Gastrointestinal (3) Flashcards

1
Q

Define haemorrhoids

A

Enlargement, engorgement and protrusion of the haemorrhoidal vascular cushions in the anal canal which have a tendency to bleed or prolapse

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2
Q

Describe haemorrhoid classification

A

Internal haemorrhoids lie ABOVE the dentate line
External haemorrhoids lie BELOW the dentate line

Dentate line = divides upper 2/3 and lower 1/3 of the anal canal and represents the hindgut-proctodeum junction

1st Degree - haemorrhoids that do NOT prolapse
2nd Degree - prolapse with defecation but
reduce spontaneously
3rd Degree - prolapse and require manual reduction
4th Degree - prolapse that CANNOT be reduced

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3
Q

What are the risk factors of haemorrhoids?

A

Age 45-65
History of constipation
Increased intra-abdominal pressure: pregnancy and ascites
Presence of space occupying pelvic lesion
Prolonged straining
Derangement of the internal anal sphincter
Portal hypertension

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4
Q

Summarise the epidemiology of haemorrhoids?

A

More common in white patients
Most common at 45-65 years
Very common

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5
Q

What are the presenting symptoms of haemorrhoids?

A

Usually ASYMPTOMATIC
Bleeding - bright red blood on the toilet paper and drips
into the pan after passage of stool. NOT mixed with stool.
ABSENCE of alarm symptoms (weight loss, anaemia, change in bowel habit, passage of
clotted or dark blood, mucus mixed with the stool)

Itching
Anal lumps
Prolapsing tissue
Perianal pain
Sensation of incomplete evacuation
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6
Q

What are the signs on physical examination of haemorrhoids?

A

1st or 2nd degree haemorrhoids are NOT usually visible on external inspection
Internal haemorrhoids are NOT normally palpable on DRE unless they are thrombosed
Haemorrhoids are usually visible on proctoscopy

Anal mass
Tender palpable perianal lesion

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7
Q

What are the appropriate investigations for haemorrhoids?

A

DRE
Anoscopic examination
Proctoscopy
Colonoscopy/flexible sigmoidoscopy - exclude IBD, cancer
FBC - check for anaemia
Stool for occult haem - if no haemorrhoidal tissue seen on examination

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8
Q

What is the management of haemorrhoids?

A

Conservative:
High-fibre diet and increased fluid intake
Bulk laxatives
Topical creams (e.g. local anaesthetics, corticosteroids)

Injection Sclerotherapy - Induces fibrosis of the dilated veins
Banding - Barron’s bands are applied proximal to the
haemorrhoids which then fall off after a few days.
Infrared photocoagulation

Surgery:
Reserved for symptomatic 3rd and 4th degree haemorrhoids
Milligan-Morgan haemorrhoidectomy - excision of three haemorrhoidal cushions

Stapled haemorrhoidectomy is an alternative method

Post-operatively the patient should be given laxatives
to avoid constipation

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9
Q

What are the possible complications of haemorrhoids?

A
Anaemia
Thrombosis
Incarceration
Faecal incontinence
Pelvic sepsis
Anal stenosis
Bleeding
Prolapse
Gangrene
Injection Sclerotherapy Complications
Prostatitis
Perineal sepsis
Impotence
Retroperitoneal sepsis
Hepatic abscess
Haemorrhoidectomy Complications
Pain
Bleeding
Incontinence
Anal stricture
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10
Q

What is the prognosis of haemorrhoids?

A

Often chronic with high rate of recurrence
Treatment results in resolution or improvement of symptoms with low rates of recurrence.
Surgical haemorrhoidectomy confers the best long-term effect with less than 20% symptom recurrence.

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11
Q

Define hepatocellular carcinoma

A

Primary malignancy of the liver parenchyma usually in a cirrhotic liver

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12
Q

What is the aetiology/risk factors of hepatocellular carcinoma?

A

Associated with chronic liver damage:

Cirrhosis
Chronic HBV infection
Chronic HCV infection
Chronic heavy alcohol use
Diabetes
Obesity
Family history
Aflatoxin – Aspergillus flavus toxin on stored grains
Autoimmune conditions e.g. PBC, PSC, haemochromatosis
Metabolic conditions e.g. alpha-1 antitrypsin deficiency
OCP
Smoking
Male
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13
Q

Summarise the epidemiology of hepatocellular carcinoma

A

COMMON
1-2% of all malignancies
LESS common than liver metastases
High incidence in regions where hepatitis B and C are endemic

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14
Q

What are the presenting symptoms of hepatocellular carcinoma?

A
Malaise
Weight loss
Loss of appetite/anorexia
Abdominal distention
Jaundice
RUQ pain
Early satiety
Leg oedema

History of Exposure to Carcinogens:
High alcohol intake
Hepatitis B or C (e.g. sexual activity, IV drug use)
Aflatoxins

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15
Q

What are the signs on physical examination of hepatocellular carcinoma?

A
Cachexia
Lymphadenopathy
Hepatomegaly (may be nodular)
Jaundice
Ascites
Bruit over the liver
Hepatic encephalopathy
Splenomegaly
Asterixis
Spider naevi
Palmar erythema
Fetor hepaticus
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16
Q

What are the appropriate investigations for hepatocellular carcinoma?

A
Bloods
FBC - low MCV and platelets
Urea - high
Sodium - low
ESR
LFTs - high ALP, AST, ALT, bilirubin, low albumin
Clotting
Alpha-fetoprotein - tumour marker for liver cancer
Hepatitis serology

PT time - normal or elevated

Imaging:
Abdominal US
CT/MRI - GOLD STANDARD for staging

Histology/Cytology - Ascitic tap my be sent for cytological analysis

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17
Q

Define a hernia

  • Direct Inguinal
  • Indirect Inguinal
  • Femoral
  • Epigastric
  • Umbilical
A

Abnormal protrusion of a viscus through a defect in its containing compartment and its coverings into an abnormal position

Inguinal hernias are above and medial to pubic tubercle

Direct Inguinal Hernia:
Protrusion of the hernial sac directly through a weakness in the transversalis fascia and posterior wall of the inguinal canal.
Arises medial to the inferior epigastric vessels
WEAKNESS IN ABDOMINAL WALL EVOLVES INTO LOCALISED HOLE

Indirect Inguinal Hernia:
Protrusion of the hernial sac through the deep inguinal ring, following the path of the inguinal canal. Occurs lateral to inferior epigastric artery. Due to lax deep ring or patent processus vaginalis.

Femoral hernia - inferior and lateral to the pubic tubercle.

Epigastric – at site of midline union of rectus muscles

Umbilical – present in 3% at birth (normally resolves <3 years), transversalis fascia defect

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18
Q

What is the aetiology/risk factors for an inguinal hernia?

A

Congenital - abdominal contents enter the inguinal canal through a patent processus vaginalis

Acquired - due to increased intra-abdominal pressure along with muscle and transversalis fascia weakness. Degeneration, fatty changes etc

Risk Factors:
Male
Prematurity
Chronic lung disease
Age
Obesity
Raised intra-abdominal pressure (e.g. chronic cough)
Constipation
Bladder outflow obstruction
Intraperitoneal fluid (e.g. ascites)
Connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome)
Smoking
Family history
AAA 
Previous RLQ incision
Heavy lifting
BPH
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19
Q

Summarise the epidemiology of hernias

A

COMMON
Peak age in adults: 55-85 yrs
9 x more common in MALES
Groin hernias affect 27% of men and 3% of women at some point in their life

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20
Q

What are the presenting symptoms of hernias?

A

Asymptomatic
Patient notices a ‘lump in the groin’
May cause discomfort and pain
May be irreducible
May present because it has increased in size
May present because of complications (e.g. bowel obstruction) - nausea and vomiting, constipation

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21
Q

What are the signs on physical examination of a hernia?

A

Visible or palpable groin lump that extends to the scrotum (males) or labia (women)
Check for cough impulse
Indirect hernias can be reduced and controlled by applying pressure over the deep inguinal ring
Auscultation - there may be bowel sounds over the hernia
Tenderness if strangulated
Check for signs of complication

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22
Q

What are appropriate investigations for hernia?

A

Mainly a clinical diagnosis

Bloods:
FBC
U&amp;Es
CRP
Clotting
Group and save (if operation is likely)

ABGs - may show lactic acidosis from bowel ischaemia

Imaging:
Erect CXR - check for perforation
USS - exclude other causes of groin lump
AXR - check for obstruction

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23
Q

What is the management for hernias?

A

If small, asymptomatic hernia then watchful waiting

Surgical
Usually elective repair of uncomplicated hernias
Mesh Repair - The hernia is surgically reduced and a mesh is inserted to reinforce the defect in the transversalis fascia
Laparoscopic Mesh Repair
Prophylactic antibiotics given

EMERGENCY: If obstructed or strangulated, laparotomy with bowel resection may be indicated if the bowel is
gangrenous - NG feeding, fluid resuscitation

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24
Q

What are the possible complications of hernias?

A

Incarceration
Strangulation
Bowel obstruction

Surgery Complications:
Pain
Wound infection
Haematoma
Penile/scrotal oedema
Mesh infection
Testicular ischaemia
Urinary retention
Bowel obstruction
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25
Q

What is the prognosis of hernias?

A

Prognosis is excellent after surgical repair.
The incidence of recurrent hernia with mesh repair is reported to be less than 2%.
Moderate to severe chronic groin pain is reported to occur in 10% to 12% of patients after inguinal hernia repair.
Groin pain higher incidence after open repair compared to laparoscopic repair.

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26
Q

Define hiatus hernia

A

The protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm. It most commonly contains a variable portion of the stomach but can contain transverse colon, omentum, small bowel, or spleen.

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27
Q

What are the types of hiatus hernia?

A

Congenital
Traumatic
Non-traumatic

Sliding (90-95%) - the hernia moves in and out of the chest. Usually protrusion of gastro-oesophageal junction followed by body of stomach above diaphragm which causes a decreased LOS pressure.

Paraoesophageal (rolling) (5-10%) - the hernia goes through a whole in the diaphragm next to the oesophagus. The fundus or body of stomach usually herniate and the gastro-oesophageal junction remains below the diaphragm.
This can produce rotation and twisting of the stomach, leading to intermittent strangulation with obstruction and ischaemia.

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28
Q

What is the aetiology/risk factors of a hiatus hernia?

A

Aetiology is unknown however can be congenital, traumatic and non-traumatic (sliding or para-oesophageal)

Risk factors:
Obesity
Previous gastro-oesophageal procedure
Elevated intra-abdominal pressure: Chronic cough, Ascites, Multiparity, pregnancy
Low-fibre diet
Male
Advanced age
Structural abnormality of oesophageal hiatus
Chronic oesophagitis
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29
Q

Summarise the epidemiology of hiatus hernias

A

Estimates of the prevalence of hiatus hernia in western populations range up to 50%.
The prevalence may be lower in eastern populations.
The incidence of symptomatic cases of hiatus hernia is closely related to the diagnosis of GORD
Sliding hernias are the most common.
70% of patients are over 70 years old.

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30
Q

What are the presenting symptoms of hiatus hernias?

A

Mostly asymptomatic

Sliding hernias most likely to cause symptoms. Present with symptoms of GORD:
Heartburn
Regurgitation
Waterbrash

Chest pain (oesophageal spasm)
Dysphagia/odynophagia (oesophagitis)
Haematemesis
Cough/wheeze (aspiration)

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31
Q

What are the signs on physical examination of hiatus hernias?

A

No signs

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32
Q

What are the appropriate investigations for hiatus hernias?

A

CXR - gastric air bubble may be seen above the diaphragm
Upper gastrointestinal series (X ray of upper GI tract) - shows intrathoracic stomach

OGD - inflammation of oesophagus and proximal migration of gastro-oesophageal junction
CT or MRI

Oesophageal manometry or pH monitoring - double hump configuration

Bloods
FBC - check for iron deficiency anaemia

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33
Q

What is the management of a hiatus hernia?

A

Medical:
Modify lifestyle factors (e.g. lose weight)
Inhibit acid production (e.g. PPIs)
Enhance upper GI motility

Surgical with or without anti-reflux procedure:
Necessary in a MINORITY of patients - those with complications of reflux disease despite medical treatment or pulmonary complications (e.g. aspiration pneumonia)

Nissen Fundoplication:
The stomach is pulled down through the oesophageal hiatus and part of the stomach is wrapped (360 degrees) around the oesophagus to make a new
sphincter and reduce the likelihood of herniation

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34
Q

What are the possible complications of hiatus hernias?

A
Oesophageal:
Intermittent bleeding
Oesophagitis
Erosions
Barrett's oesophagus
Oesophageal strictures

Non-Oesophageal:
Incarceration of para-oesophageal hiatus hernia - strangulation and perforation
Gastric volvulus
Obstruction

Surgical complications:
Dysphagia
Haemorrhage
Fundal necrosis
Diarrhoea
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35
Q

What are the possible complications of a hiatus hernia?

A

Generally GOOD

Sliding hernias have a better prognosis than rolling hernias

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36
Q

Define intestinal ischaemia

A

Obstruction of a mesenteric vessel causing reduced blood flow to the GI tract leading to bowel inflammation, odeoma, ulceration, ISCHEMIA AND NECROSIS.

Most commonly affects the splenic flexure (the watershed between the SMA and IMA).

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37
Q

Explain the aetiology of intestinal ischaemia

A

Embolus (60%)
Thrombosis (40%)

Can be a consequence of:
Volvulus
Intussusception
Bowel strangulation
Failed surgical resection
Arterial inflow obstruction:
Atheroma
Thrombosis
Embolism (cardiac arrhythmia)
Vasculitis

Venous outflow obstruction
Reduced perfusion - Hypotension, Shock

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38
Q

What are the risk factors of intestinal ischaemia?

A
AF
Endocarditis (can throw emboli)

Arterial Thrombosis: hypercholesterolaemia, hypertension, diabetes mellitus, smoking

Venous Thrombosis: portal hypertension, splenectomy, septic thrombophlebitis, OCP, thrombophilia

Old age
Hypercoagulable states
Myocardial infarction
History of vasculitis

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39
Q

Summarise the epidemiology of intestinal ischaemia

A

Uncommon
More common in elderly (60-80 years)
More common in those with co-morbidities (AF, MI, atherosclerosis)

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40
Q

What are the presenting symptoms of intestinal ischaemia?

A
Severe acute colicky abdominal pain
Vomiting/nausea
Rectal bleeding
History of chronic mesenteric artery insufficiency
Gross weight loss
Post-prandial abdominal pain
History of heart or liver disease
Melaena
Diarrhoea
41
Q

What are the signs on physical examination of intestinal ischaemia?

A
Diffuse abdominal tenderness
Abdominal distension
Tender palpable mass (ischaemic bowel)
Bowel sounds may be absent
Disproportionate degree of cardiovascular collapse
Abdominal bruit
Fever
Tachycardia
42
Q

What are the appropriate investigations for intestinal ischaemia?

A

Diagnosis based on clinical suspicion or after laparotomy

AXR - thickening of small bowel folds and signs of obstruction, bowel dilation and thickening of walls

Bloods:
ABG - lactic acidosis
FBC - leukocytosis, anaemia
U&amp;Es
LFTs
Clotting - underlying prothrombotic condition
Lactate - elevated
Cross-match

Mesenteric Angiography if stable

ECG - may show arrhythmia
Erect CXR - check for perforation
Contrast CT/CT angiogram
Sigmoidoscopy/colonoscopy

43
Q

Define intestinal obstruction

A

A mechanical disruption in the patency of the GI tract, resulting in a combination of vomiting, absolute constipation, and abdominal pain.

44
Q

Explain the aetiology/risk factors of intestinal obstruction

A
Small bowel: 
Previous surgery (adhesions) – 80%
Hernia
Crohn’s disease
Malignancy
Appendicitis
Volvulus
Intussusception (children)
Ileus

Large bowel:
Malignancy (90%)
Volvulus (5%)
Benign stricture (3%)

45
Q

Summarise the epidemiology of intestinal obstruction

A

COMMON
More common in the ELDERLY due to increasing incidence of adhesions, hernias and malignancy
Lifetime incidence between 0.1% and 5% in patients who have not undergone previous surgery
Rises to over 60% in patients who have undergone previous surgery

46
Q

What are the presenting symptoms of intestinal obstruction?

A
Severe gripping colicky pain with periods of ease
Abdominal distension
Frequent vomiting (it may be bile-stained or faeculent)
Absolute constipation
Obstipation (failure to pass stool or
flatus)
Nausea
Fever
47
Q

What are the signs on physical examination of intestinal obstruction?

A
Abdominal distension
Abdominal tenderness
Peritonitis - absent bowel sounds, guarding, rebound tenderness
Palpable abdominal mass
Palpable rectal mass
Tachycardia
Hypotension
Tinkling bowel sounds or no bowel sounds if advanced
Visible peristalsis
Abdominal scars from previous surgeries

DRE - hard faeces or empty rectum

Signs of malignancy - Weight loss, Rectal bleeding

48
Q

What are the appropriate investigations for intestinal obstruction?

A

Abdo X-Ray: Dilated intestinal loops, valvulae conniventes (small bowel - diameter more than 3cm) or haustra (large bowel - diameter more than 6cm)

Partial SBO: gas throughout the abdomen and into the rectum
Complete SBO: no distal gas, and staggered air-fluid levels
Complicated SBO: free air under the diaphragm suggestive of perforation; thumb-printing of the bowel suggestive of ischaemia

Bloods:
FBC - high WCC
Urea - increased if dehydrated
Electrolyes - low K+, Na+

Abdo CT
Water soluble contrast enema
Barium follow through

49
Q

What is the management of intestinal obstruction?

A

IV fluid resuscitation and nasogastric decompression
Electrolyte replacement
Monitor vital signs, urine output, fluid balance
Correction of underlying cause
Analgesia and anti-emetic

Pre-operative prophylactic antibiotic and surgery (emergency laparotomy)

50
Q

What are the complications of intestinal obstruction?

A
Dehydration
Bowel perforation
Peritonitis
Toxaemia
Gangrene of ischaemic bowel wall
Sepsis
Multi-organ failure
Intra-abdominal abscess
Short bowel syndrome
51
Q

What is the prognosis of intestinal obstruction?

A

Medical emergency.
Patients treated in a timely manner have a very good prognosis.
In untreated patients, obstruction progresses to intestinal necrosis, perforation, sepsis, and multi-organ failure.

52
Q

Define liver abscess

A
Purulent collections in the liver parenchyma that result from bacterial, fungal, or parasitic infection of the liver which has spread from:
Biliary tree
Portal vein (from appendicitis)
Hepatic vein
Bacteraemia
Trauma
53
Q

Explain the aetiology of liver abscess

A
Pyogenic (producing pus):
E.coli
Klebsiella sp.
Streptococcus milleri
Enterococcus
Bacteroides
Staphylococci

Amoebic:
Entamoeba histolytica

54
Q

What are the risk factors of liver abscess?

A
Biliary tract abnormalities
Age >50 years
Malignancy
Diabetes mellitus
Interventional biliary or hepatic procedures
Travel in endemic areas
Underlying malignancy
55
Q

Summarise the epidemiology of liver abscess

A
Uncommon
Higher incidence in Asia
Slightly more common in men
Incidence increases with age
Pyogenic most common in industrial world
Amoebic most common worldwide
Fungal infections can occur in immunocompromised
56
Q

What are the presenting symptoms of liver abscess?

A
Abdominal pain - RUQ/epigastric may be referred to shoulder
Nausea and vomiting
Cough, SOB, chest pain
Weight loss
Fatigue
Fevers and chills
Anorexia
Night sweats
Jaundice
Diarrhoea
History of foreign travel
57
Q

What are the signs on physical examination of liver abscess?

A
RUQ tenderness
Hepatomegaly
Ascites
Signs of pleural effusion in right lower zone - dullness to percussion, reduced breath sounds
Signs of shock
Jaundice
58
Q

What are the appropriate investigations for liver abscess?

A

Bloods:
FBC - Mild anaemia, Leukocytosis, elevted neutrophil

LFTs - High ALP, mildly high bilirubin and AST and ALT, low albumin
High ESR and CRP

PT to see if aspiration can occur
Liver USS - guide aspiration of abscess
Contrast enhanced CT abdo

Blood cultures: Amoebic and hydatid serology
Stool MC&S - for E. histolytica
Culture of aspirated fluid and gram stain

CXR - check for right pleural effusion or atelectasis, raised hemidiaphragm

Aspiration and culture of the abscess material

59
Q

Define liver failure

A

Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy.

60
Q

Describe the classification of liver failure

A

Liver failure is classified based on the time interval between the onset of jaundice and the development of encephalopathy.

Hyper-acute = <7 days
Acute = 1-4 weeks
Sub-acute = 4-12 weeks
61
Q

Explain the aetiology of liver failure

A

Viral:
Hepatitis A, B, C, D and E

Drugs: Paracetamol overdose, idiosyncratic drug reactions, long-term alcohol use

Autoimmune hepatitis
Budd-Chiari syndrome
Pregnancy-related 
Malignancy (e.g. lymphoma) 
Haemochromatosis 
Mushroom poisoning (Amanita phalloides) 
Wilson's disease
62
Q

What are the risk factors of liver failure?

A

Alcohol abuse
Poor nutritional status (depletion of glutathione stores)
Pregnancy (hepatitis E)
Chronic hepatitis B

63
Q

What are the three main features of liver failure? Describe their pathogenesis

A

Jaundice: decreased secretion of conjugated bilirubin

Encephalopathy: Nitrogenous products (e.g. ammonia) is absorbed in the gut and goes via the portal circulation to the liver. If the liver is failing, these toxic products can go through the liver and reach the brain and exert its effects

Coagulopathy: Reduced synthesis of clotting factors and reduced platelets. Platelet functional abnormalities associated with jaundice or renal failure

64
Q

Summarise the epidemiology of liver failure

A

Paracetamol overdose accounts for over 50% of acute liver failure in the UK
Rare

65
Q

What are the presenting symptoms of liver failure?

A
May be asymptomatic
Fever
Nausea and vomiting
Abdominal pain
Jaundice
Malaise
66
Q

What are the symptoms of hepatic encephalopathy?

A

Sleep reversal -> Lethargy -> Somnolence -> Stupor

Reduced awareness and attention span -> Poor memory and confusion

67
Q

What are the signs on physical examination of liver failure?

A
Jaundice
Asterixis
Bruising or bleeding
Encephalopathy
Fetor hepaticus 
Hepatomegaly

Abdo or RUQ tenderness
Ascites and splenomegaly (less common if acute or hyper-acute)
Signs of secondary causes (e.g. bronze skin colour, Kayser-Fleisher rings in Wilson’s)
Pyrexia: may indicate infection or liver necrosis

Signs of hepatic encephalopathy
• Asterixis
• Hyperreflexia
• Nystagmus
• Clonus
• Rigidity

Signs of cerebral oedema
• Hypertonia
• Decerbrate posturing
• Loss of pupillary reflexes

68
Q

What are appropriate investigations for liver failure?

A
Identify the cause: 
Viral serology 
Paracetamol levels 
Autoantibodies (e.g. ASM, Anti-LKM) 
Ferritin (haemochromatosis) 
Caeruloplasmin and urinary copper (Wilson's disease) 

Bloods:
FBC - low Hb (if GI bleed), high WCC (if infection)
U&Es - May show renal failure (hepatorenal syndrome)
Glucose
LFTs - high bilirubin, high AST, ALT, ALP, GGT, low albumin
ESR/CRP
Coagulation screen

ABG: to determine blood pH
Group and save
Liver US/CT
Ascitic Tap: If neutrophils > 250/mm3 = spontaneous bacterial peritonitis
Doppler scan of hepatic or portal veins: check for Budd-Chiari syndrome
EEG: monitor encephalopathy

69
Q

What is the management of liver failure?

A

Resuscitation - ABC

Treat the cause:
N-acetylcysteine for paracetamol overdose

Treatment/prevention of complications:
Monitor - vital signs, PT, pH, creatinine, urine output, encephalopathy
Manage encephalopathy: lactulose and phosphate enemas
Antibiotic and antifungal prophylaxis
Hypoglycaemia treatment
Coagulopathy treatment - IV vitamin K, FFP, platelet infusions
Gastric mucosa protection - PPIs or sucralfate

AVOID sedatives or drugs metabolised by the liver
Cerebral oedema - decrease ICP with mannitol

Renal Failure:
Haemodialysis
Nutritional support

Surgical - liver transplant

70
Q

What are the possible complications of liver failure?

A
Infection 
Coagulopathy
Hypoglycaemia 
Disturbance of electrolyte balance and acid-base balance 
Disturbance of cardiovascular system 
Hepatorenal syndrome 
Cerebral oedema (causing raised ICP) 
Respiratory failure
71
Q

What is the prognosis of liver failure?

A

Depends on severity and aetiology

72
Q

Define Mallory-Weiss tear

A

A tear or laceration of the lining of the oesophagus along the right border of or near the gastro-oesophageal junction which causes upper GI bleeding as a result of recent violent vomiting or straining to vomit.

73
Q

What is the aetiology of Mallory-Weiss tear?

A
Coughing
Retching
Vomiting
Straining
Hiccups
Closed-chest pressure or cardiopulmonary resuscitation
Acute abdominal blunt trauma
Alcohol
Medications (aspirin or NSAIDs). 

Most common causes: chronic alcohol abuse, bulimia, trauma, intense coughing and gastritis.

Hiatal hernia is considered a precipitating factor, causing an oesophageal tear to occur.

Conditions that may induce vomiting:
GI disease: food poisoning, infectious gastroenteritis, peptic ulcer disease, malrotation, intussusception, volvulus, gastric outlet obstruction, and gastroparesis
Hepatobiliary disease: hepatitis, gallstones, and cholecystitis
Renal disease: nephrolithiasis, renal failure, and ureteropelvic obstruction
Neurological disease: tumours, hydrocephalus, congenital disease, trauma, meningitis, pseudotumour cerebri, migraine headaches, and seizures
Psychiatric disease: anorexia nervosa, bulimia, and cyclic vomiting syndrome.

74
Q

Summarise the epidemiology of Mallory-Weiss tear

A

Common - 50-150 per 100,000 people per year
Mortality between 8-14%
Mallory-Weiss tear responsible for 3-15% of upper GI bleeds
More common in men
In women of childbearing age, most common cause is hyperemesis gravidarum
Most common between 30-50 years

75
Q

What are the presenting symptoms of Mallory-Weiss tear?

A

Small and self-limiting haematemesis - flecks or streaks of blood mixed with gastric contents and/or mucus, coffee ground vomit, bright-red bloody emesis
Light headedness/dizziness (symptoms of hypovolaemia)
Dysphagia
Odynophagia
Meleana
Abdominal pain
Involuntary retching

76
Q

What are the signs on physical examination of Mallory-Weiss tear?

A

Postural hypotension

Signs of anaemia - tachycardia, pallor, fatigue

77
Q

What are appropriate investigations for Mallory-Weiss tear?

A
Bloods:
FBC - may show anaemia
Urea - high if ongoing bleeding
LFTs - normal, rule out underlying liver-disease
PT - normal

CXR - usually normal, used to check for oesophageal perforation

OGD - DIAGNOSTIC OF MWT. Tear or laceration shows as red longitudinal defect

78
Q

What is the management of a Mallory-Weiss tear?

A

80-90% of the time, the bleeding from a Mallory-Weiss tear will stop on its own
Urgent evaluation and monitoring
Endoscopy with or without intervention

If bleeding does not stop - Surgery
Injection sclerotherapy
Coagulation therapy
Arteriography

If severe blood loss - transfusions

Anti-reflux medications may also be prescribed

79
Q

What are the possible complications of a Mallory-Weiss tear?

A

Boerhaave’s Perforation - spontaneous perforation of oesophagus resulting from a sudden increase in intraoesophageal pressure combined with negative intrathoracic pressure
Re-bleeding
Hypovolaemic shock
Hypokalaemia due to vomiting

80
Q

What is the prognosis of a Mallory-Weiss tear?

A

For most patients, bleeding is self-limited, and will have stopped by the time of endoscopy.
Prognosis is excellent in patients without associated disease or complications.
A routine second endoscopic evaluation is not recommended unless the patient remains symptomatic after initial treatment.
Re-bleeding occurs in 8-15% of patients, usually within 24 hours.

81
Q

Define acute pancreatitis

A

A sudden inflammation of the pancreas due to autodigestion by its own enzymes with variable involvement of other regional tissues or remote organ systems.

Mild: minimal organ dysfunction and uneventful recovery
Severe: organ failure and/or local complications i.e. necrosis, abscesses and pseudocyst

82
Q

Explain the aetiology of acute pancreatitis

A
Most common causes are gallstones and ethanol
I - diopathic - 10-20%
G - allstones
E - thanol
T - rauma
S - teroids
M - umps
A - utoimmune
S - scorpion sting
H - yperlipidaemia/hypercalcaemia
E - RCP
D - rugs (diuretics, valproic acid, azathioprine)
83
Q

Summarise the epidemiology of acute pancreatitis

A

In the UK - 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

Alcoholic pancreatitis is seen more frequently in men

Peak age = 60 years old

84
Q

What are the presenting symptoms of acute pancreatitis?

A
Severe sudden onset epigastric pain which radiates to the back and is better on bending over/leaning forwards
Pain made worse by movement 
Nausea
Vomiting
Anorexia
85
Q

What are the signs on physical examination of acute pancreatitis?

A

Cullen sign - bruising around umbilicus
Grey-Turner’s sign - bruising across flanks
Epigastric tenderness without guarding or rebound
Decreased bowel sounds if severe
Fever
Shock - tachypnoea, tachycardia, hypotension
Signs of hypocalcaemia - Chocstek’s sign (Facial muscle spasm when facial nerve is tapped), Trousseau’s sign (Carpopedal spasm when pressure cuff is applied).

Signs of cause:
Hepatomegaly - alcohol
Xantholasma - hyperlipidaemia
Parotid grand swelling - mumps

86
Q

What are the appropriate investigations for acute pancreatitis?

A

Bloods:
FBC - leukocytosis, increased haematocrit
Amylase and lipase - more than 3 times upper limit of normal
CRP/ESR - raised
U&Es (to check for dehydration)
Serum calcium - LOW - saponification: calcium binds to digested lipids from pancreas to form soap
LFTs - may be deranged if gallstone pancreatitis or alcohol
ABG - hypoxia or metabolic acidosis

USS: check for evidence of gallstones in biliary tree
Erect CXR: may be pleural effusion. Rule out perforation
AXR: exclude other causes of acute abdomen
CT Scan: if diagnosis is uncertain or if persisting organ failure - show inflammation, necrosis, pseudocysts

87
Q

What is the management of acute pancreatitis?

A
Fluid resuscitation
Analgesia
Bowel rest if necessary
Cessation of alcohol
ERCP and elective cholecystectomy post-pancreatitis if gallstones are cause
88
Q

What are the possible complications of acute pancreatitis?

A
Local:
Pancreatic necrosis
Liquefactive haemorrhagic necrosis
Pancreatic pseudocyst
Pancreatic abscess
Systemic:
DIC
ARDS
Pleural effusion
Sepsis
Multiorgan dysfunction
Renal failure
Hypocalceamia

Long term: CHRONIC PANCREATITIS

89
Q

What is the presentation of a pancreatic pseudocyst?

A

Following a bout of acute pancreatitis:
Abdominal pain
Anorexia/loss of appetite
Palpable mass in abdomen

Pancreatic abscess presents the same but with fever and high WCC

90
Q

What is the prognosis of acute pancreatitis?

A

80% of patients with acute pancreatitis have mild disease and will improve within 3 to 7 days of conservative management.
Overall mortality rate is low (approximately 5%)
Mortality rate rises to 25% to 30% in severe acute pancreatitis

91
Q

Define chronic pancreatitis

A

Persistent inflammation of the pancreas causing progressive injury to the pancreas and surrounding structures, resulting in irreversible scarring, calcification and parenchymal atrophy leading to loss of endocrine and exocrine function.

92
Q

Summarise the aetiology of chronic pancreatitis

A
Main causes are alcohol (70%) and idiopathic (20%)
Repeated bouts of acute pancreatitis
Gallstones
Tumour causing duct obstruction
Trauma
Cystic fibrosis
Hyperlipidaemia
Hypercalcaemia
93
Q

Summarise the epidemiology of chronic pancreatitis

A

Most common cause in children = cystic fibrosis
Prevalence 0.04-5%
Alcoholic chronic pancreatitis presentation 36-44y/o

94
Q

What are the presenting symptoms of chronic pancreatitis?

A

Repeated bouts of epigastric pain which radiates to the back
Pain relieved by sitting forward
Pain can be aggravated by eating or drinking alcohol
Weight loss
Steatorrhoea - greasy, smelly stools
Bloating

95
Q

What are the signs on physical examination of chronic pancreatitis?

A

Weight loss
Jaundice - if caused by pancreatic tumour causing obstruction of CBD
Epigastric tenderness

96
Q

What are the appropriate investigations for chronic pancreatitis?

A

Bloods:
Serum amylase/lipase - may be normal due to pancreatic insufficiency
Bilirubin and ALP - may be elevated if due to tumour compressing CBD
Glucose - high due to Diabetes mellitus following loss of endocrine function
Ig4 high if autoimmune

Ultrasound - may show gallstones
ERCP or MRCP: may show stenosis and dilatation of ducts - chains of lakes pattern
AXR: pancreatic calcification
CT Scan: May show pancreatic calcification and pancreatic cysts
Tests of pancreatic exocrine function: Faecal elastase (pancreatic exocrine function) - LOW
72hr stool collection - high fat due to fat malabsorption

97
Q

What is the management of chronic pancreatitis?

A
Adequate fluid intake
Alcohol cessation
Low fat meals
Reduce meat intake
Glycaemic control
Oral pancreatic enzyme replacement
Nutritional supplements
98
Q

What are the possible complications of chronic pancreatitis?

A
Local:
Pseudocysts 
Biliary duct stricture 
Duodenal obstruction 
Pancreatic ascites 
Pancreatic carcinoma 
Systemic: 
Diabetes mellitus
Vitamin A, D, E, K (fat soluble vitamins) deficiency
Steatorrhoea 
Chronic pain syndromes 
Dependence on strong analgesics
99
Q

What is the prognosis of chronic pancreatitis?

A

Ten-year survival after diagnosis is 20% to 30% lower than the general population
Chronic pain usually decreases
Depends on aetiology
Leading cause of death in alcoholic pancreatitis is CVS disease