Abdominal Conditions Flashcards
1
Q
What is GORD
A
Gastro-oesophageal reflux disease
Symptoms or complications resulting from the reflux of gastric contents into the oral cavity or lung
2
Q
How does GORD present
A
Heartburn (burning sensation in chest) usually after eating, which may be worse at night Chest pain (retrosternal or epigastric) Difficulty swallowing (dysphasia) Regurgitation of food or sour liquid (acid) Sensation of lump in throat Chronic nocturnal cough Laryngitis Hoarse voice New or worsening asthma Disrupted sleep
3
Q
What is ERD
A
Erosive reflux disease, where erosions are present on endoscopic examination of a patient present with GORD
4
Q
What is NERD
A
Nonerosive reflux disease, where no erosions are present on endoscopic examination of a patient present with GORD
5
Q
What is the epidemiology of GORD
A
Common condition that affects between 10% and 30% of people in developed countries
There is a global variation, with less than 10% prevalence in East Asia
All age groups affected and no evidence for clear predictive factors
6
Q
What is the aetiology of GORD
A
The lower oesophageal sphincter regulates food passage from the oesophagus to the stomach and contains both intrinsic smooth muscle and skeletal muscle.
Episodes of transient lower oesophageal sphincter relaxation are normal but occur more frequently in GORD, causing reflux of gastric contents into the oesophagus.
This relaxation is more common after meals and is stimulated by fat in the duodenum
More likely to occur if there is a hiatal sac containing acid
Those with severe reflux often have a hiatus hernia and decreased resting lower oesophageal sphincter pressure but pressure can be high in mild to moderate reflux
7
Q
What are the risk factors for GORD
A
Obesity Hiatal hernia Pregnancy Connective tissue disorders (eg scleroderma) Delayed stomach emptying Older age Family history of heart burn or GORD Smoking Eating large meals or late at night Eating certain trigger foods (eg fatty or fried food) Drinking certain beverages (eg alcohol or coffee) Taking NSAIDs Psychological stress
8
Q
What is a hiatal hernia
A
Bulging of the top of the stomach into the diaphragm
9
Q
What is the difference between the lining of the oesophagus and that of the stomach
A
Oesophagus has squamous epithelial lining which is more sensitive to the effects of stomach acid than the stomach is due to its columnar epithelial lining which is more protective against stomach acid
10
Q
What other conditions present similarly to GORD
A
Acute coronary syndrome Stable angina Functional oesophageal disorder/ functional heartburn Achalasia Functional (non-ulcer) dyspepsia Peptic ulcer disease Eosinophilic oesophagitis Proton pump inhibitor responsive oesophageal eosinophilia Malignancy Laryngipharyngeal reflux
11
Q
What investigations would be performed for suspected GORD
A
PPI trial OesophagoGastroDuodenoscopy (OGD) Ambulatory pH monitoring Oesophageal manometry Combined impedance pH testing Barium swallow Oesophageal capsule endoscopy
12
Q
What does endoscopy assess for
A
Peptic ulcers
Oesophageal malignancy
Gastric malignancy
13
Q
Who would be admitted urgently for endoscopy
A
Patients with evidence of a GI bleed (melaena or coffee ground vomitining)
14
Q
What are the key red flag features for referral for endoscopy
A
Dysphagia at any age gets a 2 week wait referral Aged over 55 (generally the cut off for urgent vs routine referrals) Weight loss Upper abdominal pain and reflux Treatment resistant dyspepsia Nausea and/or vomiting Low haemoglobin Raised platelet count
15
Q
What is the management plan for GORD
A
Lifestyle advice:
- Reduce tea, coffee and alcohol
- Weight loss
- Smoking cessation
- Smaller, lighter meals
- Avoid heavy meals before bedtime
- Stay upright after meals rather than lying flat
Acid neutralising medication when required:
- Gaviscon
- Rennie
Proton pump inhibitors (reduce acid secretion in the stomach) (most effective acid suppressants):
- Omeprazole
- Lansoprazole
Ranitidine as an alternative to PPIs or can be used in bedtime adjunction with PPI in those with nocturnal symptoms, it is an H2 receptor antagonist (antihistamine) which reduces stomach acid
Surgery
16
Q
What is the surgery for GORD
A
A laparoscopic fundoplication
It involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter
17
Q
What is the prognosis for a patient with GORD
A
Most patients respond to treatment with PPIs
Maintenance PPI therapy recommended for those who’s symptoms relapse when the PPI is discontinued as well as for those with erosive oesophagitis or Barrett’s oesophagus
Barretts oesophagus may result after prolonged GORD
Oesophageal adenocarcinoma may be a serious though rare complication of GORD
18
Q
What is Helicobacter Pylori
A
H.pylori is a gram negative aerobic bacteria which lives in the stomach
It causes damage to the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer.
It avoids the acidic stomach environment by breaking into the gastric mucosa, thereby eclipsing the epithelial cells underneath the mucosa to the stomach acid.
H.pylori also produces ammonia, to neutralise the stomach acid, which directly damages the epithelial cells along with other chemicals the bacteria produce
19
Q
Who is offered an H.pylori test
A
Anyone with dyspepsia who has had 2 weeks without use of a PPI in order to achieve an accurate result.
20
Q
What are the 3 tests for H.pylori
A
Urea breath test (using radiolabelled carbon 13)
Stool antigen test
Rapid ureas test
21
Q
What is a Rapid Urease test
A
AKA the CLO test (Campylobacter-like organism test)
It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is then added to the sample. If H.pylori are present they will produce urease enzymes which converts the urea to ammonia, which makes the solution more alkali, resulting in a positive result when pH tested.
22
Q
What is eradication regime for treatment of H.pylori
A
Triple therapy with a PPI plus 2 antibiotics for 7 days
(eg. omeprazole, amoxicillin and clarithromycin)
The urea breath test then can be used as a test of eradication after treatment period but not routinely necessary.
23
Q
What is Barretts Oesophagus
A
Constant reflux of acid results in the lower oesophageal epithelium changing through metaplasia from squamous to columnar, with this change being called Barretts oesophagus. Typically once this change happens, a patient’s symptoms will improve
It is considered to be premalignant and is a risk factor for the development of adenocarcinoma of the oesophagus
24
Q
How is Barretts oesophagus managed
A
Regular endoscopy to monitor for adenocarcinoma
Treatment with PPIs and new evidence for regular aspirin use result in reduced risk of adenocarcinoma development
Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the columnar epithelium so it is replaced with normal cells. However this is not recommended in patients with no dysplasia but has a role in those with low and high dysplasia in preventing progression to cancer.
25
What is a peptic ulcer
A break in the mucosal lining of the stomach or duodenum more than 5mm in diameter with depth to the submucosa.
Ulcers smaller than this without obvious depth are called erosions
26
What is the epidemiology of peptic ulcers
Varied worldwide prevalence of ~0.12% to 1.5%
Incidence increases with age with gastric ulcers peaking from 50-69y/o and duodenal ulcers peaking 10 to 20 years earlier
Both sexes similarly affected
27
What is the aetiology of peptic ulcers
Two major causes:
- H.pylori infection
- Use of aspirin or NSAIDs
Rarer causes include:
- Gastric ischaemia (stress ulcers)
- Zollinger-Ellison syndrome
- Infections
- Crohn's disease
- Idiopathic
28
What is the pathophysiology of peptic ulcers
The stomach mucosa is prone to ulceration from:
-the breakdown of the protective layer of the stomach and duodenum
-the increase in stomach acid
There is a protective layer in the stomach comprised of mucus and bicarbonate secreted by the stomach mucosa, which can be broken down by medications (eg steroids or NSAIDs), or H.pylori
Increased acid can result from:
-stress
-alcohol
-caffeine
-smoking
-spicy foods
29
What are the risk factors for peptic ulcers
```
H.pylori infection
NSAID use
Smoking
Increasing age
Personal or family history of peptic ulcer disease
Patient in intensive care
```
30
How do peptic ulcers present
Epigastric discomfort or pain or tenderness
Pointing sign (show site of pain with one finger)
Nausea and vomiting
Early satiety
Weight loss
Diarrhoea
Anaemia (iron deficiency type)
GI bleed (coffee ground vomiting and melaena)
Hypotension
Septic shock
Succussion splash
Dyspepsia
Eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers
31
What other conditions present similarly to peptic ulcers
```
Oesophageal cancer
Stomach cancer
GORD
Gastroparesis
Billiary colic
Acute pancreatitis
Non-ulcer dyspepsia (functional dyspepsia)
Coeliac disease
IBS
Pleuritic pain
Pericarditis
```
32
How would a patient with suspected peptic ulcer be investigated
Upper GO endoscopy with rapid urease test (CLO test) to check for H.pylori
Biopsy should be considered to exclude malignancy
FBC
Fasting serum gastrin level
Urine NSAID screen
33
What should be discussed with a patient in peptic ulcer cases
```
Advise to avoid NSAID use
Continue to use aspirin if indicated for secondary prevention of cardiac events
Discuss risk and benefits of other anticoagulants
If H.pylori present, complete course of therapy, even if symptoms resolve
Seek medical attention if develop:
-blood in stools
-black tarry stools
-vomiting
-abdominal pain
Advise for long term management:
-smoking cessation
-annual review of condition
-Self-treatment with antacid
```
34
What is the treatment plan for patient with a peptic ulcer
Stop NSAID used where possible
Start high dose proton pump inhibitors for 4-8 weeks
Referral to specialist if unexplained or treatment resistant Gastro-oesophageal symptoms, or if H.pylori has not responded to second line eradication therapy
Endoscopy can be used to monitor the ulcer to ensure it heals and to assess for further ulcers
35
What are the potential complications of a peptic ulcer
Bleeding- common but potentially life threatening
Perforation- resulting in an 'acute abdomen' and peritonitis, requiring urgent surgical repair, usually laparoscopic
Scarring and strictures of the muscle and mucosa can lead to a narrowing of the pylorus (exit od the stomach) causing difficulty in emptying the stomach contents which is known as pyloric stenosis
36
How does pyloric stenosis present
```
Upper abdominal pain
Distension
Nausea
Vomiting
Particularly worse after eating
```
37
What is the prognosis for those with a peptic ulcer
With PPI therapy, duodenal ulcers usually heal within 4 weeks and gastric ulcers usually heal within 8 weeks
For those with peptic ulcers caused by H.pylori, prognosis after eradication is good with recurrence risk of duodenal ulcer being ~20% and that of gastric ulcer being ~30%
For those associated with NSAID use, discontinuation of NSAIDs will lead to low rate of ulcer recurrence
38
What is an upper GI bleed
A medical emergency involving some form of bleeding from the oesophagus, stomach or duodenum
39
What causes an upper GI bleed
Oesophageal varices
Mallory-Weiss tear (tear of the oesophageal mucous membrane)
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum
40
How does an upper GI bleed present
Haematemesis (vomiting blood)
Coffee ground vomit (vomiting digested blood which looks like coffee grounds)
Melaena (tar like, black, greasy and offensive stools caused by digested blood
Haemodynamic instability (occurs in large blood loss, causing low blood pressure, tachycardia and other songs of shock)
May have symptoms of underlying pathology such as:
-epigastric pain and dyspepsia in peptic ulcers
-jaundice for ascites in liver disease with oesophageal varices
41
What is the Glasgow-Blatchford score
Used as a scoring system in suspected upper GI bleeds on initial presentation to establish the patients risk of having an upper GI bleed to help form a management plan.
A score > 0 indicated high risk (use an online calculator to calculate the score)
Takes into account various features indicateing an upper GI bleed:
-Drop in Hb
-Rise in urea
-Blood pressure
-Heart rate
-Melaena
-Syncopy
42
Why does urea rise in an upper GI bleed
Blood in the GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is urea and this urea is then absorbed in the intestines
43
What is the Rockall Score
Used for patient that have had an endoscopy yo provide a percentage risk of rebreeding and mortality.
Use an online calculator to calculate the score
Takes in to account the risk factors from clinical presentation and endoscopy findings:
-Age
-Features of shock (tachycardia, hypotension etc)
-Co-morbidities
-Cause of bleeding (Mallory-Weiss, malignancy etc)
-Endoscopic stigmata of recent haemorrage such as clots or visible bleeding vessels
44
What is the management plan for those with an upper GI bleed
ABATED
A-ABCDE approach to immediate resuscitation
B-Bloods (FBC (Hb and platelets for coagulation), UandEs (urea), INR, LFTs (liver disease), Crossmatch for 2 units of blood)
A-Access (2 large-bore cannula)
T-Transfuse
E-Endoscopy
D-Drugs (stop anticoagulants and NSAIDs)
If oesophageal varices are suspected give:
- Terlipressin
- Prophylactic broad spectrum antibiotics
Definitive treatment is OGD to provide interventions that stop the bleeding (eg. variceal banding or cauterisation of the bleeding vessel)
NICE recommend against using a PPI prior to endoscopy but some senior doctors may still do this
45
What are the risk factors for an upper GI bleed
Chronic vomiting
Alcoholism
Medications such as NSAIDs and anticoagulants
GI surgery
46
What is the epidemiology of those with upper GI bleed
Most common GI emergency in UK
Incidence in the UK ranges from 50-150 per 100,000 per year
Men more commonly affected than women
Those in lower socioeconomic groups more commonly affected than those in higher groups
Incidence rises sharply with age
Accounts for ~5000 deaths per year in the UK
47
What are the differentials for those presenting with symptoms of an upper GI bleed
```
Peptic ulcer disease
Oesophageal varices
Oesophagitis
Mallory-Weiss tear
Boerhaave syndrome (spontaneous oesophageal perforation)
Gastric varices
Arteriovenous malformation
Dieulafoy's lesions
Upper GI tumours
Aortoenteric fistulae (AEF)
Coagulopathy
```
48
What is the prognosis after an upper GI bleed
Mortality of 2-10%
49
What should be transfused in those with an upper GI bleed
Transfusion is based on the individual presentation:
- Transfuse blood, platelets and clotting factors (fresh frozen plasma) in those with massive haemorrhage
- Transfusing more blood than necessary can be harmful
- Platelets should be given in active bleeding and thrombocytopenia
- Prothrombin Complex Concentrate can be given to those taking warfarin that are actively bleeding
50
What is indicative of thrombocytopenia
Platelets < 50
51
What are the two types of inflammatory bowel disease
Crohn's disease and Ulcerative colitis
52
What is Crohn's disease
A disorder of unknown aetiology characterised by a transmural inflammation of the GI tract. It may involve any or all parts of the entire GI tract from mouth to perianal area, although it is usually seen in the terminal ilium and perianal locations
Characterised by skip lesions, where normal bowel mucosa is found between diseased areas.
The inflammation often leads to fibrosis causing intestinal obstruction and can also result in sinus tracts that burrow through and penetrate the serosa, thereby leading to perforations and fistulae
53
What is inflammatory bowel disease
An umbrella term of the diseases which cause inflammation of the walls of the GI tract and have periods of remission and exacerbation
54
What is Ulcerative colitis
A type of IBD which characteristically involves the rectum and extends proximally to affect a variable length of the colon.
It is recognised as a multifactorial polygenic disease with unknown exact aetiology.
55
What are the Crohn's disease features which distinguish it from Ulcerative colitis
(think crows NESTS)
N- No blood or mucus
E- Entire GI tract
S- Skip lesions on endoscopy
T- Terminal ileum most affected and Transmural (full thickness) inflammation
S- Smoking is a risk factor (don't set the NEST on fire)
Crohn's is also associated with weight loss, strictures and fistulae
56
What are the Ulcerative colitis features which distinguish it from Crohn's disease
```
(remember U C CLOSEUP)
C- Continuous inflammation
L- Limited to colon and rectum
O- Only superficial mucosa affected
S- Smoking is protective
E- Excrete blood and mucus
U- Use aminosalicylates
P- Primary sclerosis cholangitis
```
57
What is the epidemiology of IBD
~0.3% prevalence in North America
~3 million adults in USA
Equally prevalent among men and women
More common in white people and Ashkenazi Jews
58
What are the risk factors for Crohn's disease
```
White ancestry
Age 15-40 or 60-80
Family history of CD
Cigarette smoker
High refined sugar diet
Oral contraceptive pill
Not breastfed
NSAID use
```
59
What are the risk factors for Ulcerative Colitis
```
Family history of IBD
HLA-B27 positive
Infection
NSAID use
Non-smoker or former smoker
```
60
How does Crohn's disease present
```
Abdominal pain
Prolonged diarrhoea
Perianal lesions
Bowel obstruction
Blood in stools
Fever
Fatigue
Abdominal tenderness
Weight loss
Oral lesions
Abdominal maa
Extra-intestinal manifestations (eg erythema nodosum or pyoderma gangrenosum)
```
61
How does Ulcerative colitis present
```
Rectal bleeding
Diarrhoea
Blood in stools
Abdominal pain
Arthritis and spondylitis
Malnutrition
Abdominal tenderness
Fever
Weight loss
Constipation
Skin rash
Uveitis and episcleritis
Pallor
```
62
What are the differentials for IBD
```
Both types (CD and UC) are differentials for each other
Infectious colitis
Indeterminate colitis
Pseudomembranous colitis
Ischaemic colitis
Radiation colitis
Yersinia enterocolitica
Internal tuberculosis
Amoebiasis
Cytomegalovirus colitis
Colorectal cancer
Diverticular disease
Acute appendicitis
Ectopic pregnancy
Pelvic inflammatory disease
Endometriosis
Irritable bowel syndrome
Vasculitis
```
63
How would IBD be investigated
Routine bloods for anaemia, infection, thyroid, kidney and liver function
CRP indicated inflammation and active disease
Faecal calprotectin is released by the intestines when inflamed so useful as a screening test and is more than 90% sensitive and specific to IBD in adults
Endoscopy (OGD and colonoscopy) with biopsy is diagnostic
Imaging with ultrasound, CT and MRI can be used to look for complications such as fistulae, abscesses and strictures
64
What is the management plan for those with Crohn's disease
Inducing remission:
- First line is steroid (eg oral prednisolone or IV hydrocortisone)
- If steroids alone don't work, consider adding immunosuppressant under specialist guidance (eg methotrexate, azathioprine or infliximab)
Mainting remission:
Treatment is tailored to patient based on risks, side effects, nature of disease and wishes. It is reasonable to not take medications whilst well.
-First line are azathioprine or mercaptopurine
-Alternatives are methotrexate, infliximab, adalimumab
Surgery:
If the disease is only affecting with distal ileum, it is possible to surgically resect this area and prevent further flares.
Surgery can also be used to treat strictures and fistulae secondary to Crohn's disease
65
What is the management plan for those with Ulcerative Colitis
Inducing remission:
Mild to moderate disease:
-First line - Aminosalicylate (eg mesalazine oral or rectal)
-Second line - Corticosteroids (eg prednisolone)
Severe disease:
-First line - IV corticosteroids (hydrocortisone)
-Second line - IV cyclosporin
Maintaining remission:
- Aminosalicylate
- Azathioprine
- Mercaptopurine
Surgery:
Panproctocolectomy to remove the colon and rectum will remove the disease as these are the sites typically affected.
The patient is then left with either a permanent ileostomy or and ileo-anal anastomosis (J-pouch), where the ileum is folded back on itself and fashioned into a larger pouch which functions as a rectum. This J-pouch is then attached to the anus and collects stools prior to the patient passing the motion.
66
What are the important discussions to have with a patient with IBD
Smoking cessation in CD
Maintain healthy balanced diet to prevent malnutrition
Avoid dairy products
Low fat diet after terminal ileum resection with medium triglyceride supplementation
Preoperative nutrition is of high importance to reduce post surgical complications
Regular exercise
Avoid NSAIDs
Avoid oral contraceptives
Advise on preventative vaccines if immunosuppressive treatments used
Seek medical advice if have any of the following symptoms:
-fever or chills
-bloody stools
-severe abdominal pain
-abdominal bloating and inability to pass stool or gas
-dizziness
-dehydration
-pus draining from anal area or abdominal wall
-intractable vomiting
-worsening of usual symptoms
-weight loss
Provide contacts for local support groups and educational sources (eg Crohn's and Colitis UK)
67
What is IBS
Irritable bowel syndrome is a chronic condition characterised by abdominal pain associated with bowel dysfunction. It is a diagnosis of exclusion meaning that a diagnosis is only made when other pathology is excluded. It is a functional bowel disorder meaning there is no identifiable disease underlying the symptoms and is the result of the abnormal functioning of an otherwise normal bowel
68
What is the epidemiology of IBS
Occurs in up to 20% of the population
| Affects women more than men and is more common in younger adults
69
What is the aetiology of IBS
Probably multifactorial and evidence suggests motility, inflammatory, genetic, immunological, psychological and dietary components
70
What are the risk factors for IBS
```
Physical and sexual abuse
PTSD
Age <50y/o
Female
Previous enteric infection
Stress
```
71
How does IBS present
```
Abdominal discomfort
Diarrhoea
Constipation
Fluctuating bowel habits
Change in bowel habits associated with pain
Abdominal bloating or distension
Normal examination of the abdomen
Passage of mucus with stool
Urgency of defecation
Symptoms worsen after eating
Symptoms improved by opening bowels
```
72
What are the criteria for diagnosis of IBS
Other pathology to be excluded:
- Normal FBC, ESR and CRP blood tests
- Faecal calprotectin negative to exclude IBD
- Negative coeliac disease serology (anti-TTG antibodies)
- Cancer is not suspect or is excluded if suspected
```
Symptoms should suggest IBS:
Abdominal pain and/or discomfort:
- relived on opening bowels or
-associated with a change in bowel habit
And 2 of:
- abnormal stool passage
- bloating
- worse symptoms after eating
- mucus with stools
```
73
What is the management of IBS
Provide reassurance that there is no serious underlying pathology
General healthy diet and exercise advice:
- Adequate fluid intake
- Regular small meals
- Reduce process foods
- Limit caffeine and alcohol
- Low FODMAP diet guided by a dietician
- Trial of probiotic supplements for 4 weeks
First line medication:
- Loperamide for diarrhoea
- Laxatives for constipation (avoid lactulose as it can cause bloating, Linaclotide is a specialist laxative for those who don't respond to first line laxatives)
- Antispasmodics for cramps (eg. buscopan)
Second line medication:
-Tricyclic antidepressants (ie amitriptyline 5-10mg at night)
Third line medication:
-SSRI antidepressants
CBT offered to help patients psychologically manage the condition and reduce distress associated with symptoms
74
What is acute gastritis
Inflammation of the stomach which presents with nausea and vomiting
75
What is enteritis
Inflammation the intestines which presents with diarrhoea
76
What is gastroenteritis
Inflammation all the way from the stomach to the intestines which presents with nausea, vomiting and diarrhoea
77
What is the most common type of gastroenteritis
Viral
78
What is the prognosis for gastroenteritis
It is very infectious so people with the diagnosis should isolate until 48 hours symptom free.
Most people recover well but it can be potentially fatal, especially in very young or very old people or those with comorbidities
79
What are the causes of gastroenteritis
Viral:
- Rotavirus
- Norovirus
- Adenovirus (less common)
Bacterial:
- E. coli
- Campylobacter Jejuni (most common bacterial cause worldwide)
- Shigella
- Salmonella
- Bacillus Cereus
- Yersinia Enterocolitica
- Staphylococcus Aureus toxin
Parasitic:
-Giardiasis
80
What are the characteristics of E. coli gastroenteritis
A normal intestinal bacteria with certain strain that cause gastroenteritis.
It is spread through contact with infected faeces, unwashed salads or contaminated water.
E.coli 0157 produces the Shiga toxin which causes abdominal cramps, bloody diarrhoea and vomiting. The Shiga toxin destroys blood cells and leads to haemolytic uraemic syndrome
The use of antibiotics increases the risk of haemolytic uraemic syndrome and so antibiotics should be avoided if this type of gastroenteritis is suspected
81
What are the characteristics of Campylobacter Jejuni gastroenteritis
AKA traveller's diarrhoea
Campylobacter means curved bacteria
It is a gram negative bacteria which is curved or spiral shaped
It is spread by:
- raw or improperly cooked poultry
- untreated water
- unpasteurised milk
Incubation is usually 2-5 days and symptoms resolve after 3 to 6 days. Symptoms are:
- abdominal cramps
- diarrhoea often with blood
- vomiting
- fever
Antibiotics can be considered after isolating the organism where patients have severe symptoms or other risk factors such as HIV or heart failure. Popular choices are azithromycin or ciprofloxacin
82
What are the characteristics of Shigella gastroenteritis
Shigella is a gram negative bacteria spread by faeces contaminating drinking water, swimming pools and food.
The incubation period is 2-5 days and symptoms usually resolve within a week without treatment.
It causes bloody diarrhoea. abdominal cramps and fever
Shigella can produce the Shiga toxin and cause haemolytic uraemic syndrome
Treatment of severe cases is with azithromycin or ciprofloxacin
83
What are the characteristics of Salmonella gastroenteritis
Salmonella is spread by eating raw eggs or poultry and food contaminated with the infected faeces of small animals
Incubation period is 12 hours to 3 days and symptoms usually resolve within 1 week
Symptoms are watery diarrhoea that can be associated with mucus and/or blood, abdominal pain, and vomiting
Antibiotics are only necessary in severe cases and guided by stool culture and sensitivities
84
What are the characteristics of Bacillus Cereus gastroenteritis
Bacillus Cereus is a gram positive rod that is spread through inadequately cooked food and grows well on food not immediately refrigerated after cooking. The typical food is fried rice left out at room temperature
Whilst growing on the food it produced the toxin cereulide that causes abdominal cramping and vomiting within 5 hours of ingestion. When it arrives in the intestines it produces different toxins which cause a watery diarrhoea which occurs more than 8 hours after ingestion. All of the symptoms usually resolve within 24 hours
Typical course is vomiting after 5 hours, diarrhoea after 8 hours and resolution of symptoms after 24 hours
85
What are the characteristics of Yersinia Enterocolitica gastroenteritis
Yersinia is a gram negative bacillus. Pigs are key carriers and consumption of raw or undercooked pork can cause infection. It is also spread through contamination with the urine or faeces of other mammals such as rats and rabbits
Most frequently affects children, causing watery or bloody diarrhoea, abdominal pain, fever and lymphadenopathy. Older children or adults can present with right sided abdominal pain due to mesenteric lymphadenitis (inflammation in the intestinal lymph nodes) and fever, which can give the impression of appendicitis
Incubation is 4 to 7 days with symptoms lasting 3 weeks or more.
Antibiotics are only necessary in severe cases and guided by stool culture and sensitivities
86
What are the characteristics of Staphylococcus Aureus Toxin caused gastroenteritis
Staphylococcus Aureus can produce enterotoxins when going on food such as eggs, dairy and meat . When eaten, these toxins cause small intestine inflammation, causing symptoms of diarrhoea, perfuse vomiting, abdominal cramps and fever. These symptoms start within hours of ingestion and settle within 12 to 24 hours.
It is not the bacteria causing the enteritis but the staphylococcus enterotoxin
87
What are the characteristics of Giardiasis
Giardia lamblia is a type of microscopic parasite which lives in the small intestines of mammals (pets, farmyard animals or humans) It releases cysts in the stools of infected mammals which contaminate food or watering are eaten, infecting the new host (faecal-oral transmission)
Infection may mot cause any symptoms or it may cause chronic diarrhoea.
Diagnosis made by stool microscopy.
Treatment is with metronidazole
88
What are the principles of gastroenteritis management
Good hygiene to help prevent gastroenteritis
Isolation of patients with symptoms immediately to prevent spread
A sample of faeces can be tested with microscopy, culture and sensitivities to establish cause and antibiotic sensitivity
Assess patients for dehydration
Attempt a fluid challenge and if able to tolerate oral fluid and are adequately hydrated, consider outpatient management
If tolerated and not vomiting then use rehydration solutions (eg. dioralyte)
If dehydrated then IV fluids can be used to rehydrate them and prevent dehydration until oral intake adequate again.
Slowly introduce a light diet once oral intake tolerated
Advise to stay off work/school for 48 hours after symptoms have completely resolved
Antidiarrhoeals and antiemetics are not recommended
Antibiotics only to be given in those at risk of complications and once the causative organism is confirmed
89
What are some potential post gastroenteritis complications
Lactose intolerance
IBS
Reactive arthritis
Guillain-Barré syndrome
90
What are the symptoms of chronic pancreatitis
```
Dull epigastric pain which bores through to the back and is relieved by sitting forward or placing a hot water bottle on epigastrium or back and worse ~ 30 mins after eating
Bloating/distension
SOB
Steatorrhoea
Weightloss and malnutrition
Diabetes/ glucose intolerance
Nausea and vomiting
Skin nodules
Painful joints
Low-trauma fracture
Jaundice
Symptoms relapse and worsen over time
```
91
What are the causes of chronic pancreatitis
```
Alcohol
Smoking
Idiopathic
Autoimmunity
Family history
Cystic fibrosis
Haemochromatosis
Pancreatic duct obstruction (stone/tumour)
Congenital (pancreas divisum
```
92
How is suspected chronic pancreatitis investigated
```
MRI or CT scan looking for pancreatic calcifications
s-MRCP
Endoscopic ultrasonography
Histological examination
Genetic testing
Faecal elastase-1 (indirect pancreatic function test)
Faecal fat
Steatocrit
Direct pancreatic function tests
IgG4 levels
Therapeutic trial of corticosteroids
```
93
What is the Sarles Classification
Sarles classification of chronic pancreatitis, classifies into 3 major groups:
- Obstructive pancreatitis
- Inflammatory pancreatitis
- Lithogenic or calcifying chronic pancreatitis
94
What is the TIGAR-O classification
The TIGAR-O aetiological classification of chronic pancreatitis looks at the various causes of the disease and consists of six groups:
- Toxic-metabolic
- Idiopathic
- Genetic
- Autoimmune
- Recurrent and severe acute pancreatitis
- Obstructive
95
What are the toxic metabolic classified chronic pancreatitis types
```
Alcohol
Tobacco smoking
Hypercalcaemia
Hyperlipidaemia
Chronic kidney disease
Medicines (phenacetin abuse)
Toxins (organotin compounds eg. di-N-butyltin dichloride (DBTC))
```
96
What are the idiopathic classified chronic pancreatitis types
Early onset
Late onset
Tropical
97
What are the genetic classified chronic pancreatitis types
- Hereditary pancreatitis (cationic trypsinogen mutations)
- Cystic fibrosis transmembrane conductance regulator (CFTR) mutations
- Serine protease inhibitor Kazal type 1 (SPINK1) mutations
- Chymotrypsinogen C (CTRC) mutations
- Calcium-sensing receptor (CaSR, CSR) mutations
- Claudin-2 (CLDN2) mutations
- Carboxypeptidase A1 (CPA1)
- Fucosyltransferase 2 (FUT2) non-secretor status
- ABO blood group type B
98
What are the autoimmune classified chronic pancreatitis types
Isolated autoimmune chronic pancreatitis
| Syndromic autoimmune chronic pancreatitis associated with Sjogren's syndrome, IBD, primary billiard cirrhosis
99
What are the recurrent and severe acute classified chronic pancreatitis types
Post-necrotic (severe acute pancreatitis)
Recurrent acute pancreatitis
Vascular diseases/ ischaemia
Post-irradiation
100
What are the obstructive classified chronic pancreatitis types
```
Pancreas divisum
Sphincter of Oddi disorders
Duct obstruction (eg solid tumor, intra-suctal papillary mucinous neoplasm)
Peri-ampullary duodenal wall cysts
Post-traumatic pancreatic duct scars
```
101
What is the Cambridge classification for chronic pancreatitis
The Cambridge classification of endoscopic retrograde cholangiopancreatography (ERCP) (and ultrasound [US] or computed tomography [CT] imaging) grades the severity of pancreatic structural changes based on abnormalities of the main duct and side branches.
102
What is steatorrhea
An increase in fat excretion in the stools
103
What are the risk factors for chronic pancreatitis
```
Alcohol
Smoking
Family history
Coeliac disease
Psoriasis
High-fat, high protein diet
Tropical geography
```
104
How is chronic pancreatitis managed
- alcohol and smoking cessation
- dietary advice and supplementation of fat-soluble vitamins due to malabsorption of fat and protein
- pancreatic enzyme replacement therapy
- PPI or H2 antagonist may be needed for gastric acid suppression to improve absorption
- Pain can be managed with simple analgesia and adjunct weak opioid if necessary, and increasing up the pain ladder may be needed as the illness progresses
- Endoscopic treatment to dilate strictures, remove stones or drain pseudocysts
- Surgical management is last resort and has three general strategies:
- - decompression (drainage)
- - denervation
- - resection
105
What is pancreatitis
A clinical diagnosis defined by pancreatic inflammation
106
What is chronic pancreatitis
Characterised by recurrent or persistent abdominal pain and progressive injury to the pancreas and surrounding structures, resulting in scarring and loss of function
107
What are the differentials in cases of suspected chronic pancreatitis
```
Pancreatic cancer
Acute pancreatitis
Biliary colic
Peptic ulcer disease
Mesenteric ischaemia
Abdominal aortic aneurysm
MI
Intestinal obstruction
IBS
Gastroparesis
Somatisation disorder
Radiculopathy
Post-herpetic neuralgia
Abdominal wall pain
Nephrolithiasis
```
108
What advice should be given to a patient following diagnosis of chronic pancreatitis
Lead and healthy lifestyle (low-fat diet, no alcohol and no smoking)
Give contact details for help with smoking or alcohol cessation
109
What is acute pancreatitis
A self-liming and reversible pancreatic injury associated with mid-epigastric abdominal pain and elevated serum pancreatic enzymes
A disorder of the exocrine pancreas and is associated with acinar cell injury with local and systemic inflammatory responses
110
How does acute pancreatitis present
- Sudden onset mid-epigastric or left upper quadrant pain that radiates to the back and is constant and severe, described as like being stabbed with a knife, and worsens with movement and sometimes better when curled in foetal position, is the most common presenting symptom
- Tender and distended abdomen with voluntary guarding to palpation of the upper abdomen
- Nausea and vomiting
- Hypovolaemia
- Pleural effusion
- Anorexia
- Organ dysfunction
- dyspnoea
- Jaundice
- Hypocalcaemia (rare)
- Ecchymotic bruising and discolouration
111
What are the signs of hypovolaemia
```
Hypotension
Oliguria
Dry mucous membranes
Decreased skin turgor
Sweating
Tachycardia
Tachypnoea
```
112
What is the epidemiology of acute pancreatitis
Incidence is approximately 56 per 100,000 per year in the UK, with the overall mortality rate being around 5%, rising to 25% in severe disease.
In the UK, around 50% of cases are caused by gallstones, 25% by alcohol, and 25% by other factors
Gallstone pancreatitis is more common in white women >60 years of age, especially among patients with microlithiasis. Alcoholic pancreatitis is seen more frequently in men
113
What are the risk factors for acute pancreatitis
```
Middle aged women
Young to middle aged men
Gallstones
Alcohol
Hypertriglyceridaemia
Use of causative drugs (eg. azathioprine, thiazide diuretics, furosemide)
ERCP
Trauma
Systemic lupus erythematosus
Sjogren's syndrome
Hypercalcaemia
Mumps
Coxsackievirus
Mycoplasma pneumoniae
Pancreas divisum
Pancreatic cancer
Sphincter of Oddi dysfunction
Family history of pancreatitis
```
114
What are some causes of acute pancreatitis
```
Gallstones
Alcohol
Idiopathic
Malignancy
Trauma
Infection
Drugs
Autoimmunity
Hypercalcaemia
Hypertriglyceridaemia
```
115
What is the Atlanta classification of acute pancreatitis
The revised classification of acute pancreatitis identifies an early and a late phase of the disease. Severity is classified as mild, moderate, or severe.
Mild:
- Most common
- No organ failure
- No local or systemic complications
- Resolves within 1 week
Moderate:
-Presence of transient organ failure which resolves within 48 hours and/or local complications or exacerbation of comorbid disease
Severe:
- Persistent organ failure (>48 hours)
- Local complications are peri-pancreatic fluid collections, pancreatic and peri-pancreatic necrosis, pseudocyst, and walled off necrosis
116
What are the differentials in suspected acute pancreatitis
```
Peptic ulcer disease
Perforated viscous
Oesophageal spasms
Intestinal obstruction
Abdominal aortic aneurysm
Cholangitis
Choledocholithiasis
Cholecystitis
Viral gastroenteritis
Hepatitis
Mesenteric ischaemia
Myocardial infarction
```
117
What are the important discussions to have with a patient with acute pancreatitis
Advise on modifiable lifestyle risk factors, alcohol, dietary advice of low fat meals of carbohydrates and proteins with a gradual increase in quantity over a period of 3-6 days as tolerated
118
What is the management plan in acute pancreatitis
Goals: provide supportive treatment to reduce the risk of progression to organ failure and/or local complications.
Initial supportive treatment with fluid resuscitation, oxygen, pain control, an antiemetic and nutrition support.
Treat underlying cause and local complications
119
What is gallstone disease
AKA Cholelithiaisis
The presence of solid concretions in the gallbladder
Gallstones form in the gallbladder but may exit into the bile ducts (choledocholithiasis)
Symptoms issue if a stone obstructs the cystic, bile or pancreatic duct.
120
What is the epidemiology of gallstone disease
10-15% of adults in the US and Europe
Prevalence rates are low in Africa and Asia
Generally asymptomatic in >80% of people
Age, obesity and female sex hormones are important etiological factors
121
What causes gallstone formation
Most gallstones in developed countries (>90%) consist of cholesterol.
Cholesterol gallstone formation begins with the secretion of bile supersaturated with cholesterol from the liver.
Initiated by nucleating factors such as mucin, microscopic crystals then percipitate in the gallbladder where hypomotility provides time for stone growth.
122
What are the risk factors for Gallstone disease
```
Increasing age
Female sex
Obesity
Diabetes
Metabolic syndrome
Family history of gallstones
Gene mutation
Pregnancy
Exogenous oestrogen
Non-alcoholic liver disease
Prolonged fasting/rapid weight loss
Total parenteral nutrition
Medication
Terminal ileum disease or resection
Haemoglobinopathy
Hispanic and Native-American ethnicity
Low-fibre diet
H-pylori gallbladder infection
```
123
How does gallstone disease present
Right upper quadrant or epigastric pain or tenderness (typically lasting >30 minutes)
Postprandial pain (around an hour after eating)
Nausea
Jaundice
124
What are the differentials in suspected gallstone disease
```
Peptic ulcer disease
Gallbladder cancer
Gallbladder polyps
Acalculous cholecystitis
Sphincter of Oddi dysfunction (SOD)
Non-biliary acute pancreatitis
```
125
How would a patient with suspected gallstones be investigated
Abdominal ultrasound
Serum LFTs
FBC
Serum lipase or amylase
Magnetic resonance cholangiopancreatography (MRCP)
Endoscopic ultrasound scan
Abdominal CT scan
126
What are the important discussions to have with a patient with gallstone disease
Reassure that asymptomatic gallbladder stones found incidentally do not need treatment unless they develop symptoms (provided the gallbladder and biliary tree are normal)
Advise to avoid food and drink that triggers their symptoms until they have their gallbladder or stones removed
Explain that do not need to avoid food and drink the triggered their symptoms after they have had it removed
Consult doctor if develop abdominal pain, fever, nausea, vomiting, anorexia or mental status changes after surgery.
127
What is the management plan for patients with gallstone disease
Treat biliary colic with an NSAID drug (diclofenac or indometacin) in combination with an anti-spasmodic if needed
Paracetamol might be sufficient in some cases
For severe symptoms, use an opioid (ideally buprenorphine)
Symptomatic gallstones with no cholecystitis, offer patient laproscopic cholecystectomy
Offer bile duct clearance and laparoscopic cholecystectomy to patients with bile duct stones, whether symptomatic or asymptomatic.
Clear bile duct either:
-With endoscopic retherograde cholangiopanreatography (ERCP) before or at the same time as laparoscopic cholecystectomy
-Surgically via laparoscopic bile duct exploration at the time of laparoscopic cholecystectomy
128
What is the prognosis for a patient with gallstone disease
Outlook for those who have a cholecystectomy is favourable
Same for those whith choledocholithiasis who undergo ERCP with biliiary sphincterotomy and stone extraction, followed later by cholecystectomy
129
What is hepatitis?
Hepatitis describes inflammation in the liver. this can vary from a chronic low level inflammation to acute and severe inflammation that leads to large areas of necrosis and liver failure
130
What are the causes of hepatitis
```
Alcoholic hepatitis
Non alcoholic fatty liver disease
Viral hepatitis
Autoimmune hepatitis
Drug induced hepatitis
```
131
How does hepatitis present
Can be asymptomatic or present with non-specific symptoms:
- abdominal pain
- fatigue
- pruritis (itching)
- muscle and joint aches
- nausea and vomiting
- jaundice
- fever (viral hepatitis)
132
What are the usual biochemical findings in hepatitis
Liver function tests become deranged with high transaminases (AST and ALT) and proportionally less of a rise in ALP. This is referred to as a hepatic picture
Bilirubin can also rise as a result of inflammation of liver cells
133
What are transaminases
AST and ALT
| Liver enzymes which are released into the blood as a result of inflammation of the liver cells
134
A rise in which chemical causes jaundice
Bilirubin
135
What is Hepatitis A
The most common viral hepatitis worldwide but relatively rare in the UK with less than 1000 cases in England and Wales in 2017
It is an RNA virus
Transmitted faecal-orally in contaminated food and water
It is a notifiable disease
136
How does Hep A present
Nausea
Vomiting
Anorexia
Jaundice
137
What is a complication of Hep A and how would this present
Cholestasis - slowing of bile flow through the biliary system
Dark urine
Pale stools
Moderate hepatomegaly
138
What is the management of Hep A
Resolves without treatment in ~1 to 3 months
Manage with simple analgesia
Vaccination available to reduce chance of developing the infection
139
What is Hepatitis B
A DNA virus
Transmitted by direct contact with blood or bodily fluids (eg sexually or shared needle use) or by vertical transmission during childbirth
140
What is the prognosis for those with Hep B
Most people recover within 2 months but 10-15% go on to become chronic hepatitis carriers when the virus DNA becomes integrated into their own DNA and so they continue to produce proteins
141
How are patients tested for Hep B
Test HBcAb (core antibodies) for previous infection and HBsAg (surface antigen) for active infection. If these are both positive then further testing for HBeAg (E antigen which is a marker of viral replication and implies high infectivity) and HBV DNA (for direct count of the viral load)
IgM version of HBcAB implies an active infection and will give a high titre with an acute infection and a low titre with a chronic infection. The IgG version indicated a past infection where HBsAg is negative.
The presence of HBeAg implies an acute phase of the infection where the virus is actively replicating.
The level of HBeAg correlates with the infectivity of the patient, where hight means they are highly infectious to others
142
How does the Hep B vaccine work
Involves injecting the hep B surface antigen
HBsAb demonstrates an immune response to HBsAg.
HBsAg is given in the vaccine so having a positive HBsAb may simply indicate the patient has been vaccinated and created an immune response to the vaccine so vaccinated people are tested for HBsAb to confirm their response
The vaccine requires 3 doses at different intervals
143
What is the management for Hep B
Have a low threshold for screening patients at risk of hep B
Screen for other blood born viruses (hep a, b and HIV) and other STDs
Refer to gastroenterology, hepatology or infectious diseases for specialist management
Notify PHE
Smoking and alcohol cessation
Educate about reducing transmission and informing at risk contacts
Test for complications (fibroscan for cirrhosis and ultrasound for hepatocellular carcinoma)
Antiviral meds can be used to slow progression of disease and reduce infectivity
Liver transplantation for end stage liver disease
144
What is Hep C
An RNA virus spread by blood and body fluids
| No vaccine available but now curable with direct acting antiviral meds
145
What is the prognosis for those with hep C
1 in 4 fights off the virus and makes a fill recovery
| 3 in 4 it becomes chronic
146
What are the complications of Hep C
Liver cirrhosis and associated complications of cirrhosis
| Hepatocellular carcinoma
147
How is Hep C tested for
Hepatitis C antibody screening test
Hepatitis C RNA testing is used to confirm diagnosis of Hep C, calculate viral load and assess for the individual genotype
148
What is the management for Hep C
Have a low threshold for screening patients at risk of hep B
Screen for other blood born viruses (hep a, b and HIV) and other STDs
Refer to gastroenterology, hepatology or infectious diseases for specialist management
Notify PHE
Smoking and alcohol cessation
Educate about reducing transmission and informing at risk contacts
Test for complications (fibroscan for cirrhosis and ultrasound for hepatocellular carcinoma)
Antiviral treatment with direct acting antivirals is tailored to the specific viral genotype and successfully cures >90% and is taken for 8-12 weeks
Liver transplantation for end stage liver disease
149
What is Hepatitis D
An RNA virus
Can only survive in patients who also have Hep B
Attaches self to HBsAg to survive and cannot survive without this protein
Very low rates in UK
Increases with complications and severity of Hep B
No treatment for Hep D
Notifiable disease
150
What is Hep E
An RNA virus
Transmitted faecal-orally
Very rare in UK
Normally causes very mild illness which resolves within a month and no treatment needed
Rarely it can progress to chronic hepatitis and liver failure, more often this is in those immunocompromised
No vaccine
Notifiable disease
151
What is Autoimmune Hepatitis
A rare cause of chronic hepatitis
Unknown exact aetiology
The T cells of the immune system recognise the liver cells as being harmful and alert the rest of the immune system to attack these cells
152
What are the two types of Autoimmune Hepatitis and how are they distinguishable
Type 1:
- in adults
- in woman around late forties or fifties present around or post menopause with fatigue and features of liver disease on examination
- less acute presentation
- Antibodies:
- - Anti-nuclear antibodies (ANA)
- - Anti-smooth muscle antibodies (anti-actin)
- - Anti-soluble liver antigen (anti-SLA/LP)
Type 2:
- in children
- patients in teenage years or early twenties present with acute hepatitis with high transaminases and jaundice
- Antibodies:
- - Anti-liver kidney microsomes-1 (anti-LKM1)
- - Anti-liver cytosol antigen type 1 (anti-LC1)
153
How is Autoimmune Hepatitis diagnosed
Liver biopsy
154
How is Autoimmune Hepatitis treated
With high dose steroids (prednisolone) that are tapered over time as other immunosuppressants (eg. azathioprine) are introduced.
Immunosuppression is usually successful in inducing remission but is usually required life long.
Liver transplantation may be required in end stage liver disease, however autoimmune hepatitis can recur in the transplanted liver
155
What is appendicitis
Inflammation of the appendix
156
What is the epidemiology of appendicitis
Peak incidence is in patients aged 10-20 y/o
| It can occur at any age but is less common in younger children and adults over 50 y/o
157
How does appendicitis present
- Abdominal pain that starts centrally and moves down to the right iliac fossa within the first 24 hours, eventually becoming localised in the RIF
- Tender on palpation at McBurney's point
- Loss of appetite (anorexia)
- Nausea and vomiting
- Rovsing's sign
- Guarding on abdominal palpation
- Rebound tenderness in RIF
- Percussion tenderness
158
Where is McBurney's point
A specific area one third of the distance from the anterior superior iliac spine to the umbilicus
159
What is Rovsin's sign
Palpation of the left iliac fossa causes pain in the right iliac fossa
160
What is rebound tenderness
Increased pain when suddenly release the pressure of deep palpation
161
What do rebound tenderness and percussion tenderness in suspected appendicitis indicate
Peritonitis and therefore a potentially ruptured appendix
162
What is percussion tenderness
Pain and tenderness when percussing the abdomen
163
What are the differentials of suspected appendicitis
Ectopic pregnancy
Ovarian cysts
Meckel's diverticulum
Mesenteric adenitis
164
How is suspected appendicitis investigated
CT scan
Ultrasound to exclude ovarian and gynaecological pathology and in children due to CT scan having too high a dose of radiation
Raised inflammatory markers
Mostly a clinical diagnosis, where unclear, observation period used, with repeated examinations to see if symptoms resolve or worsen
If clinical presentation suggestive of appendicitis but investigations are negative, next step id a diagnostic laparoscopy to visualise appendix directly, the surgeon can proceed to an appendicectomy during same procedure id indicated
165
What are the complications of an appendicectomy
```
Bleeding, infection, pain and scars
Damage to bowel, bladder or other organs
Removal of normal healthy appendix
Anaesthetic risks
Venous thromboembolism
```
166
How is appendicitis managed
Emergency admission to hospital under surgical team
Removal of the inflamed appendix (appendicectomy) is the definitive management for acute appendicitis
Laparoscopic surgery is associated with fewer risks and faster recovery compared to open surgery (laparotomy)
167
What is a bowel obstruction
When the passage of food, fluids and gas, through the intestines, becomes blocked.
Obstruction results in a build up of gas and faecal matter proximal (before) to the obstruction causing back-pressure, resulting in vomiting and dilation of the intestines proximal to the obstruction.
Bowel obstruction is a surgical emergency.
Small bowel obstruction is more common than large bowel obstruction
168
What is third-spacing in a bowel obstruction
The abnormal loss of fluid, resulting from the fluid usually secreted from the GI tract to be absorbed by the colon, being unable to reach the colon due to the obstruction and thereby unable to be absorbed.
The result is fluid loss from the intravascular space into the GI tract, leading to hypovolaemia and shock.
The higher up the intestine the obstruction is, the greater the fluid losses as there is less bowel over which the fluid can be reabsorbed
169
What are the causes of bowel obstruction
Top three (accounting for ~90%) are:
- Adhesions (small bowel)
- Hernias (small bowel)
- Malignancy (large bowel)
Other causes are:
- Volvulus (large bowel)
- Diverticular disease
- Strictures (eg secondary to Crohn's disease)
- Intussusception (in kids age 6 months to 2 years)
170
What are adhesions within the bowel
Pieces of scar tissue that bind the abdominal contents together.
They can cause kinking or squeezing of the bowel, leading to obstruction
171
What are the main causes of intestinal adhesions
Abdominal or pelvic surgery (particularly open surgery)
Peritonitis
Abdominal or pelvic infection (eg. pelvic inflammatory disease)
Endometriosis
Congenital
Secondary to radiotherapy treatment
172
What is a closed loop bowel obstruction
A situation where there are two points of obstruction along the bowel, resulting in a middle section sandwiched between two points of obstruction
May happen with:
-Adhesions which compress two areas of bowel
-Hernias that isolate a section of bowel blocking either end
-Volvulus where the twist isolates a section of intestine
-A single point of obstruction in the large bowel with an ileocaecal valve that is competent, resulting in an isolated section of bowel with contents that cannot flow in either direction
Since the contents of a closed loop section of bowel do not have an open end where they can drain and decompress, the section will continue to expand, leading to ischaemia and perforation
This type of obstruction requires emergency surgery
173
What is a competent ileocaecal valve
It does not allow any movement back into the ileum from the caecum and
174
How does a bowel obstruction present
Vomiting (particularly green bilious vomiting)
Abdominal distension
Diffuse abdominal pain
Absolute constipation and lack of flatulence
Tinkling bowel sounds on ausculation in early bowel obstruction
175
What are the X ray findings for bowel obstruction
Distended loops of bowel
Valvulae conniventes in the small bowel which are mucosal folds that form lines extending the full width of the bow eland are seen on an abdominal x-ray as lines across the entire width of the bowel
Haustra are like pouches formed by the muscles in the walls of the bowel and form lines that do not extend the full width of the bowel and are seen on an abdominal x-ray as lines that extend only part of the way across the bowel
176
What are the normal upper limits for the diameter of bowel
3cm small bowel
6cm colon
9cm caecum
177
How is bowel obstruction initially managed
```
Start with ABCDE approach
Patients with bowel obstruction may be haemodynamically unstable and require urgent intervention if they have developed:
-hypovolaemic shock
-bowel ischaemia
-bowel perforation
-sepsis
```
A full set of bloods, look especially for:
- electrolyte imbalances (U and Es)
- metabolic alkalosis due to vomiting stomach acid (venous blood gas)
- bowel ischaemia (raised lactate on either VBG or lab sample)
Initial management is known as drip and suck:
- nil by mouth
- IV fluids to hydrate and correct electrolyte imbalances
- NG tube with free drainage to allow stomach contents to freely drain and reduce the risk of vomiting and aspiration
Abdominal Xray or CT scan
Erect chest X ray can demonstrate air under the diaphragm when there is an inter abdominal perforation
Contrast abdominal CT usually required to confirm diagnosis and establish the site and cause of the obstruction and diagnose an intra-abdominal perforation if one is present
178
How is a bowel obstruction surgically managed
When conservative management fails, surgery is required
Definitive management with surgery to correct underlying cause:
-Exploratory surgery in patients with unclear underlying cause
-Adhesiolysis to treat adhesions
-Hernia repair
-Emergency resection go the obstructing tumour
May be laparoscopy or laparotomy
Stents may be inserted into the bowel (during colonoscopy) in patients with obstruction due to a tumour to hold the tumour out of the way and create space for the bowel contents to move through
179
What is a hernia
Hernias occur when there is a weak pint in a cavity wall, usually affecting the muscle or fascia.
This weakness allows a body organ (eg. bowel) that would normally be contained within the cavity, to pass through the cavity wall
180
What are inguinal hernias
Present with a soft lump in the inguinal region in the groin
There are two types:
-Indirect
-Direct
181
What are the differentials for a lump in the inguinal region
```
Inguinal hernia
Femoral hernia
Lymph node
Saphena varix
Femoral aneurysm
Abscess
Undescended/ectopic testes
Kidney transplant
```
182
What is saphena varix
Dilation of saphenous vein at the junction with the femoral vein in the groin
183
What is an indirect inguinal hernia
Where the bowel herniated through the inguinal canal
Normally after tests descend through the inguinal canal the deep inguinal ring closes and the processus vaginalis is obliterated.
However, in some patients, the inguinal ring remains patent and the processus vaginalis remains intact, so leaves a tract from the abdominal contents, through the inguinal canal and into the scrotum.
The bowel can herniate along this tract and create an indirect inguinal hernia
184
What is the inguinal canal
A tube that runs between the deep inguinal ring (where it connects to the peritoneal cavity) and the superficial inguinal ring (where it connects to the scrotum/ or superior to the pubic tubercle in females)
In males, allows spermatic cord and contents to travel inside the peritoneal cavity, though the abdominal wall and into the scrotum
In females, the round ligament is attaches to the uterus and passes through the deep inguinal ring, inguinal canal and then attaches to the labia majora
185
What is the processes vaginalis
During foetal development, the processus vaginalis is a pouch of peritoneum that extends from the abdominal cavity through the inguinal canal to allow the testes to descend from the abdominal cavity, through the inguinal canal and into the scrotum.
186
What is the specific finding of indirect inguinal hernias which helps to differentiate them from direct inguinal hernias
When an indirect hernia is reduced and pressure is applied with two finger tips to the deep inguinal ring (at the mid- way point from the ASIS to the pubic tubercle) the hernia will remain reduced
187
What is a direct inguinal hernia
Occurs due to weakness in the abdominal wall at Hesselbach's triangle.
The hernia protrudes directly through the abdominal wall, through Hesselbach's triangle and not along a canal or tract like in an indirect type.
Pressure over the deep inguinal ring will not stop the herniation
188
What are the boundaries of Hesselbach's triangle
RIP mnemonic
R- rectus abdominis muscle (medial border)
I- inferior epigastric vessels (superior/ lateral border)
P- puppet's ligament (inguinal ligament) (inferior border
189
What are femoral hernias
Involve herniation of the abdominal contents through the femoral canal which is below the inguinal ligament at the top of the thigh
The opening between the peritoneal cavity and the femoral canal is the femoral ring which only leaves a narrow opening for femoral hernias.
190
What are femoral hernias at high risk of
Incarceration
Obstruction
Strangulation
191
What are the boundaries of the femoral canal
```
FLIP mnemonic
F – Femoral vein laterally
L – Lacunar ligament medially
I – Inguinal ligament anteriorly
P – Pectineal ligament posteriorly
```
192
What are the boundaries of the femoral triangle
SAIL mnemonic
S – Sartorius – lateral border
A – Adductor longus – medial border
IL – Inguinal Ligament – superior border
193
What are the contents of the femoral triangle
From lateral to medial across the top of the thigh, use NAVY-C
N – femoral Nerve
A – femoral Artery
V – femoral Vein
Y-C – Y-fronts and femoral Canal (containing lymphatic vessels and nodes)
194
How do hernias tend to present
A soft lump protruding from the abdominal wall
The lump may be reducible (it can be pushed back into the normal place)
The lump may protrude on coughing (raising intra-abdominal pressure) or standing (pulled out by gravity)
Aching, pulling or dragging sensation
195
What are the three key complications of hernias
Incarceration (it is irreducible)
Obstruction (causes a blockage of passage of faeces through the bowel)
Strangulation (non-reducible and the base becomes so tight that it cuts off the blood supply causing ischaemia)
196
Why is the neck size of a hernia important
Hernias that have a wide neck, meaning that the size of the opening that allows abdominal contents through is large, are at lower risk of complications. While the contents can easily pass out of this opening, they can also easily be put back, which puts them at a lower risk of incarceration, obstruction and strangulation. When assessing a hernia, always comment on the size of the neck/defect (narrow or wide), as this will help formulate a risk assessment and management plan for the hernia (such as how urgently they need to be operated on).
