patients that are less suitable for ERCP, or where ERCP has failed.
19
Q
What are the key risk factors of cholangiocarcinoma?
A
- Primary sclerosing cholangitis
- Liver flukes (a parasitic infection)
20
Q
What are the signs and symptoms of cholangiocarcinomas?
A
Obstructive jaundice is the key presenting feature to remember. Obstructive jaundice is also associated with:
- Pale stools
- Dark urine
- Generalised itching
Other non-specific signs and symptoms include:
- Unexplained weight loss
- Right upper quadrant pain
- Palpable gallbladder (swelling due to an obstruction in the duct distal to the gallbladder)
- Hepatomegaly
- periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
Courvoisier’s law
21
Q
What are the investigations for cholangiocarcinomas?
A
- LFTs (abnormal)
- CA-19-9, CEA (non-specific, poor markers)
- 1st line, incidental → USS (mass, polyps, thickening)
-
1st line, suspected GB cancer → CT abdomen (diagnosis, staging)
- ERPC (gold-standard staging) - biopsy
- MRCP staging)
- Biopsy
22
Q
What is the management of cholangiocarcinomas?
A
- Management will be decided at a multidisciplinary team (MDT) meeting.
-
Curative surgery may be possible in early cases → cholecystectomy (simple → extended → extra debulking)
- It may be combined with radiotherapy and chemotherapy.
- In most cases, curative surgery is not possible. Palliative treatment may involve:
- Stents inserted to relieve the biliary obstruction
- Surgery to improve symptoms (e.g., bypassing the biliary obstruction)
- Palliative chemotherapy/radiotherapy
- End of life care with symptom control
Poor prognosis
23
Q
Define PBC.
A
Primary biliary cirrhosis is a condition where the immune system attacks the small bile ducts within the liver.
24
Q
Describe the pathophysiology of PBC.
A
The first parts to be affected are the intralobar ducts, also known as the Canals of Hering. This causes obstruction of the outflow of bile, which is called cholestasis. The back-pressure of the bile obstruction and the overall disease process ultimately leads to:
- fibrosis
- cirrhosis
- liver failure.
When there is obstruction to the outflow of bile acids, bilirubin and cholesterol, they build up in the blood as they are not being excreted.
- Bile acids cause itching
- bilirubin causes jaundice
- raised cholesterol causes cholesterol deposits in the skin called xanthelasma (xanthomas are larger nodular deposits in the skin or tendons) and blood vessels causing increased risk of cardiovascular disease.
25
Law of Ms
* **AMA**
* **Raised IgM**
* **Middle-aged women** (9: 1)
PBC
26
What are the associations with PBC?
* **Sjögren’s** (80% of patients), **RhA**, **thyroid disease**, **systemic sclerosis**
27
How does PBC present?
* Fatigue
* Pruritus
* GI disturbance and abdominal pain
* Jaundice
* Pale stools
* ***Xanthoma*** and ***xanthelasma***
* Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
28
How do we investigate PBC?
* Cholestatic liver biochemistry (**raised GGT/ALP**, normal transaminases)
* Autoantibodies (**AMA** [98% of patients]; **raised serum IgM**)
* Biopsy (this is required for a definitive diagnosis _but not often carried out_; only perform if doubt of dx)
29
What is the management of PBC?
1st line : Ursodeoxycholic acid ± obeticholic acid
± cholestyramine (for itching)
Immunosuppression (e.g. with steroids) is considered in some patients
**2nd line** (end-stage): Liver transplantation (e.g. if bilirubin \> 100 (PBC is a major indication)
30
What are the complications of PBC?
* Symptomatic pruritus
* Fatigue
* Steatorrhoea (greasy stools due to lack of bile salts to digest fats)
* Distal renal tubular acidosis
* Hypothyroidism
* Osteoporosis
* Hepatocellular carcinoma
31
Define PSC.
***Primary sclerosing cholangitis*** is a condition where the intrahepatic or/and extrahepatic ducts become strictured and fibrotic.
32
Describe the pathophysiology of PSC.
* There's an obstruction to the flow of bile out of the liver and into the intestines.
* Sclerosis refers to the stiffening and hardening of the bile ducts, and cholangitis is inflammation of the bile ducts.
* Chronic bile obstruction eventually leads to liver inflammation (hepatitis), fibrosis and cirrhosis.
33
What are the associations of PSC? What are the RFs?
* UC (4% of patients with UC have PSC; _80% of patients with PSC have UC_) - pANCA
* Crohn’s
* HIV
* Male
* Aged 30-40
* Ulcerative Colitis
* Family History
34
Describe the presentation of PSC.
* Jaundice
* Chronic right upper quadrant pain
* Pruritus
* Fatigue
* Hepatomegaly
35
What are the investigations for PSC?
* LFTs - Raised ALP, raised bilirubin
* Autoantibodies - pANCA, ANA, aCL
* The _gold standard investigation_ for diagnosis is an **MRCP** - it may show bile duct lesions or strictures.
* Biopsy of bile duct (fibrous, obliterative cholangitis often described as 'onion skin')
36
How do we manage PSC?
**_observation**_ (surveillance colonoscopy, DEXA) → _**liver transplant_**
Prevention: Ursodeoxycholic acid
Avoid alcohol (RF for cholangiocarcinoma)
* ERCP can be used to dilate and stent any strictures
* ***Colestyramine*** is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
* Monitoring for complications (such as cholangiocarcinoma, cirrhosis and oesophageal varices)
37
What are the complications of PSC?
_cholangiocarcinoma_ (in 10%), _colorectal cancer_, _hepatic osteoporosis/osteopenia_
38
What drugs cause a hepatocellular picture?
* paracetamol
* sodium valproate, phenytoin
* MAOIs
* halothane
* anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
* statins
* alcohol
* amiodarone
* methyldopa
* nitrofurantoin
39
What drugs cause cholestasis (+/- hepatitis)?
* combined oral contraceptive pill
* antibiotics: flucloxacillin, co-amoxiclav, erythromycin\*
* anabolic steroids, testosterones
* phenothiazines: chlorpromazine, prochlorperazine
* sulphonylureas
* fibrates
* rare reported causes: nifedipine
40
What drugs cause cirrhosis?
* methotrexate
* methyldopa
* amiodarone
41
What is haemochromatosis?
Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6
42
How does haemochromatosis present?
* early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
* 'bronze' skin pigmentation
* diabetes mellitus
* liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
* cardiac failure (2nd to dilated cardiomyopathy)
* hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
* arthritis (especially of the hands)
43
How should haemochromatosis be investigated?
* general population: transferrin saturation is considered the most useful marker. Ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
* testing family members: genetic testing for HFE mutation
Diagnostic tests
* molecular genetic testing for the C282Y and H63D mutations
* liver biopsy: **Perl's stain**
Typical iron study profile in patients with haemochromatosis
* transferrin saturation \> 55% in men or \> 50% in women
* raised ferritin (e.g. \> 500 ug/l) and iron
* low TIBC
Joint x-rays characteristically show chondrocalcinosis
44
How should haemochromatosis be managed?
* Venesection is the first-line treatment
* monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
* desferrioxamine may be used second-line
45
What histology do pancreatic cancers have?
80% Adenocarcinomas
46
What are the associations with pancreatic cancers?
* increasing age
* smoking
* diabetes
* chronic pancreatitis (alcohol does not appear an independent risk factor though)
* hereditary non-polyposis colorectal carcinoma
* multiple endocrine neoplasia
* BRCA2 gene
* KRAS gene mutation
47
How do pancreatic cancers present?
* classically painless jaundice
* pale stools, dark urine, and pruritus
* cholestatic liver function tests
* Courvoisier's law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
* however, patients typically present in a non-specific way with anorexia, weight loss, epigastric pain
* loss of exocrine function (e.g. steatorrhoea)
* loss of endocrine function (e.g. diabetes mellitus)
* atypical back pain is often seen
* migratory thrombophlebitis (Trousseau sign) is more common than with other cancers
48
What are the investigations for pancreatic cancers?
* ultrasound has a sensitivity of around 60-90%
* high-resolution CT scanning is the investigation of choice if the diagnosis is suspected
* imaging may demonstrate the 'double duct' sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
49
How should a variceal bleed be managed?
* ABC: patients should ideally be resuscitated prior to endoscopy
* correct clotting: FFP, vitamin K
* vasoactive agents:
* terlipressin \> octreotide
* prophylactic IV antibiotics have been shown to reduce mortality in patients with liver cirrhosis. Quinolones are typically used.
* endoscopy: endoscopic variceal band ligation is superior to endoscopic sclerotherapy. NICE recommend band ligation
* **Sengstaken-Blakemore tube** if uncontrolled haemorrhage
* **Transjugular Intrahepatic Portosystemic Shunt (TIPSS)** if above measures fail
* connects the hepatic vein to the portal vein
* exacerbation of hepatic encephalopathy is a common complication
50
How can we prevents variceal bleeds?
* Propanolol
* endoscopic variceal band ligation - It should be performed at two-weekly intervals until all varices have been eradicated. Proton pump inhibitor cover is given to prevent EVL-induced ulceration.
51
What are the risk factors behind peptic ulcer disease?
* H.pylori
* Drugs
* NSAIDs
* SSRIs
* Corticosteroids
* Bisphosphonates
* Zollinger Ellison syndrome - excessive levels of gastrin, usually from gastrin secreting tumour
* Alcohol and smoking
52
How to PUD present?
* epigastric pain
* nausea
* duodenal ulcers
* more common the gastric
* epigastric pain when hungry, relieved by eating
* gastric ulcer
* worsened by eating
52
What Ix would you do for a suspected PUD?
* H.pylori test - urea breath test or stool antigen
53
How are PUDs managed?
* if *Helicobacter pylori* is negative then proton pump inhibitors (PPIs) should be given until the ulcer is healed
* if *Helicobacter pylori* is positive then eradication therapy should be given
54
What is the H.pylori eradication therapy?
* A proton pump inhibitor, plus [amoxicillin](https://bnf.nice.org.uk/drugs/amoxicillin/), and *either* [clarithromycin](https://bnf.nice.org.uk/drugs/clarithromycin/) or [metronidazole](https://bnf.nice.org.uk/drugs/metronidazole/)
* Penicillin allergy -
* A proton pump inhibitor, plus [clarithromycin](https://bnf.nice.org.uk/drugs/clarithromycin/), and [metronidazole](https://bnf.nice.org.uk/drugs/metronidazole/).
For 7 days
55
How do perforated peptic ulcers present?
* Epigastric pain, tachycardia, cool extermitires
* Generalised pain worse on movement
* Abdominal distention, pyrexia, hypotension
56
How ix would you do for a perforated peptic ulcer?
* Although the diagnosis is largely clinical, UptoDate recommend that plain x-rays are the first form of imaging to obtain
* An upright ('erect') chest x-ray is usually required when a patient presents with acute *upper* abdominal pain
* This is a useful test, as approximately 75% of patients with a perforated peptic ulcer will have free air under the diaphragm
57
How would a perforated peptic ulcer be managed?
PPU is a surgical emergency associated with high mortality if left untreated.
In general, all patients with PPU require:
* prompt resuscitation
* intravenous antibiotics
* analgesia
* proton pump inhibitory medications
* nasogastric tube
* urinary catheter
* surgical source control.
58
What is the most common complication of PUD?
Bleeding - from gastroduodenal artery
59
how would a bleeding peptic ulcer present?
The most common presenting symptom is haematemesis. Other features include:
* melaena
* hypotension, tachycardia
60
How would a bleeding peptic ulcer be managed?
* ABC approach as with any upper gastrointestinal haemorrhage
* IV proton pump inhibitor
* the first-line treatment is endoscopic intervention
* if this fails (approximately 10% of patients) then either:
* urgent interventional angiography with transarterial embolization or
* surgery
61
Define dyspepsia.
A group of symptoms that alert doctors to consider disease of the upper GI tract (not a diagnosis).
These symptoms, which typically are present for 4 weeks or more, include upper abdominal pain or discomfort, heartburn, gastric reflux, nausea or vomiting
62
Define GORD.
Symptoms of oesophagitis secondary to refluxed gastric contents
* endoscopically determined oesophagitis
* endoscopy-negative reflux disease.
63
What are the investigations for GORD? When are the indicated?
Upper GI Endoscopy
* age \> 55 years
* symptoms \> 4 weeks or persistent symptoms despite treatment
* dysphagia
* relapsing symptoms
* weight loss
If endoscopy negative consider 24-hr oesophageal pH monitoring (gold standard)
64
What lifestyle advice can be given for GORD?
* Healthy eating
* Weight reduction
* Smoking cessation
* Avoid precipitants (smoking, alcohol, coffee, chocolate, fatty foods, eat earlier)
65
How would you manage patients with GORD?
**Uninvestigated GORD** - Offer empirical full-dose PPI therapy for 4 weeks to people with dyspepsia.
If symptoms return after initial care strategies, step down PPI therapy to the lowest dose needed to control symptoms. Discuss using the treatment on an 'as-needed' basis with people to manage their own symptoms.
Offer H2 receptor antagonist (H2RA) therapy if there is an inadequate response to a PPI.
**Investigated GORD** - full-dose PPI for 4 or 8 weeks.
If symptoms recur after initial treatment, offer a PPI at the lowest dose possible to control symptoms.Discuss using the treatment on an 'as-needed' basis with people to manage their own symptoms.
Offer H2 receptor antagonist (H2RA) therapy if there is an inadequate response to a PPI.
66
What are the complications of GORD?
* oesophagitis
* ulcers
* anaemia
* benign strictures
* Barrett's oesophagus
* oesophageal carcinoma
67
How do we divide Barretts oesophagus?
Barrett's can be subdivided into short (\<3cm) and long (\>3cm). The length of the affected segment correlates strongly with the chances of identifying metaplasia.
68
What does Barretts oesophagus look like on histology?
the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)
69
What are the RFs for Barretts oesophagus?
* gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
* male gender (7:1 ratio)
* smoking
* central obesity
70
How is Barretts oesophagus managed?
* high-dose proton pump inhibitor
* endoscopic surveillance with biopsies - every 3-5 yrs
* If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
* radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia
* endoscopic mucosal resection
71
What are the 2 types of oesophageal cancers? What is the epidemiology, location and RFS?
72
How would oesophageal cancers present?
* dysphagia: the most common presenting symptom
* anorexia and weight loss
* vomiting
* other possible features include: odynophagia, hoarseness, melaena, cough
73
What are the investigations for oesophageal cancer?
* Upper GI endoscopy with biopsy is used for diagnosis
* Endoscopic US - locoregional staging
* CT Scan of the chest, abdo and pelvis is used for initial staging
* FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans.
* Laparoscopy is sometimes performed to detect occult peritoneal disease
74
How are oesophageal cancers managed? What is the biggest challenge
* Operable disease is best managed by surgical resection - the most common procedure is an Ivor-Lewis type oesophagectomy
* The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
* In addition to surgical resection many patients will be treated with adjuvant chemotherapy
