Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

!Final Year > Gastrointestinal (2) > Flashcards

Gastrointestinal (2) Flashcards

1
Q

What is Gastro-oesophageal reflux disease (GORD)?

A

Inflammation of the oesophagus caused by reflux of gastric acid and/or bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the aetiology of Gastro-oesophageal reflux disease (GORD)?

A
  1. The lower oesophageal sphincter (LOS) regulates food passage from the oesophagus to the stomach
  2. Episodes of transient lower oesophageal sphincter relaxation are a normal phenomenon, but they occur more frequently in GORD
  3. This causes reflux of gastric contents into the oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the epidemiology of Gastro-oesophageal reflux disease (GORD)?

A
  1. GORD is a common condition that affects between 10% and 30% of people in developed countries
  2. All age groups are affected but risk increases with age and obesity
  3. FH association
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the features of GORD?

A
  1. Substernal burning discomfort or heartburn:
    a. Aggravated by lying supine or bending
    b. Large meals and drinking alcohol
  2. Regurgitation of gastric contents
  3. Dysphagia (caused by formation of peptic stricture after long-standing reflux)
  4. Bloating/ early satiety
  5. Pain relieved by antacids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the features of aspiration from GORD?

A

RARE, may result in:
1. Voice hoarseness
2. Laryngitis
3. Nocturnal cough and wheeze with (out) pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the indications for an upper GI endoscopy in GORD?

A
  1. Age > 55 years
    2 Symptoms > 4 weeks or persistent symptoms despite treatment
  2. Dysphagia
  3. Relapsing symptoms
  4. Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the gold standard test for GORD?

A

24-hr oesophageal pH monitoring
Often performed if endoscopy is indicated and negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is the management of GORD divided?

A

Endoscopy findings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the management of GORD if endoscopy shows oesophagitis?

A
  1. Full dose proton pump inhibitor (PPI) for 1-2 months
  2. If response then low dose treatment as required
  3. If no response then double-dose PPI for 1 month
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the management of GORD if endoscopy does not show reflux disease?

A
  1. Full dose PPI for 1 month
  2. If response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
  3. If no response then Histamine type 2 receptor antagonist or prokinetic for one month
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the management of GORD that has not been investigated by endoscopy?

A
  1. Review medications for possible causes of dyspepsia
  2. Lifestyle advice
  3. Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some of the complications of GORD?

A
  1. Oesophagitis
  2. Ulcers
  3. Anaemia
  4. Benign strictures
  5. Barrett’s oesophagus
  6. Oesophageal carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Gastroenteritis?

A

Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Infectious Colitis?

A

Inflammation of the colon due to a virus or bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the aetiology of Gastroenteritis and Infectious Colitis?

A

Can be caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is traveller’s diarrhoea?

A
  1. Defined as at least 3 loose to watery stools in 24 hours with or without one of more of:
    a.abdominal cramps
    b. fever
    c. nausea/ vomiting or
    d. blood in the stool
  2. The most common cause is Escherichia coli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is acute food poisoning?

A
  1. Describes the sudden onset of nausea, vomiting and diarrhoea after the ingestion of a toxin
  2. Typically caused by Staphylococcus aureus, Bacillus cereus or Clostridium perfringens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some of the causative bacterial organisms for gastroenteritis?

A
  1. E.coli: traveller’s diarrhoea
  2. Giardiasis
  3. Cholera
  4. Shigella
  5. Staph Aureus
  6. Campylobacter
  7. Baccilus cereus
  8. Amoebiasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the typical presentation of gastroenteritis caused by E.coli?

A

Watery stools
Abdominal cramps and nausea
Common amongst travellers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the typical presentation of gastroenteritis caused by Giardiasis?

A

Prolonged, non-bloody diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the typical presentation of gastroenteritis caused by cholera?

A
  1. Profuse, watery diarrhoea ‘rice water stools’
  2. Severe dehydration resulting in weight loss
  3. Not common amongst travellers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the typical presentation of gastroenteritis caused by shigella?

A
  1. Bloody diarrhoea
  2. Vomiting and abdominal pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the typical presentation of gastroenteritis caused by staphylococcus aureus?

A

Severe vomiting
Short incubation period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the typical presentation of gastroenteritis caused by Campylobacter?

A
  1. A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
  2. May mimic appendicitis
  3. Complications include Guillain-Barre syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the typical presentation of gastroenteritis caused by Bacillus cereus?

A

Two types of illness are seen:
1. vomiting within 6 hours, stereotypically due to rice
2. diarrhoeal illness occurring after 6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the most common cause of gastroenteritis?

A

Norovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the signs of Gastroenteritis and Infectious Colitis on physical examination?

A
  1. Diffuse abdominal tenderness
  2. Abdominal distension
  3. Bowel sounds are often increased
    If severe:
    a. Pyrexia
    b. Dehydration
    c. Hypotension
    d. Peripheral shutdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the investigations for gastroenteritis and infective colitis?

A
  1. Bloods: FBC, blood culture (helps identification if bacteriaemia present), U&Es: dehydration
  2. Stool:
    a. Faecal microscopy for polymorphs, parasites, oocysts, culture, electron microscopy (used to diagnose viral infections)
    b. Analysis for toxins, particularly for pseudomembranous
    colitis (Clostridium difficile toxin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the management for Gastroenteritis and Infectious Colitis?

A

Most infections are self-limiting:
1. Bed rest
2. Fluid and electrolyte replacement with oral rehydration solution (containing glucose and salt)
3. IV rehydration may be necessary in those with severe vomiting
4. Antibiotic treatment is only warranted if severe or the infective agent has been identified (e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter)

Public health:
-Often a notifiable disease
-Educate on basic hygiene and cooking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the complications of Gastroenteritis and Infectious Colitis?

A
  1. Dehydration
  2. Electrolyte imbalance
  3. Pre-renal failure
  4. Secondary lactose intolerance (particularly in infants)
  5. Sepsis and shock (particularly Salmonella and Shigella)
  6. Haemolytic uraemic syndrome is associated with toxins from E. coli
  7. Guillian–Barre syndrome may occur weeks after recovery from Campylobacter gastroenteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is diarrhoea?

A

> 3 loose or watery stool per day:
1. Acute diarrhoea < 14 days
2. Chronic diarrhoea > 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the causes for acute diarhhoea?

A
  1. Gastroenteritis: may be accompanied by abdominal pain or nausea/vomiting
  2. Diverticulitis: lassically causes left lower quadrant pain, diarrhoea and fever
  3. Antibiotic therapy: ,ore common with broad spectrum antibiotics (C diff)
  4. Constipation causing overflow: A history of alternating diarrhoea and constipation may be given -may lead to faecal incontinence in the elderly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the causes of chronic diarrhoea?

A
  1. IBS: Very common, most consistent features are abdominal pain, bloating and change in bowel habit (constipation or diarrhoea)
  2. UC: Bloody diarrhoea may be seen, crampy abdominal pain and weight loss are also common
  3. Crohn’s disease: less likely compared to UC
  4. Colorectal cancer: depends on site of tumour
  5. Coeliac disease: children may present with failure to thrive, diarrhoea and abdominal distension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are some other conditions in which diarrhoea may be a feature?

A
  1. Thyrotoxicosis
  2. Laxative abuse
  3. Appendicitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is gastrointestinal perforation?

A

Also known as ruptured bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the aetiology of gastrointestinal perforation?

A

The most common causes of GI perforation are peptic ulcers (gastric or duodenal) and sigmoid diverticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the different causes of gastrointestinal perforation?

A
  1. Chemical: peptic ulcer, foreign body
  2. Infection: diverticulitis, cholecystitis
  3. Ischaemia: mesenteric ischaemia, malignancy (LBO)
  4. Inflammation: toxic megacolon (C. diff or UC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the traumatic causes of gastrointestinal perforation?

A

Iatrogenic:
1. Recent surgery (including anastomotic leak)
2. Endoscopy or overzealous NG tube insertion
3. Penetrating or blunt trauma: Shear forces
Direct rupture:
1. Excessive vomiting leading to oesophageal perforation (Boerhaave Syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the most common cause of gastrointestinal perforation?

A

Ulcerative disease: duodenal ulcers causing 2- to 3-times more than gastric ulcers do

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the presenting symptoms of gastrointestinal perforation?

A
  1. Main feature is pain: typically this is rapid onset and sharp in nature
  2. Patients are systemically unwell therefore may also have associated malaise, vomiting, and lethargy
  3. Thoracic perforation: such as a oesophageal rupture
    a. Pain, ranging from chest or neck pain to pain radiating to the back, typically worsening on inspiration
    b. There may be associated vomiting and respiratory symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the signs of gastrointestinal perforation on physical examination?

A
  1. Patients will look unwell and often have features of sepsis
  2. On examining their abdomen, they will have features of peritonism: may be localised or generalised (a rigid abdomen)
  3. Thoracic perforation:
    auscultation and percussion may reveal signs of a pleural effusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the gold standard investigation for gastrointestinal perforation?

A

CT scan: demonstrating air outside the gastrointestinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the findings of gastrointestinal perforation on abdominal x-ray (and chest x-ray)?

A
  1. Free air under the diaphragm
  2. Rigler’s sign: both sides of the bowel wall can be seen, due to free intra-abdominal air acting as an additional contrast
  3. Psoas sign: loss of the sharp delineation of the psoas muscle border, secondary to fluid in the retroperitoneum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the management of gastrointestinal perforation?

A
  1. Conservative:
    a. For patients who have localised perforation (diverticular disease) or sealed upper GI perforation without generalised peritonism
    b. Can also be for patients not suitable for surgery e.g. elderly patients with extensive co-morbidities
  2. Medical: Prophylactic broad spectrum antibiotics, should be given to almost all patients, particularly those requiring surgery
  3. Surgical:
    a. Identification and management of underlying cause e.g. repairing perforated peptic ulcer with an omental patc, resecting a perforated diverticulae (e.g. via a Hartmann’s procedure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the complications of gastrointestinal perforation?

A
  1. Infection: peritonitis and sepsis
  2. Haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the prognosis of gastrointestinal perforation?

A
  1. Most patients require urgent surgery
  2. Prognosis is dependent on early recognition and prompt resuscitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is haemochromatosis?

A

An autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the aetiology of haemochromatosis?

A

Caused by inheritance of mutations in the HFE gene on both copies of chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the epidemiology of haemochromatosis?

A
  1. 1 in 10 people of European descent carry a mutation in the genes affecting iron metabolism, mainly HFE
  2. Prevalence in people of European descent = 1 in 200, making it more common than cystic fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the early features of haemochromatosis?

A

Often asymptomatic and initial symptoms are often non-specific e.g. lethargy and arthralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the features of haemochromatosis?

A
  1. Early symptoms: fatigue, erectile dysfunction and arthralgia (often of the hands)
  2. ‘bronze’ skin pigmentation
  3. Diabetes mellitus
  4. Liver:
    a. Stigmata of chronic liver disease
    b. Hepatomegaly
    c. Cirrhosis
    d. Hepatocellular deposition
  5. Arthritis (especially of the hands)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are some of the cardiac and endocrine features of haemochromatosis?

A
  1. Cardiac failure secondary to dilated cardiomyopathy
  2. Hypogonadism: secondary to cirrhosis and pituitary dysfunction = hypogonadotrophic hypogonadism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is important to exclude in suspected haemochromatosis?

A

Causes of secondary iron overload e.g. multiple transfusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the signs of Haemochromatosis on physical examination?

A

May be normal, but with severe iron overload:
1. Skin: Pigmentation (slate-grey) resulting from increase in melanin deposits
2. Liver: Hepatosplenomegaly
3. Heart: Signs of heart failure, arrhythmias
4. Hypogonadism: Testicular atrophy, loss of hair, gynaecomastia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the best investigations to screen for iron overload?

A
  1. In the general population: transferrin saturation is considered the most useful marker (plus ferritin)
  2. In family members: genetic testing for HFE mutation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is a typical iron study profile in a patient with haemochromatosis?

A
  1. Transferrin saturation > 55% in men or > 50% in women
  2. Raised ferritin (e.g. > 500 ug/l) and iron
  3. Low TIBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What other investigations are useful in haemochromatosis?

A
  1. Iron studies: specifically transferrin
  2. LFTs
  3. MRI for liver and cardiac involvement
  4. Liver biopsy: now only for patients with suspected cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the management for haemochromatosis?

A
  1. First line: Venesection
  2. May use desferrioxamine as second line
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What should be monitored during venesection as part of the management for haemochromatosis?

A

Transferrin saturation:
Should be kept below 50% and the serum ferritin concentration below 50 ug/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the complications of haemochromatosis?

A

Reversible with treatment:
1. Cardiomyopathy
2. Skin pigmentation
Irreversible:
1. Liver cirrhosis
2. Diabetes mellitus
3. Hypogonadotrophic hypogonadism
4. Arthropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are haemorrhoids?

A

Vascular-rich connective tissue cushions located within the anal canal: become haemorrhoids when they become enlarged, congested and symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How can haemorrhoids be classified?

A

External and internal:
1. External:
a. originate below the dentate line
b. prone to thrombosis
c. may be painful
2. Internal:
a. originate above the dentate line
b. do not generally cause pain
c. Can be graded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the grading system of internal haemorrhoids?

A

Grade I: Do not prolapse out of the anal canal
Grade II: Prolapse on defecation but reduce spontaneously
Grade III: Can be manually reduced
Grade IV: Cannot be reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the aetiology of haemorrhoids?

A
  1. Excessive straining due to either chronic constipation or diarrhoea (most common)
  2. Increase in intra-abdominal pressure by pregnancy or ascites
  3. Presence of space-occupying lesions within the pelvis may cause a concomitant decrease in vascular return and increase in anal vascular engorgement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the epidemiology of haemorrhoids?

A
  1. Prevalence is approximately 4% and is more common in white patients than in black patients
  2. Presentation peaks between the ages of 45-65 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the clinical features of haemorrhoids?

A
  1. Painless rectal bleeding (most common symptom)
  2. Can be itchy: pruritus
  3. Pain, usually only if thrombosed
  4. Faecal incontinence with third or fourth degree haemorrhoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the signs of haemorrhoids on physical examination?

A
  1. Tender palpable perianal lesion: can form adjacent to the anal canal on the anal margin when there is acute thrombosis
  2. Internal haemorrhoids are not usually palpable on DRE
  3. Anal mass: may be present with prolapsing haemorrhoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the investigations for haemorrhoids?

A
  1. Anoscopic examination: most specific and conclusive diagnostic test
  2. Colonoscopy/flexible sigmoidoscopy: exclude serious pathology such as inflammatory bowel disease or cancer
  3. Bloods only if there is concern that the patient has experienced significant prolonged rectal bleeding and signs of anaemia are present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the management of haemorrhoids?

A
  1. Conservative: soften stools by increasing dietary fibre and fluid intake
  2. Medical: topical local anaesthetics and steroids may be used to help symptoms
  3. Surgical: ranges from outpatient treatment to newer treatments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the outpatient treatment for haemorrhoids?

A

Rubber band ligation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Who is eligible for surgical management of haemorrhoids?

A

Reserved for large symptomatic haemorrhoids which do not respond to outpatient treatments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the new surgical techniques in the management of haemorrhoids?

A

Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the features of an acutely thrombosed external haemorrhoid?

A
  1. Typically present with significant pain
  2. Examination reveals a purplish, oedematous, tender subcutaneous perianal mass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the management of an acute thrombosed external haemorrhoid?

A
  1. Patient presents within 72 hours: then referral should be considered for excision
  2. Otherwise patients can usually be managed with stool softeners, ice packs and analgesia
  3. Symptoms usually settle within 10 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the complications of haemorrhoids?

A
  1. Anaemia from continuous or excessive bleeding
  2. Acute thrombosis of a haemorrhoid
  3. Incarceration: prolapsing haemorrhoidal tissue can become incarcerated and be unable to be reduced into the anal canal, causing severe pain- urgent surgical haemorrhoidectomy
  4. Faecal incontinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What leads to the best long term prognosis of haemorrhoids?

A

Surgical haemorrhoidectomy: lowers the risk of recurrence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is a haemorrhoidectomy?

A

An operation to remove haemorrhoids-swollen blood vessels in the anal canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the indications for a haemorrhoidectomy?

A
  1. Relieve persistent discomfort/pain
  2. Prevent bleeding from the anus
  3. Surgically correct strangulated haemorrhoids: when the anal sphincter squeezes the prolapsed haemorrhoid and interrupts blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the possible complications of a haemorrhoidectomy?

A

From surgery:
1. Bleeding
2. Constipation
3. Infection
4. Excessive bleeding (seek advice)
Further complications of haemorrhoids:
1. Incontinence of stool: very rare (less than 1%)
2. Recurrent haemorrhoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is hepatocellular carcinoma?

A

Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the epidemiology of hepatocellular carcinoma?

A

The third most common cause of cancer worldwide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the most common causes of hepatocellular carcinoma?

A
  1. Chronic hepatitis B is the most common cause worldwide
  2. Chronic hepatitis C is the most common cause in Europe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the main risk factor for developing hepatocellular cancer?

A

Liver cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the most common causes of liver cirrhosis?

A

Secondary to:
1. Hepatitis B and C
2. Alcohol
3. Haemochromatosis
4. Primary biliary cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are some of the risk factors of hepatocellular cancer?

A
  1. Alpha-1 antitrypsin deficiency
  2. Glycogen storage disease
  3. Drugs: OCP, anabolic steroids
  4. Porphyria cutanea tarda
  5. Diabetes mellitus, metabolic syndrome
  6. Male sex
  7. Aflatoxins: Aspergillus flavus fungal toxin found on grains or biological weapons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the features of hepatocellular cancer?

A
  1. Tends to present late, features of liver failure:
    a. Jaundice
    b. Ascites
    c. RUQ pain,
    d. Hepatosplenomegaly
    e. Pruritus
  2. Possibly present as decompensated chronic liver disease: encephalopathy, asterixis, spider naevi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the tumour marker for hepatocellular carcinoma?

A

AFP: alpha-fetoprotein, will be raised, has high sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the screening for hepatocellular carcinoma?

A

Ultrasound ± AFP in high risk groups:
1. Patients with liver cirrhosis secondary to Hep B and C, haemochromatosis
2. Men with liver cirrhosis secondary to alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the management of hepatocellular carcinoma?

A
  1. In early disease: surgical resection
  2. Definitive management: liver transplantation
  3. Radiofrequency ablation
  4. Transarterial chemoembolisation
  5. Sorafenib: a multikinase inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the prognosis of hepatocellular carcinoma?

A

A very aggressive type of cancer, depends upon stage and overall functional status of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is a hernia?

A

The protrusion of abdominal or pelvic contents through a weakness in the muscle or tissue wall that holds it in place e.g. the abdominal wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the different types of hernia?

A
  1. Inguinal hernia
  2. Femoral hernia
  3. Umbilical
  4. Paraumbilical
  5. Epigastric
  6. Obturator
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the risk factors for abdominal wall hernias?

A
  1. Obesity
  2. Ascites
  3. Increasing age
  4. Surgical wounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the features of abdominal wall hernias?

A
  1. Palpable lump
  2. Cough impulse
  3. Pain
  4. Obstruction: more common in femoral hernias
  5. Strangulation: may compromise the bowel blood supply leading to infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the cough impulse for inguinal hernias?

A

Helps to distinguish between direct and indirect inguinal hernias:
1. Reduce the hernia and occlude the deep internal ring with 2 fingers
2. Ask the patient to cough (or stand)
3. If the hernia is restrained it is indirect
4. If not it is direct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is an inguinal hernia?

A
  1. Accounts for 75% of abdominal wall hernias
  2. Around 95% of patients are male
  3. Above and medial to pubic tubercle
  4. Presents as a groin lump: disappears on pressure or when lying down
  5. Discomfort and ache often worse with activity
  6. Strangulation is rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is a femoral hernia?

A
  1. Below and lateral to the pubic tubercle
  2. More common in women, particularly multiparous ones
  3. High risk of obstruction and strangulation
  4. Surgical repair is required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is an epigastric hernia?

A
  1. Lump in the midline between umbilicus and the xiphisternum
  2. Risk factors include extensive physical training or coughing (from lung diseases), obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is an incisional hernia?

A

May occur in up to 10% of abdominal operations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is an obturator hernia?

A
  1. A hernia which passes through the obturator foramen
  2. More common in females and typical presents with bowel obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the management of inguinal hernias?

A
  1. Treat medically fit patients even if they are asymptomatic
  2. A hernia truss may be an option for patients not fit for surgery but probably has little role in other patients
  3. Mesh repair is associated with the lowest recurrence rate:
  4. Unilateral inguinal hernias are generally repaired with an open approach
  5. Bilateral and recurrent inguinal hernias are generally repaired laparoscopically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What advice should be given to patients who had open repair management of their inguinal hernia?

A

Return to non-manual work after 2-3 weeks (following laparoscopic repair after 1-2 weeks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the complications of inguinal hernia mesh repair?

A

Early: bruising, wound infection
Late: chronic pain, recurrence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How are femoral hernias diagnosed?

A

Usually clinical, although ultrasound is an option

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are some of the differentials for a femoral hernia?

A
  1. Lymphadenopathy
  2. Abscess
  3. Femoral artery aneurysm
  4. Hydrocoele or varicocele in males
  5. Lipoma
  6. Inguinal hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the management of femoral hernias?

A
  1. Surgical repair is a necessity, given the risk of strangulation, and can be carried out either laparoscopically or via a laparotomy
  2. Hernia support belts/trusses should not be used for femoral hernias (risk of strangulation)
  3. In an emergency situation, a laparotomy may be the only option
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are the complications of a femoral hernia?

A
  1. Incarceration: where the herniated tissue cannot be reduced
  2. Strangulation: surgical emergency!
  3. Bowel obstruction: surgical emergency
  4. Bowel ischaemia and resection due to the above, which may lead to significant morbidity and mortality for the patient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is femoral hernia strangualtion?

A
  1. A surgical emergency where the blood supply to the herniated tissue is compromised, leading to ischemia or necrosis
  2. These hernias will be tender and likely non-reducible, and may also present with a systemically unwell patient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the investigations for a strangulated hernia?

A
  1. Imaging can be used in cases of suspected strangulation, however, it is not considered necessary and is more useful in excluding other pathologies
  2. FBC and ABG analysis can help point towards the diagnosis by showing:
    a. Leukocytosis
    b. Raised lactate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the management of a strangulated femoral hernia?

A

Surgical repair, a laparotomy may be the only option

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What type of hernia carries a high risk of strangulation?

A

Femoral hernias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is a hiatus hernia?

A

Describes the herniation of part of the stomach above the diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are the two types of hiatus hernia?

A
  1. Sliding: (95% of hiatus hernias), the gastroesophageal junction moves above the diaphragm
  2. Rolling: the gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What are the risk factors for hiatus hernias?

A
  1. Obesity
  2. Increased intra-abdominal pressure e.g. ascites, multiparity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the features of a hiatus hernia?

A
  1. Heartburn
  2. Dysphagia
  3. Regurgitation
  4. Chest pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is the most sensitive test for a hiatus hernia?

A

Barium swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

How are hiatus hernias commonly found?

A

Incidentally: due to presenting symptoms the patients have an endoscopy which shows the displacement of the gastroesophageal junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the management of hiatus hernias?

A
  1. Conservative: all patients benefit from weight loss
  2. Medical: proton pump inhibitor therapy
  3. Surgical: only really has a role in symptomatic paraesophageal hernias (other part of the stomach herniates)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is intestinal ischaemia and how can it be divided?

A

Bowel ischaemia:
1. Acute mesenteric ischaemia
2. Chronic mesenteric ischaemia
3. Ischaemic colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What are the predisposing factors for intestinal ischaemia?

A
  1. Increasing age
  2. AF (mesenteric ischaemia)
  3. Other causes of emboli: malignancy, endocarditis
  4. CVD risk factors: HTN, smoking, DM
  5. Cocaine (ischaemic colitis in young people)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What are the features of intestinal ischaemia?

A
  1. Abdominal pain
  2. Rectal bleeding
  3. Diarrhoea
  4. Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is a common feature in acute mesenteric ischaemia?

A

The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are the findings of intestinal ischaemia on bloods?

A

Elevated white blood cell count and lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the investigation of choice for intestinal ischaemia?

A

CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What is acute mesenteric ischaemia caused by?

A
  1. Typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel e.g. superior mesenteric artery
  2. Classically patients have a history of AF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is the management of acute mesenteric ischaemia?

A
  1. Urgent surgery is usually required
  2. Poor prognosis, especially if surgery delayed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is chronic mesenteric ischaemia?

A
  1. A relatively rare clinical diagnosis due to it’s non-specific features
  2. May be thought of as ‘intestinal angina’
  3. Colickly, intermittent abdominal pain occurs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is ischaemic colitis?

A
  1. Describes an acute but transient compromise in the blood flow to the large bowel
  2. This may lead to inflammation, ulceration and haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Where is a common site for ischaemic colitis?

A

More likely to occur in ‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What are the signs of ischaemic colitis on abdominal x-ray?

A

‘Thumbprinting’ may be seen due to mucosal oedema/haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is the management of ischaemic colitis?

A
  1. Usually supportive
  2. Surgery may be required in a minority of cases if conservative measures fail
  3. Indications for surgery include:
    a. Generalised peritonitis
    b. Perforation
    c. Ongoing haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is small bowel obstruction?

A

Where the passage of food, fluids and gas, through the small intestines becomes blocked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What are the common causes of small bowel obstruction?

A
  1. Adhesions (e.g. following previous surgery): most common
  2. Hernias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are the features of small bowel obstruction?

A
  1. Diffuse, central abdominal pain
  2. Nausea and vomiting
  3. Typically bilious vomiting
  4. ‘constipation’ with complete obstruction and lack of flatulence
  5. Abdominal distension may be apparent, particularly with lower levels of obstruction
  6. ‘tinkling’ bowel sounds (more common in early bowel obstruction)
135
Q

What is the first line imaging in small bowel obstruction?

A

Abdominal x-ray: distended small bowel loops with fluid levels
1. Considered dilated if small bowel is >3cm diameter

136
Q

What is the definitive investigation for small bowel obstruction?

A

CT: most sensitive, particularly in early obstruction

137
Q

What is the management of small bowel obstruction?

A
  1. Intial steps:
    a. NBM
    b. IV fluids
    c. nasogastric tube with free drainage
  2. Some patients settle with conservative management but otherwise will require surgery
138
Q

What is large bowel obstruction?

A

When the passage of food, fluids and gas, through the large intestines becomes blocked

139
Q

What is the most common cause of large bowel obstruction?

A

Tumours:
1. 60% of cases
2. Can be the initial presenting complaint of colonic malignancy (30% of cases)
3. Particularly more distal colonic and rectal tumours, as these tend to obstruct earlier due to the smaller lumen diameter

140
Q

What are the causes of large bowel obstruction?

A
  1. Tumours (60%)
  2. Volvulus
  3. Diverticular disease
141
Q

What are the clinical features of large bowel obstruction?

A
  1. Feature suggestive of obstruction plus underlying causes (e.g. any recent symptoms suggestive of colorectal cancer)
  2. Absence of passing flatus or stool
  3. Abdominal pain
  4. Abdominal distention
  5. Late: nausea and vomiting, may suggest a more proximal lesion
  6. Peritonism: if there is associated bowel perforation
142
Q

What is the first line investigation for large bowel obstruction?

A

Abdominal x-ray:
1. Normal diameter limits are 10-12 cm for caecum, 8 cm for ascending colon, and 6.5 cm for recto-sigmoid
2. Diameter greater than this is diagnostic of obstruction
3. Presence of free intra-peritoneal gas indicates colonic perforation

143
Q

What is the best investigation for large bowel obstruction?

A

CT:
1. High sensitivity and specificity for identifying obstruction (over 90% each)
2. Can identify the aetiology of obstruction itself

144
Q

What is the management of large bowel obstruction?

A
  1. Initial steps:
    a. NBM
    b. IV fluids
    c. nasogastric tube with free drainage
  2. Urgency of management depends on whether perforation is suspected
  3. If the cause of obstruction itself does not require surgery: conservative management for up to 72 hours can be trialled
  4. Around 75% will eventually require surgery
  5. IV antibiotics will be given if perforation suspected or surgery planned
145
Q

What is the surgical management of large bowel obstruction?

A
  1. Emergency surgery necessary if: there is any overt peritonitis or evidence of bowel perforation,
  2. Procedure:
    a. Irrigation of the abdominal cavity
    b. Resection of perforated segment and ischaemic bowel
    c. Address the underlying cause of the obstruction itself
146
Q

What is the difference in imaging in small and large bowel obstruction?

A

On abdominal x-ray:
Small bowel:
1. Maximum normal diameter = 35 mm
2. Valvulae conniventes extend all the way across
Large bowel:
1. Maximum normal diameter = 55 mm
2. Haustra extend about a third of the way across

147
Q

What is Ileus?

A
  1. The slowing of GI motility accompanied by distention, in the absence of a mechanical intestinal obstruction
  2. Diagnosis of exclusion after bowel obstruction has been ruled out
  3. It usually occurs in response to physiological stress, including surgery, sepsis, metabolic derangements, and Gl diseases
148
Q

What are the complications of Intestinal obstruction?

A
  1. Intestinal necrosis
  2. Sepsis
  3. Multi-organ failure
  4. Intestinal perforation: lead to intra-abdominal abscess
  5. From surgery: short bowel syndrome: extensive removal of small intestine resulting in inadequate absorption of enteral nutrition
149
Q

What are Liver abscesses?

A

Localised infections in the liver parenchyma resulting in a walled off collection of pus

150
Q

What is the aetiology of liver abscesses?

A

The most common organisms:
1. Staphylococcus aureus in children
2. Escherichia coli in adults

151
Q

What are the presenting symptoms of a Liver abscess?

A
  1. Non-specific symptoms: fever, malaise, nausea, anorexia, night sweats, weight loss
  2. RUQ or epigastric pain, which may be referred to shoulder (diaphragmatic irritation)
  3. Diarrhoea
  4. 1/3 of patients have chest symptoms, including cough, shortness of breath, and chest pain
152
Q

What are the appropriate investigations for Liver abscesses?

A
  1. Bloods:
    a. Inflammatory and infection markers
    b. LFTS: raised ALP (most common finding), prothrombin time
    c. Blood cultures: pyogenic abscesses
  2. Ultrasound:
    a. Can be used to guide aspiration of the abscess
    b. Gram stain and culture of aspirated abscess fluid
  3. Non-contrast CT: demonstrates hypodense liver lesions, gas within the lesion is highly suggestive of a pyogenic abscess
153
Q

What is the management of liver abscesses?

A

Drainage (typically percutaneous) and antibiotics:
1. amoxicillin + ciprofloxacin + metronidazole
2. If penicillin allergic: ciprofloxacin + clindamycin

154
Q

What are Liver cysts?

A

Fluid filled sacs in the liver, that can be congenital

155
Q

What is the aetiology of Liver cysts?

A
  1. Inherited disorders can cause cysts, including polycystic liver disease, congenital hepatic fibrosis
  2. Majority of cystic disease is caused by simple cysts- caused from a malformation of your bile ducts
156
Q

What is the epidemiology of Liver cysts?

A
  1. Congenital causes are present at birth
  2. Simple cysts are estimated to affect between 1% and 2.5% of the population
  3. Affect all ages, but occur more frequently in the population as age increases
157
Q

What are the presenting symptoms/signs of Liver cysts?

A
  1. Usually have no symptoms
  2. Larger cysts may occasionally cause some dull pain and/ or swelling RUQ- hepatomegaly
158
Q

What are the investigations for Liver cysts?

A
  1. Bloods:
    a. FBC: lack of signs of infection: abscess
    b. CRP: elevated if inflamed
    c. LFTs: elevated AlkPhos and bilirubin if bile duct is obstructed
  2. Ultrasound or CT scan: localise structure of mass, exclude abscess
  3. Aspiration of fluid: exclude infection
159
Q

What is the management of Liver cysts?

A
  1. Simple liver cysts generally do not require treatment unless they become large enough to cause pain
  2. Aspiration and then stick the walls together using sclerosant or remove part of the wall of the cyst, called laparoscopic de-roofing
160
Q

What is acute liver failure?

A

Describes the rapid onset of hepatocellular dysfunction leading to a variety of systemic complications

161
Q

What are the causes of acute liver failure?

A
  1. Paracetamol overdose
  2. Alcohol
  3. Viral hepatitis (usually A or B)
  4. Acute fatty liver of pregnancy
162
Q

What are the features of acute liver failure?

A
  1. May be asymptomatic
  2. Jaundice
  3. Fever, nausea, malaise
  4. Abdominal pain
163
Q

What are the signs of liver failure on examination?

A
  1. Bruising: coagulopathy: raised prothrombin time
  2. Hypoalbuminaemia
  3. Hepatic encephalopathy
  4. Renal failure is common (‘hepatorenal syndrome’)
164
Q

What is Budd-Chiari syndrome?

A
  1. A very rare condition involving the occlusion of the hepatic veins that drain the liver
  2. It presents with the classical triad of abdominal pain, ascites, and liver enlargement
165
Q

What is the pathogenesis of the manifestation in Liver failure?

A
  1. Jaundice: decreased secretion of conjugated bilirubin
  2. Encephalopathy: increased delivery of gut-derived products into the systemic circulation and brain
    from the reduced extraction of nitrogenous products by liver and portal systemic shunting- ammonia may play a part
  3. Coagulopathy: reduced synthesis of clotting factors and so reduced platelets (hypersplenism if chronic portal hypertension)
166
Q

What are the investigations for Liver failure?

A

A to E approach:
1. Bloods:
a. LFTs: hyperbilirubinaemia, elevated liver enzymes
Prothrombin time >1.5
b. FBC: thrombocytopenia
c. U&Es for renal failure
2. ABG: metabolic acidosis. elevated lactate- presence of acidosis is an important prognostic indicator, particularly in paracetamol overdose
3. Identify cause e.g. paracetamol level, urine toxicology, pregnancy, viral hepatitis serology, autoimmune markers

167
Q

What tests are the most accurate marker of liver function?

A

Prothrombin time and albumin

168
Q

What is the management for Liver failure?

A
  1. Resuscitation (ABC approach): ITU care and specialist unit support essential
  2. Treat the cause if possible: N-acetylcysteine for paracetamol overdose
  3. Invasive ventilatory support often required plus coagulopathy treatment: IV Vitamin K, FFP, platelet infusions if required, gastric mucosa protection (PPI)
  4. Antiviral therapy should be considered
  5. Avoid: Sedatives or drugs metabolized by the liver
  6. Liver transplantation should be considered in all patients with acute liver failure who fulfil prognostic criteria for a high risk of mortality
169
Q

What is the prognostic criteria for a high risk of mortality in Liver failure?

A

According to the United Network for Organ Sharing (UNOS):
1. Age >18 years
2. Life expectancy without a liver transplant of <7 days
3. Onset of encephalopathy within 8 weeks of the first symptoms of liver disease
4. Absence of pre-existing liver disease
4. Admission to an intensive care unit, and 1 of the following:
a. Ventilator dependence
b. Requirement of renal replacement therapy
c. INR >2.0

170
Q

What are the contraindications of Liver transplantation?

A
  1. Severe infection or septic shock
  2. Brain death
  3. Severe cardiopulmonary disease or ARDS
  4. Multi-organ failure
  5. Extrahepatic malignancy
  6. Others: ongoing alcohol or illicit drug abuse, or a history of repeated suicide attempts
171
Q

What are the complications of Liver failure?

A
  1. Rapidly progressing hepatic encephalopathy
  2. Coagulopathy
  3. Infection
    4.. Hepatorenal syndrome (concurrent hepatic and renal failure)
  4. Metabolic disorders: hypoglycaemia, acid–base and electrolyte disturbances
  5. Cerebral oedema
  6. GI bleeding due to coagulopathy
172
Q

What is the prognosis of Liver failure?

A

Depends on the severity and aetiology:
1. Secondary to paracetamol overdose, acute hepatitis A, or shock liver is associated with a favourable prognosis
2. In contrast, resulting from idiosyncratic drug-induced liver injury, acute hepatitis B, or indeterminate cause has a much lower rate of spontaneous recovery

173
Q

What is hepatic encephalopathy?

A
  1. Often associated with acute liver failure it may also be seen with chronic disease
  2. Features:
    a. Confusion
    b. Asterix/ liver flap
174
Q

What are the grades of hepatic encephalopathy?

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

175
Q

What are the precipitating factors for hepatic encephalopathy?

A
  1. Infection e.g. spontaneous bacterial peritonitis
  2. GI bleed
  3. Post transjugular intrahepatic portosystemic shunt
  4. Constipation
  5. Drugs: sedatives, diuretics
    hypokalaemia
  6. Renal failure
176
Q

What is the management of hepatic encephalopathy?

A
  1. Treat any underlying precipitating cause
  2. NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
    a. Lactulose promotes the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
177
Q

What is Mallory-Weiss tear?

A

A syndrome characterised by a tear or laceration often along the right border of, or near, the gastro-oesophageal junction

178
Q

What is the aetiology of a Mallory-Weiss tear?

A

Most cases seem to occur as a result of a sudden rise in abdominal pressure or transmural pressure gradient across the gastro-oesophageal junction with a corresponding low intrathoracic pressure e.g. retching, vomiting, chronic cough

179
Q

What are the causes of a Mallort-Weiss tear?

A
  1. Coughing (chronic e.g. COPD, bronchiectasis)
  2. Retching, vomiting and straining
  3. Closed-chest pressure or cardiopulmonary resuscitation
  4. Acute abdominal blunt trauma
  5. Alcohol and medications (aspirin or other NSAIDs)
  6. Chemotherapeutic agents
  7. Hiatal hernia, which is present in 40% to 100% of people with MWT, is considered by many to be a precipitating factor, causing an oesophageal tear to occur
180
Q

What is the epidemiology of Mallory-Weiss tears?

A
  1. Admission to hospital for non-variceal upper GI bleeding is common
  2. Age of presentation may vary but is most common in people aged between 30- 50 years
  3. More common in men than in women in a ratio of 3:1
  4. In women of childbearing age, the most common cause is hyperemesis gravidarum (severe nausea and vomiting)
181
Q

What are the presenting symptoms and signs of a Mallory-Weiss tear?

A
  1. Haematemesis: varies from flecks or streaks of blood mixed with gastric contents and/or mucus, blackish or ‘coffee ground’, to a bright-red bloody emesis
  2. Light headedness/dizziness
  3. Postural/orthostatic hypotension
182
Q

What is the typical history of a Mallory-Weiss tear?

A

Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting (rare to have malena)

183
Q

What are some differentials for an acute upper GI bleed?

A

Oesophageal:
1. Varices
2. Oesophagitis
3. Cancer
4. Mallory-Weiss tear
Gastric:
1. Ulcer
2. Cancer
3. Gastritis
Duodenal:
1. Ulcer

184
Q

What is the Glasgow-Blatchford score for assessing acute upper GI bleeds?

A

The first assessment which helps clinicians decide whether patient patients can be managed as outpatients or not

185
Q

What is the Glasgow-Blatchford score for assessing acute upper GI bleeds?

A

The first assessment which helps clinicians decide whether patient patients can be managed as outpatients or not

186
Q

What is the blatchford score?

A

Assessing the admission risk for patients who present with an acute upper GI bleed (if 0 may be considered for early discharge):
1. Urea level
2. Haemoglobin
3. Systolic BP
4. Others including:
a. Pulse
b. Melena
c. Syncope
d. Hepatic disease
e. Cardiac failure

187
Q

What is the best investigation for acute upper GI bleed?

A

Endoscopy within 24 hours - but should only be performed after resuscitation

188
Q

What is the resuscitation of patients with an acute upper GI bleed?

A
  1. ABC, wide-bore intravenous access x 2
  2. Platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
  3. Fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time or activated partial thromboplastin time greater than 1.5 times normal
  4. Prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
189
Q

What is the specific management for a Mallory-Weiss tear?

A

Usually ceases spontaneously

190
Q

What is the management of an acute upper GI bleed divided into?

A

Variceal vs non-variceal bleeding

191
Q

What is variceal bleeding?

A
  1. Complication of portal hypertension secondary to liver cirrhosis
  2. Usually associated with large volumes of blood (can haemorrhage)
  3. Often associated with haemodynamic compromise
  4. May stop spontaneously but re-bleeds are common until appropriately managed
192
Q

What is the management of variceal bleeding?

A
  1. Terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
  2. Band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
  3. Transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
193
Q

What is the management of non-variceal bleeding?

A
  1. NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper GI bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
  2. If further bleeding then options include repeat endoscopy, interventional radiology and surgery
194
Q

What are the complications of Mallory-Weiss tears?

A
  1. MI or infraction: usually related to the acuity, severity of bleeding, and associated CAD
  2. Hypovolaemic shock/death: usually related to acuity and severity of bleeding; however, it is rare in patients with early stabilisation and prompt treatment
  3. Oesophageal perforation:
    Gastric ischaemia
  4. Metabolic disturbance: intractable vomiting
195
Q

What is the prognosis of Mallory-Weiss tears?

A
  1. For most patients, bleeding is self-limited, and will have stopped by the time of endoscopy
  2. Prognosis is excellent in patients without associated disease or complications
  3. A routine second endoscopic evaluation is not recommended unless the patient remains symptomatic after initial treatment
196
Q

What is Nasogastric tube insertion?

A

The insertion of a tube from the patients nose into their stomach for either feeding or aspiration

197
Q

What are the indications of Nasogastric tube insertion?

A
  1. To empty the upper gastrointestinal tract or for feeding
  2. Insertion may be for prophylactic or therapeutic reasons e.g. bowel obstruction
198
Q

What are the possible contraindications of a NG tube insertion?

A
  1. Ear, nose and throat abnormalities or infections
  2. Facial/neck fractures including base of skull
  3. Possible strictures of the oesophagus
  4. Oesophageal varices
  5. Anatomical abnormalities (oesophageal diverticulae)
  6. High risk of aspiration
199
Q

What are the possible complications of Nasogastric tube insertion?

A

Main: aspiration and tissue trauma- if placed incorrectly into the trachea and lung it can cause pneumonia and death

200
Q

How is an NG tube insertion checked that it is in the correct position?

A

pH test (NG tube is aspirated and the contents are checked using pH paper) and CXR

201
Q

What is Nissen fundoplication?

A

Surgical procedure to treat severe and ongoing acid reflux (GORD) and hiatal hernia

202
Q

What is Non-alcoholic fatty liver disease?

A
  1. Now the most common cause of liver disease in the developed world
  2. Includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis (in non-alcoholics)
203
Q

What is the aetiology of non-alcoholic fatty liver disease?

A

It is largely caused by obesity and describes a spectrum of disease ranging from:
1. Steatosis - fat in the liver
2. Steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH)
3. Progressive disease may cause fibrosis and liver cirrhosis

204
Q

What is non-alcoholic steatohepatitis (NASH)?

A
  1. A term used to describe liver changes similar to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse
  2. It is relatively common and thought to affect around 3-4% of the general population
  3. The progression of disease in patients with NASH may be responsible for a proportion of patients previously labelled as cryptogenic cirrhosis
205
Q

What are the associated factors in non-alcoholic fatty liver disease?

A
  1. Obesity
  2. T2 DM
  3. Hyperlipidaemia
  4. Jejunoileal bypass
  5. Sudden weight loss/starvation
206
Q

What are the features of non-alcoholic fatty liver disease?

A
  1. Usually asymptomatic
  2. Hepatomegaly
  3. ALT is typically greater than AST
  4. Increased echogenicity on ultrasound
  5. Absence of chronic alcoholic disease signs
207
Q

What are the signs of chronic alcoholic disease?

A
  1. Spider naevi
  2. Palmar erythema
  3. Dupuytren’s contracture
  4. Gynaecomsastia
  5. Parotid gland enlargement
208
Q

What are the guidelines on investigation and management of non-alcoholic fatty liver disease?

A
  1. No evidence to support screening for NAFLD in adults, even in at risk groups (e.g. T2DM)
  2. The guidelines are therefore based on the management of the incidental finding of NAFLD - typically asymptomatic fatty changes on liver ultrasound
209
Q

What are the initial investigations that would be performed in patients presenting with features of non-alcoholic fatty liver disease?

A
  1. Bloods:
    a. FBC
    b. LFTs: deranged, AST>ALT, elevated GGT and Alk Phos
  2. Test for aetiology e.g. HbA1c
  3. Ultrasound
210
Q

What are the features of non-alcoholic fatty liver disease on ultrasound?

A

1) Diffuse hyperechoic echotexture (bright liver)
2) Increased liver echogenicity compared with kidney
3) Vascular blurring
4) Deep attenuation

211
Q

What investigation is recommended in patients with non-alcoholic fatty liver disease on ultrasound?

A

Enhanced liver fibrosis (ELF) blood test:
1. To check for advanced fibrosis
2. A combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1
3. An algorithm based on these values results in an ELF blood test score, similar to triple testing for Down’s syndrome

212
Q

What is the management of patients with advanced fibrosis secondary to non-alcoholic fatty liver disease?

A
  1. Referred to a liver specialist
  2. Have a liver biopsy to stage the disease more accurately
213
Q

What is the management for patients with non-alcoholic fatty liver disease with no advanced fibrosis?

A
  1. Mainstay of treatment is lifestyle changes (particularly weight loss) and monitoring
  2. Consider pharmacological agents or surgery (Orlistat is an enteric lipase inhibitor that prevents the absorption of fats from the GI tract/ bariatric surgery)
  3. Treatment of insulin resistance and diabetes (metformin)
  4. If presence of end-stage liver failure:
    a. Transjugular intrahepatic portosystemic shunt (TIPS)
    b. Liver transplantation
214
Q

What are the complications of Non-alcoholic steatohepatitis (NASH)?

A
  1. Ascites
  2. Cirrhosis
  3. Variceal haemorrhagae
  4. Portosystemic encephalopathy
  5. Hepatocellular carinoma
  6. Hepatorenal syndrome
  7. Hepatopulmonary syndrome
  8. Death: result of the increased risk of coronary artery disease
215
Q

What is the prognosis of Non-alcoholic steatohepatitis (NASH)?

A
  1. Independent predictors of fibrosis progression include:
    a. Diabetes mellitus
    b. A low initial fibrosis stage
    c. Higher BMI
  2. Patients who have NASH progress to cirrhosis 9% to 20% of the time: up to 1/3 of these patients will die from liver failure or require liver transplantation
  3. Recurrent NAFLD following liver transplantation is now a well-recognised phenomenon
216
Q

What is oesophageal cancer?

A

A malignant tumour arising in the oesophageal mucosa. There are two major histological types:
1. Squamous cell carcinoma
2. Adenocarcinoma (now most common)

217
Q

What is oesophageal adenocarcinoma?

A
  1. Most common type of oesophageal cancer
  2. More likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett’s
  3. Majority are located near the gastroesophageal junction in the lower third of oesophagus
218
Q

What is oesophageal squamous cell carcinoma?

A
  1. Most common type of oesophageal cancer in the developing world
  2. Associated with alcohol and smoking
  3. Located in the upper 2/3rds of the oesophagus
219
Q

What are the risk factors for oesophageal cancer?

A
  1. Male sex, 7:1
  2. Squamous cell carcinoma:
    a. Alcohol
    b. Tobacco
    c. FH of oesophageal, stomach, oral or pharyngeal cancer
    d. Achalasia
  3. Adenocarcinoma:
    a. GORD
    b. Barrett’s oesophagus
    c. Obesity
220
Q

What are the features of oesophageal cancer?

A
  1. Dysphagia: the most common presenting symptom
  2. Anorexia and weight loss
  3. Vomiting
  4. Other possible features include:
    a. Odynophagia: painful swallowing
    b. Hoarseness: may indicate recurrent laryngeal nerve palsy
    c. Melaena
    d. Cough
221
Q

What is the initial and best investigation for oesophageal cancer?

A

Upper GI endoscopy with biopsy:
1. Mucosal lesion
2. Histology shows squamous carcinoma or adenocarcinoma

222
Q

What are the other useful investigations for staging of oesophageal cancer?

A
  1. Endoscopic ultrasound: is the preferred method for locoregional staging
  2. CT scanning of the chest, abdomen and pelvis: is used for initial staging
  3. FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans
  4. Laparoscopy is sometimes performed to detect occult peritoneal disease
223
Q

What is the management of oesophageal cancer?

A

Operable disease is best managed by surgical resection with adjuvant chemotherapy

224
Q

What is the most common surgical procedure of oesophageal cancer?

A

Ivor-Lewis type oesophagectomy

225
Q

What is the biggest risk of surgical resection management of oesophageal cancer?

A

Anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis

226
Q

What is pancreatic cancer?

A
  1. Malignancy arising from the exocrine or endocrine tissues of the pancreas
  2. Refers to primary pancreatic ductal adenocarcinoma, which accounts for >80% of all pancreatic neoplasms (head of pancreas)
227
Q

What is the aetiology of pancreatic cancer?

A
  1. Pancreatic cancer is a disease of older people, with a peak incidence in people 65 to 75 years of age
  2. The only consistently reported exogenous risk factor for pancreatic cancer is cigarette smoking
  3. 5-10% have a familial component
  4. Weak risk factors:
    a. Obesity
    b. Diabetes Mellitus
    c. Dietary factors ( high in meats and fat, and low serum folate)
228
Q

What are the associations of pancreatic cancer?

A
  1. Increasing age
  2. Smoking
  3. Diabetes
  4. Chronic pancreatitis (alcohol does not appear an independent risk factor though)
  5. Hereditary non-polyposis colorectal carcinoma
  6. Multiple endocrine neoplasia
  7. Genetics: BRCA2 gene, KRAS gene mutation
229
Q

What is the main problem with the presentation of pancreatic cancer?

A

Pancreatic cancer is often diagnosed late as it tends to present in a non-specific way

230
Q

What are the early/ initial symptoms of pancreatic cancer?

A

Initial symptoms (often non-specific):
a. Anorexia
b. Malaise
c. Weight loss
d. Nausea
Later symptoms: jaundice, epigastric pain

231
Q

What is the main presenting symptom that often occurs later in pancreatic cancer?

A

Painless jaundice: pale stools, dark urine, and pruritus

232
Q

What are the signs of pancreatic cancer of physical examination?

A
  1. Courvoisier’s law: states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
  2. migratory thrombophlebitis (Trousseau sign): is more common than with other cancers
233
Q

What is Courvoisier’s law?

A

In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

234
Q

What are associated features of pancreatic cancer?

A
  1. Loss of exocrine function (e.g. steatorrhoea)
  2. Loss of endocrine function (e.g. diabetes mellitus)
235
Q

What is the initial investigation for pancreatic cancer?

A

Ultrasound: has a sensitivity of around 60-90%

236
Q

What is the investigation of choice for pancreatic cancer?

A

High-resolution CT scanning:
imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts

237
Q

What are the other investigations alongside imaging for pancreatic cancer?

A

Bloods:
1. Tumour marker CA19-9 can be elevated (specific, but not diagnostic)
2. If causing obstructive jaundice: bilirubin, alkaline phosphatase, and gamma glutamyl transpeptidase elevated

238
Q

What is the management of pancreatic cancer?

A

Less than 20% are suitable for surgery at diagnosis:
1. Surgery
2. Palliation (± ERCP stenting)

239
Q

What is the surgical management of pancreatic cancer?

A

Whipple’s resection (pancreaticoduodenectomy):
1. Performed for resectable lesions in the head of pancreas
2. Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
3. Adjuvant chemotherapy following surgery

240
Q

What is acute pancreatitis?

A

An acute inflammatory process of the pancreas and is associated with acinar cell injury with local and systemic inflammatory responses (self-limiting and reversible pancreatic injury)

241
Q

What are the two most common causes of acute pancreatitis?

A

Gallstones and alcohol

242
Q

What are the other causes of acute pancreatitis?

A

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune disease
Scorpion sting
Hypercalcemia
Hypertriglyceridemia
ERCP
Drugs: furosemide, azathioprine, thiazide diuretics, sulfonamides, tetracyclines, sodium, mesalazine, oestrogen

243
Q

What is the epidemiology of acute pancreatitis?

A
  1. Common- the most common cause worldwide is alcohol consumption
  2. Peak age is 60 years
  3. In males, alcohol-induced is more common while in females, principal cause is gallstones
244
Q

What is the pathophysiology of acute pancreatitis?

A

Autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis

245
Q

What are the presenting symptoms of acute pancreatitis?

A
  1. Severe epigastric or abdominal pain:
    a. radiating to back
    b. relieved by sitting forward
    c. aggravated by movement
  2. Associated with anorexia, nausea and vomiting
246
Q

What are the signs of acute pancreatitis on examination?

A
  1. Epigastric tenderness
  2. Ileus
  3. Low-grade fever
  4. Rarer signs:
    a. periumbilical discolouration (Cullen’s sign)
    b. flank discolouration (Grey-Turner’s sign)
247
Q

What are the investigations for acute pancreatitis?

A
  1. Bloods:
    a. Amylase (>3 times of normal)
    b. Lipase
    c. FBC: neutrophilia
    d. U&Es: hypocalcaemia
    e. Hyperglycaemia
    f. LDH and AST (LFTs): raised
  2. Imaging: ultrasound e.g. for gallstones
248
Q

What is the role of serum amylase and lipase in the investigation of acute pancreatitis?

A
  1. Amylase:
    a. Raised in 75% of patients - typically > 3 times the upper limit of normal
    b. Levels do not correlate with disease severity
  2. Lipase:
    a. More sensitive and specific than serum amylase
    b. Has a longer half-life than amylase and may be useful for late presentations > 24 hours
249
Q

What conditions could lead to a raised amylase?

A
  1. Pancreatitis
  2. Pancreatic pseudocyst
  3. Mesenteric infarct
  4. Perforated viscus
  5. Acute cholecystitis
  6. Diabetic ketoacidosis
250
Q

When is imaging not needed in the diagnosis of acute pancreatitis?

A

If there is characteristic pain + amylase/lipase > 3 times normal level

251
Q

What are some of the scoring systems for acute pancreatitis?

A

Ranson score, Glasgow score and APACHE II. Factors for severe pancreatitis include:
1. Age > 55 years
2. Hypocalcaemia
3. Hyperglycaemia
4. Hypoxia
5. Neutrophilia
6. Elevated LDH and AST

252
Q

How can acute pancreatitis be stratified?

A
  1. Mild: no organ failure, no complications
  2. Moderately severe: no/ transient (<48 hours) organ failure, possible complications
  3. Severe: persistent (> 48 hours) organ failure, possible complications
253
Q

What is the key aspect of care in the management of acute pancreatitis?

A

Fluid resuscitation:
1. Aggressive early hydration with crystalloids
2. In severe cases 3-6 litres of third space fluid loss may occur
3. Aim for a urine output of > 0.5mls/kg/hr
4. May also help relieve pain by reducing lactic acidosis

254
Q

What are the other aspects of managing acute pancreatitis?

A
  1. Analgesia: IV opioids are normally required to adequately control the pain
  2. Nutrition: not routinely be made ‘nil-by-mouth’ unless there is a clear reason e.g. the patient is vomiting, enteral nutrition offered if there is moderately severe pancreatitis within 72 hours of presentation
  3. Antibiotics: not prophylactic, potential indications include infected pancreatic necrosis
  4. Surgery e.g. urgent early cholecystectomy for gallstones, ERCP for obstructed biliary system
255
Q

What is the surgical management of pancreatitis?

A
  1. Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy
  2. Patients with obstructed biliary system due to stones should undergo early ERCP
  3. Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement, fine needle aspiration is still used by some
  4. Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy
256
Q

What are the complications of acute pancreatitis?

A

Local:
1. Peripancreatic fluid collection
2. Psuedocyst
3. Pancreatic necrosis
4. Pancreatic abscess
5. Haemorrhage
Systemic: ARDS (high mortality rate around 20%)

257
Q

What are peripancreatic fluid collections?

A
  1. Complication of acute pancreatitis
  2. Occur in 25% cases
  3. Located in or near the pancreas and lack a wall of granulation or fibrous tissue
  4. May resolve or develop into pseudocysts or abscesses
  5. Since most resolve aspiration and drainage is best avoided as it may precipitate infection
258
Q

What are pancreatic pseudocysts?

A
  1. Result from organisation of peripancreatic fluid collection
  2. They may or may not communicate with the ductal system
  3. The collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or more after an attack of acute pancreatitis
  4. Most are retrogastric
    75% are associated with persistent mild elevation of amylase
  5. Investigation is with CT, ERCP and MRI or endoscopic USS
  6. Treatment is either with endoscopic or surgical cystogastrostomy or aspiration
259
Q

What is Pancreatic necrosis?

A
  1. May involve both the pancreatic parenchyma and surrounding fat
  2. Complications are directly linked to extent of parenchymal necrosis and extent of necrosis overall
  3. Early necrosectomy is associated with a high mortality rate (should be avoided)
  4. Sterile necrosis should be managed conservatively (at least initially)
260
Q

What are pancreatic abscesses?

A
  1. Complication of acute pancreatitis
  2. Intraabdominal collection of pus associated with pancreas but in the absence of necrosis
  3. Typically occur as a result of infected pseudocyst
  4. Transgastric drainage is one method of treatment, endoscopic drainage is an alternative
261
Q

What is usually the timeline of complications of acute pancreatitis?

A
  1. Peripancreatic fluid collections → pseudocyst → abscess
  2. Necrosis → infected → haemorrhage
262
Q

What is pancreatic haemorrhage following acute pancreatitis?

A
  1. Infected necrosis may involve vascular structures with resultant haemorrhage that may occur de novo or as a result of surgical necrosectomy
  2. When retroperitoneal haemorrhage occurs Grey Turner’s sign may be identified
263
Q

What is the Glasgow criteria scoring system for assessing the severity of acute pancreatitis?

A

Modified Glasgow criteria (3 or more indicates severe disease):
(P) pO2 < 7.9 kPa
(A) Age > 55
(N) WCC > 15x109/L
(C) Ca2 þ < 2 mmol/L
(uR) Urea > 16 mmol/L
(Enz) LDH > 600
(A) Albumin > 32 g/L
(Sugar) Glucose > 10 mmol/L

264
Q

What is chronic pancreatitis?

A

Chronic inflammatory disease of the pancreas characterized by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain

265
Q

What is the main cause of chronic pancreatitis?

A

Alcohol (80% of cases)

266
Q

Other than alcohol, what are the causes of chronic pancreatitis?

A
  1. Genetic: cystic fibrosis, haemochromatosis
  2. Ductal obstruction: tumours, stones, structural abnormalities including pancreas divisum and annular pancreas
267
Q

What are the features of chronic pancreatitis?

A
  1. Pain: typically worse 15 to 30 minutes following a meal
  2. Steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
  3. Diabetes mellitus develops in the majority of patients, typically occurs more than 20 years after pain begins
268
Q

What are the investigations of chronic pancreatitis?

A
  1. Abdominal x-ray shows pancreatic calcification in 30% of cases
  2. CT is more sensitive at detecting pancreatic calcification
  3. Functional tests: faecal elastase may be used to assess exocrine function if imaging inconclusive
269
Q

What is the best investigation for chronic pancreatitis?

A

CT: Sensitivity is 80%, specificity is 85% for pancreatic calcification

270
Q

What is the management of chronic pancreatitis?

A

1.Pancreatic enzyme supplements
2. Analgesia
3. Treat DM
4. Antioxidants: limited evidence base - one study suggests benefit in early disease?

271
Q

What are the complications of chronic pancreatitis?

A
  1. Local: Pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites
    Important: pancreatic cancer
  2. Systemic: Diabetes, steatorrhoea, reduced quality of life, chronic pain syndromes and dependence on strong analgesics
272
Q

What is the prognosis of chronic pancreatitis?

A
  1. Difficult to predict as pain may improve, stabilise or worsen (generally, pain decreases or disappears over time, regardless of aetiology)
  2. Surgery improves symptoms in 60–70% but results are often not sustained
  3. Life expectancy can be reduced by 10–20 years
273
Q

What is Peptic ulcer disease?

A

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter, with depth to the submucosa, most commonly gastric and duodenal

274
Q

What are the risk factors for Peptic ulcer disease?

A
  1. Helicobacter pylori is associated with the majority of peptic ulcers:
    a. 95% of duodenal ulcers
    b. 75% of gastric ulcers
  2. Drugs:
    a. NSAIDs
    b. SSRIs
    c. corticosteroids
    d. Bisphosphonates
275
Q

What is the epidemiology of Peptic ulcer disease?

A
  1. Common
  2. More common in males
  3. Duodenal ulcers have a mean age in 30s while gastric ulcers have a mean age in 50s
  4. H. pylori is usually acquired in childhood
276
Q

What type of peptic ulcer disease is more common?

A

Duodenal ulcers

277
Q

What are the features of peptic ulcer disease?

A
  1. Epigastric pain: depends on gastric (worsened by eating), or duodenal (worse when hungry, relieved by eating)
  2. Nausea
278
Q

What is the pattern of epigastric pain in gastric ulcers?

A

Epigastric pain worsened by eating

279
Q

What is the pattern of epigastric pain in duodenal ulcers?

A

Epigastric pain when hungry, relieved by eating

280
Q

How else can peptic ulcer disease present?

A

Complicated:
1. Acute bleeding
2. Perforation

281
Q

What are the investigations for peptic ulcer disease?

A
  1. History of drugs e.g. NSAID use
  2. Helicobacter pylori should be tested for via either a Urea breath test or stool antigen test (first line)
282
Q

What is the the management of uncomplicated peptic ulcer disease?

A

1.If Helicobacter pylori is negative then proton pump inhibitors (PPIs) should be given until the ulcer is healed
2. If Helicobacter pylori is positive then eradication therapy should be given:
a. PPI + amoxicillin + (clarithromycin OR metronidazole)
b. If penicillin-allergic: a PPI + metronidazole + clarithromycin

283
Q

What is the most common complication of peptic ulcer disease?

A

Bleeding

284
Q

What is the aetiology of acute bleeding in peptic ulcer disease?

A

The gastroduodenal artery can be the source of a significant gastrointestinal bleed

285
Q

What is the main feature of acute bleeding secondary to peptic ulcer disease?

A
  1. Haematemesis
  2. Other features include:
    melaena, hypotension, tachycardia
286
Q

What are the investigations and management of acute bleeding secondary to peptic ulcer disease?

A
  1. ABC approach as with any upper gastrointestinal haemorrhage
  2. IV proton pump inhibitor
  3. First line treatment: endoscopic intervention
  4. If this fails (approximately 10% of patients) then either:
    urgent interventional angiography with transarterial embolization or surgery
287
Q

What is the first line management for acute bleeding secondary to peptic ulcer disease?

A

Endoscopic intervention

288
Q

What is a less common complication of peptic ulcer disease?

A

Perforation:
1. Typically develops sudden epigastric pain, later becoming more generalised
2. Patients may describe syncope

289
Q

What are the investigations of perforation secondary to peptic ulcer disease?

A

First: plain x-rays:
1. Upright (‘erect’) chest x-ray is usually required when a patient presents with acute upper abdominal pain
2. This is a useful test, as approximately 75% of patients with a perforated peptic ulcer will have free air under the diaphragm

290
Q

What is the management of perforation secondary to peptic ulcer disease?

A

Acute:
a. Resuscitation if perforated or bleeding (IV colloids/crystalloids)
b. Close monitoring of vital signs
c. Proceed to endoscopic or surgical treatment: Truncal vagotomy (reduce acid production) and pyloroplasty (reconstruct the lining lost)

291
Q

What is the prognosis of Peptic ulcer disease?

A
  1. Overall lifetime risk is 10%
  2. Generally good prognosis as peptic ulcers associated with H. pylori can be cured by eradication (or NSAID discontinuation)
  3. With proton-pump inhibitor (PPI) therapy, duodenal ulcers typically heal within 4 weeks and gastric ulcers within 8 weeks
292
Q

What is gastritis?

A

The histological presence of gastric mucosal inflammation

293
Q

What are the two main causes of gastritis?

A

H. pylori and NSAID use (can be alcohol too)

294
Q

What are the presenting symptoms/signs of Gastritis?

A
  1. Dyspepsia (indigestion)/epigastric discomfort
  2. Nausea and vomiting
  3. Loss of appetite
  4. Absence of malignancy features
295
Q

What are the investigations for Gastritis?

A

§. Helicobacter pylori urea breath test or stool antigen: positive result if H pylori present
2. FBC: may show reduced Hb and HCT and increased MCV in autoimmune gastritis; leukocytosis in phlegmonous gastritis (caused by numerous bacterial agents)
3. Consider endoscopy:
a. For patients 60 years of age or older presenting with dyspepsia
b. Only on a case-by-case basis in younger patients with dyspepsia who have red flag features (weight loss, anaemia, dysphagia and persistent vomiting)

296
Q

What is the management of Gastritis?

A
  1. Helicobacter pylori gastritis:
    a. Triple therapy for 1–2 weeks, PPI and two antibiotics (e.g. clarithromycin + amoxicillin, metronidazole + tetracycline)
  2. Erosive gastritis:
    a. Reducing exposure to the associated agent is essential e.g. alcohol and NSAID discontinuation
    b. Symptomatic therapy with either H₂ antagonists or a PPI
297
Q

What are Perineal abscesses and fistulae?

A
  1. Perineal abscess: is a collection of pus resulting from an infection in the perineum
  2. Perineal fistula: an abnormally chronically infected tract communication between the perineal skin and the anal canal or rectum
298
Q

What is the aetiology of Perineal abscesses and fistulae?

A
  1. Abscess: Bacterial infection
  2. Fistulae are often a complication of an abscess
  3. RF for fistulae:
    a. IBD (especially Crohn’s)
    b. DM
    c. Malignancy
299
Q

What are the presenting symptoms of Perineal abscesses and fistulae?

A
  1. Throbbing pain in the perineum
  2. Intermittent discharge near the anal region (mucus or faecal)
  3. PMH or FH of IBD
300
Q

What are the signs of Perineal abscesses and fistulae on physical examination?

A
  1. Localised tender perineal mass
  2. Small skin lesion near the anus - opening of the fistula
  3. On DRE: thickened area over the abscess or fistula may be felt
301
Q

What is Goodsall’s law regarding perineal fistulas?

A

Correlate the location of the internal fistula opening based on the location of the external fistula opening:
1. If external opening is anterior to anal canal, the fistula runs radially and directly into anal canal
2. If external opening lies posterior to the transverse anal line, it will follow a curved path and open internally in the posterior midline

302
Q

What are the appropriate investigations for Perineal abscesses and fistulae?

A
  1. Bloods:
    a. FBC: leukocytosis
    b. CRP/ESR: inflammation
  2. Blood culture: positive for causative organism
  3. Imaging: MRI
303
Q

What is the management of Perineal abscesses and fistulae?

A
  1. Medical: antibiotics
  2. Surgical treatment:
    a. Open drainage of abscess
    b. Laying open if fistula, investigate via probe or dye
    c. LOW fistula: fistulotomy, care taken to prevent damage to anal sphincter
    d. HIGH fistula: seton- non-absorbable suture that is threaded through the fistula and allows drainage (fistulotomy would cause incontinence)
304
Q

What are the complications of Perineal abscesses and fistulae?

A
  1. Recurrence (high rate if abscess not completely excised)
  2. Damage to internal anal sphincter
  3. Incontinence
  4. Persisting pain
305
Q

What is Peritonitis?

A
  1. Inflammation of the peritoneum usually caused by infection from bacteria or fungi
  2. Left untreated, peritonitis can rapidly spread into the blood (sepsis) and to other organs, resulting in multiple organ failure and death
306
Q

What is the aetiology of peritonitis?

A

The two main types:
1. Primary spontaneous peritonitis: an infection that develops in the peritoneum
2. Secondary peritonitis: usually develops when an injury or infection in the abdominal cavity allows infectious organisms into the peritoneum

307
Q

What is the epidemiology of peritonitis?

A
  1. Both types of peritonitis are life-threatening
  2. The death rate from peritonitis depends on many factors, but can be as high as 40% in those who also have cirrhosis
308
Q

What are the risk factors for primary spontaneous peritonitis?

A
  1. Liver disease with cirrhosis: buildup of abdominal fluid (ascites) that can become infected
  2. Kidney failure getting peritoneal dialysis
309
Q

What are the causes for secondary peritonitis?

A
  1. Ruptured appendix, diverticulum, or stomach ulcer
  2. Digestive diseases such as Crohn’s disease and diverticulitis
  3. Pancreatitis
  4. Pelvic inflammatory disease
  5. Perforations of the bowel, stomach, intestine, gallbladder, or appendix
  6. Surgery/ trauma
310
Q

What are the presenting symptoms of peritonitis?

A
  1. Abdominal pain or tenderness
  2. Rigors , fever
  3. Not passing any urine (or passing less volume than usual)
  4. Difficulty passing gas or having a bowel movement
  5. Vomiting
  6. May have ascites if SBP
311
Q

What are the signs of peritonitis on physical examination?

A
  1. Abdominal pain or tenderness
  2. Signs of ascites:
    a. flank dullness
    b. shifting dullness
    c. fluid wave, and auscultatory percussion
  3. Signs of sepsis may be present:
    a. Hypothermia
    b. Hypotension
    c. Tachycardia
312
Q

What are the appropriate investigations for peritonitis?

A
  1. Bloods:
    a. FBC: leukocytosis, anaemia (if worsens may be a GI bleed)
    b. Creatinine: elevated hepatorenal syndrome may be present
    c. LFTs: May be useful in determining if patient has liver disease
    d. Blood cultures: growth of causative organism
  2. Paracentesis: analysis of peritoneal fluid for culture and neutrophil count
  3. Imaging: CT scan
    a. Demonstrate diffuse ascites
    b. Can exclude pneumoperitoneum in patients with secondary peritonitis
313
Q

What is the management for peritonitis?

A
  1. Patients who appear otherwise well (no signs of sepsis, encephalopathy, or GI bleeding): started on oral antibiotics: quinolone or a cephalosporin such as cefixime, continue for 5 to 10 days
  2. Patients who have signs of sepsis, encephalopathy, or GI bleeding: started on empirical broad-spectrum antibiotics e.g cephalosporin, ciprofloxacin
  3. Surgery: necessary to remove infected tissue, treat the underlying cause of the infection, and prevent the infection from spreading, especially if peritonitis is due to a ruptured appendix, stomach or colon
314
Q

What are the possible complications of peritonitis?

A
  1. High risk of sepsis/septic shock
    2.High risk of renal dysfunction/impairment
  2. Medium risk of worsening ascites
315
Q

What is spontaneous bacterial peritonitis?

A

A form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis

316
Q

What are the features of spontaneous bacterial peritonitis?

A
  1. Ascites
  2. Abdominal pain
  3. Fever
  4. May be signs of sepsis
317
Q

How is SBP diagnosed?

A
  1. A to E approach
  2. Bloods
  3. Paracentesis
    a. neutrophil count > 250 cells/ul
    b. Culture: E. coli
318
Q

What is the best investigation for SBP?

A

Paracentesis:
1. Neutrophil count > 250 cells/ul
2. Most common organism found on ascitic fluid culture is E. coli

319
Q

What is the management of SBP?

A

IV cefotaxime is usually given

320
Q

When should antibiotic prophylaxis be given to patients with acites secondary to liver cirrhosis?

A
  1. Patients who have had an episode of SBP
  2. Patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
  3. NICE: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
321
Q

What is a marker of poor prognosis of SBP?

A

Alcoholic liver disease

322
Q

What is Pilonidal sinus disease?

A

A relatively common condition where sinuses and cysts form near the upper part of the natal cleft of the buttocks

323
Q

What is the epidemiology of pilonidal disease?

A

More common in men and typically presents around the age of 20 years

324
Q

What is the pathophysiology of pilonidal disease?

A
  1. Thought to develop as a result of hair debris collecting in intergluteal pores that become stretched when a person sits or bends
  2. Over a period of time, this may lead to sinus formation, with further hairs become trapped within the sinus
  3. The opening of the sinus is lined by squamous epithelium, but most of its wall consists of granulation tissue
325
Q

What are the clinical features of pilonidal disease?

A
  1. Typically sinus presents when acute inflammation occurs, leading to an abscess:
    a. pain (may be severe)
    b. purulent discharge
    c. fluctuant swelling at the site
  2. Patients may describe cycles of being asymptomatic and periods of pain and discharge from the sinus
326
Q

What is the management of asymptomatic pilonidal disease?

A

May be managed conservatively, with a focus on local hygiene

327
Q

What is the management of symptomatic pilonidal disease?

A

1.If acute: then incision and drainage, allowing the wound to close by secondary intention
2. If chronic/recurrent: then surgical options including excision of the pits and obliteration of the underlying cavity

328
Q

What is the prognosis of Pilonidal sinus?

A
  1. Depending on the surgical technique chosen, recurrence rates are variable and average 6.9%
  2. Less likely to occur after healing by secondary intention
  3. Small risk of pilonidal abscess or necrotising fascitis: presence of fever and toxaemia should raise suspicion for severe skin infection
329
Q

What is ascites?

A

Tthe abnormal accumulation of fluid in the abdomen

330
Q

How can the causes of ascites be grouped?

A

Serum-ascites albumin gradient (SAAG):
1. SAAG > 11g/L
(indicates portal hypertension)
2. SAAG <11g/L

331
Q

What are the causes of serum ascites albumin gradient > 11g/L?

A
  1. Liver disorders (most common cause):
    a. cirrhosis/alcoholic liver disease
    b. acute liver failure
    c. liver metastases
  2. Cardiac:
    a. right heart failure
    b. constrictive pericarditis
  3. Other causes:
    a. Budd-Chiari syndrome
    b. portal vein thrombosis
332
Q

What are the causes of serum ascites albumin gradient < 11g/L?

A
  1. Hypoalbuminaemia:
    a. nephrotic syndrome
    b. severe malnutrition (e.g. Kwashiorkor)
  2. Malignancy: peritoneal carcinomatosis
  3. Infections: tuberculous peritonitis
  4. Other causes:
    a. pancreatitisis
    b. bowel obstruction
    c. biliary ascites
333
Q

What is the general management of ascites?

A
  1. Reducing dietary sodium
  2. Fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
  3. Aldosterone antagonists: e.g. spironolactone
  4. Drainage if tense ascites (therapeutic abdominal paracentesis)
  5. Consider prophylactic antibiotics to prevent SBP

!Final Year (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions