Gastrointestinal (3) Flashcards

(99 cards)

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

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

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

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

Summarise the epidemiology of haemorrhoids?

A

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define hepatocellular carcinoma

A

Primary malignancy of the liver parenchyma usually in a cirrhotic liver

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

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

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

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the prognosis of hernias?
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.
26
Define hiatus hernia
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.
27
What are the types of hiatus hernia?
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.
28
What is the aetiology/risk factors of a hiatus hernia?
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 ```
29
Summarise the epidemiology of hiatus hernias
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.
30
What are the presenting symptoms of hiatus hernias?
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)
31
What are the signs on physical examination of hiatus hernias?
No signs
32
What are the appropriate investigations for hiatus hernias?
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
33
What is the management of a hiatus hernia?
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
34
What are the possible complications of hiatus hernias?
``` 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 ```
35
What are the possible complications of a hiatus hernia?
Generally GOOD | Sliding hernias have a better prognosis than rolling hernias
36
Define intestinal ischaemia
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).
37
Explain the aetiology of intestinal ischaemia
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
38
What are the risk factors of intestinal ischaemia?
``` 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
39
Summarise the epidemiology of intestinal ischaemia
Uncommon More common in elderly (60-80 years) More common in those with co-morbidities (AF, MI, atherosclerosis)
40
What are the presenting symptoms of intestinal ischaemia?
``` 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
What are the signs on physical examination of intestinal ischaemia?
``` 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
What are the appropriate investigations for intestinal ischaemia?
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&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
Define intestinal obstruction
A mechanical disruption in the patency of the GI tract, resulting in a combination of vomiting, absolute constipation, and abdominal pain.
44
Explain the aetiology/risk factors of intestinal obstruction
``` 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
Summarise the epidemiology of intestinal obstruction
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
What are the presenting symptoms of intestinal obstruction?
``` 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
What are the signs on physical examination of intestinal obstruction?
``` 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
What are the appropriate investigations for intestinal obstruction?
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
What is the management of intestinal obstruction?
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
What are the complications of intestinal obstruction?
``` Dehydration Bowel perforation Peritonitis Toxaemia Gangrene of ischaemic bowel wall Sepsis Multi-organ failure Intra-abdominal abscess Short bowel syndrome ```
51
What is the prognosis of intestinal obstruction?
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
Define liver abscess
``` 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
Explain the aetiology of liver abscess
``` Pyogenic (producing pus): E.coli Klebsiella sp. Streptococcus milleri Enterococcus Bacteroides Staphylococci ``` Amoebic: Entamoeba histolytica
54
What are the risk factors of liver abscess?
``` Biliary tract abnormalities Age >50 years Malignancy Diabetes mellitus Interventional biliary or hepatic procedures Travel in endemic areas Underlying malignancy ```
55
Summarise the epidemiology of liver abscess
``` 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
What are the presenting symptoms of liver abscess?
``` 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
What are the signs on physical examination of liver abscess?
``` RUQ tenderness Hepatomegaly Ascites Signs of pleural effusion in right lower zone - dullness to percussion, reduced breath sounds Signs of shock Jaundice ```
58
What are the appropriate investigations for liver abscess?
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
Define liver failure
Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy.
60
Describe the classification of liver failure
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
Explain the aetiology of liver failure
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
What are the risk factors of liver failure?
Alcohol abuse Poor nutritional status (depletion of glutathione stores) Pregnancy (hepatitis E) Chronic hepatitis B
63
What are the three main features of liver failure? Describe their pathogenesis
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
Summarise the epidemiology of liver failure
Paracetamol overdose accounts for over 50% of acute liver failure in the UK Rare
65
What are the presenting symptoms of liver failure?
``` May be asymptomatic Fever Nausea and vomiting Abdominal pain Jaundice Malaise ```
66
What are the symptoms of hepatic encephalopathy?
Sleep reversal -> Lethargy -> Somnolence -> Stupor Reduced awareness and attention span -> Poor memory and confusion
67
What are the signs on physical examination of liver failure?
``` 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
What are appropriate investigations for liver failure?
``` 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
What is the management of liver failure?
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
What are the possible complications of liver failure?
``` 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
What is the prognosis of liver failure?
Depends on severity and aetiology
72
Define Mallory-Weiss tear
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
What is the aetiology of Mallory-Weiss tear?
``` 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
Summarise the epidemiology of Mallory-Weiss tear
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
What are the presenting symptoms of Mallory-Weiss tear?
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
What are the signs on physical examination of Mallory-Weiss tear?
Postural hypotension | Signs of anaemia - tachycardia, pallor, fatigue
77
What are appropriate investigations for Mallory-Weiss tear?
``` 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
What is the management of a Mallory-Weiss tear?
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
What are the possible complications of a Mallory-Weiss tear?
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
What is the prognosis of a Mallory-Weiss tear?
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
Define acute pancreatitis
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
Explain the aetiology of acute pancreatitis
``` 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
Summarise the epidemiology of acute pancreatitis
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
What are the presenting symptoms of acute pancreatitis?
``` 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
What are the signs on physical examination of acute pancreatitis?
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
What are the appropriate investigations for acute pancreatitis?
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
What is the management of acute pancreatitis?
``` Fluid resuscitation Analgesia Bowel rest if necessary Cessation of alcohol ERCP and elective cholecystectomy post-pancreatitis if gallstones are cause ```
88
What are the possible complications of acute pancreatitis?
``` 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
What is the presentation of a pancreatic pseudocyst?
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
What is the prognosis of acute pancreatitis?
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
Define chronic pancreatitis
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
Summarise the aetiology of chronic pancreatitis
``` Main causes are alcohol (70%) and idiopathic (20%) Repeated bouts of acute pancreatitis Gallstones Tumour causing duct obstruction Trauma Cystic fibrosis Hyperlipidaemia Hypercalcaemia ```
93
Summarise the epidemiology of chronic pancreatitis
Most common cause in children = cystic fibrosis Prevalence 0.04-5% Alcoholic chronic pancreatitis presentation 36-44y/o
94
What are the presenting symptoms of chronic pancreatitis?
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
What are the signs on physical examination of chronic pancreatitis?
Weight loss Jaundice - if caused by pancreatic tumour causing obstruction of CBD Epigastric tenderness
96
What are the appropriate investigations for chronic pancreatitis?
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
What is the management of chronic pancreatitis?
``` Adequate fluid intake Alcohol cessation Low fat meals Reduce meat intake Glycaemic control Oral pancreatic enzyme replacement Nutritional supplements ```
98
What are the possible complications of chronic pancreatitis?
``` 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
What is the prognosis of chronic pancreatitis?
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