Gastrointestinal Flashcards

(508 cards)

1
Q

Define achalasia

A

An oesophageal motor disorder characterised by a loss of oesophageal peristalsis and failure of the lower oesophageal sphincter (LOS) to relax in response to swallowing

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2
Q

Explain the aetiology of achalasia

A

The degeneration of ganglion cells of the myenteric plexus in the oesophagus

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3
Q

Summarise the epidemiology of achalasia

A

Annual incidence is about 1 in 100000. Usual presentation age: 25–60 years.

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4
Q

What are the presenting symptoms of achalasia?

A

Insidious onset and gradual progression of:
. intermittent dysphagia involving solids and liquids;
. difficulty belching;
. regurgitation (particularly at night);
. heartburn;
. chest pain (atypical/cramping, retrosternal);
. weight loss.

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5
Q

What are the signs of achalasia on physical examination?

A

May reveal signs of complications: aspiration pneumonia, malnutrition and weight loss may result

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6
Q

What are the appropriate investigations for achalasia?

A

1st line:
Upper gastrointestinal endoscopy- mucosa obscured by retained saliva (and to exclude malignancy)

Barium swallow: Dilated oesophagus which smoothly tapers down to the sphincter (beak- shaped). Loss of peristalsis and delayed oesophageal emptying

Oesophageal Manometry:
. incomplete LOS relaxation
. Elevated resting LOS pressure (>45 mmHg);
. absence of peristalsis in the distal (smooth muscle portion) of the oesophagus.

CXR:may show a widened mediastinum and double right heart border (dilated oesophagus), an air-fluid level in the upper chest and absence of the normal gastric air bubble.

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7
Q

What is acute cholangitis?

A

Also known as ascending Cholangitis

  • Infection of the biliary tree, most commonly caused by obstruction
  • In its less severe form, there is biliary obstruction with inflammation and bacterial seeding and growth in the biliary tree
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8
Q

What is the aetiology of acute cholangitis?

A
  • Most commonly gallstones leading to choledocholithiasis (gallstones in the bile duct) and biliary obstruction.
  • Iatrogenic biliary tract injury, most commonly caused via surgical injury cholecystectomy, can lead to benign strictures, which in turn can lead to obstructions
  • Acute prancreatitis
  • Malignant strictures (restricts flow)
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9
Q

What is the epidemiology of acute cholangitis?

A

Relatively uncommon
Male: female ratio is equal
Median age of presentation is 50-60

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10
Q

What are the presenting signs of acute cholangitis?

A

Pale stools
Pruritus
Hypotension
Mental status changes

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11
Q

What are the investigations for acute cholangitis?

A

FBC: Raised WBC, decreases platelets
Serum urea: Raised in severe cases
Serum creatinine: Raised in severe cases
ABG: Metabolic acidosis
LFT: Hyperbilinuraemia
CRP: Raised
Serum K & Mg: May be decreased
Blood cultures: Bacteria usually gram negative, but gram positive bacteria and anaerobes are also implicated in cholangitis
Tansabdominal USS: dilated bile duct, common bile duct stones- order CT with contrast if USS is negative
ERCP: best first intervention, can assist in the diagnosis of cholangitis by finding stones causing obstruction and is also therapeutic, as the procedure can be used for biliary stone extraction

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12
Q

What are the presenting symptoms of acute cholangitis?

A

Jaundice
Fever
Upper abdominal pain
Right upper quadrant tenderness

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13
Q

How is acute cholangitis managed?

A

Initial stabilisation:
-borad spectrum IV antibiotics
-correct any electrolyte imbalances and coagulation abnormalities
- give adequate analgesia
Biliary decompression:
-ERCP
-surgical incision of the common bile duct (choledochotomy with a T tube replacement)
- cholecystectomy
Consider endoscopic lithotripsy- physical destruction of gallstones

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14
Q

What are the possible complications of acute cholangitis?

A
  • Acute prancreatitis
  • Inadequate biliary drainage following performance of endoscopy, radiology or surgery
  • Hepatic abscess
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15
Q

What is the prognosis of acute cholangitis?

A

If adequate biliary drainage is quickly obtained, most patients experience rapid clinical improvement
Outcome worse for patient’s with underlying medical conditions

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16
Q

What is Alcoholic hepatitis?

A

Inflammatory liver injury and necrosis caused by chronic heavy intake of alcohol

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17
Q

What are the three stages of Alcoholic liver disease?

A
  1. Fatty liver (steatosis)
  2. Alcoholic Hepatitis
  3. Alcoholic Liver Cirrhosis
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18
Q

What is the aetiology Alcoholic hepatitis?

A

The middle stage between fatty liver (steatosis) and alcoholic liver cirrhosis.
Inflammatory liver injury, liver histopathology shows:
-centrilobar ballooning degeneration
-necrosis of hepatocytes
-steatosis (abnormal retention of lipids)
-neutrophilic inflammation
-cholestasis (impaired secretion of bile from hepatocytes and so decrease flow of bile)
-Mallory hyaline inclusions and giant mitochondria

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19
Q

What is the epidemiology of Alcoholic hepatitis?

A

10-35% of heavy drinkers develop this form of liver disease

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20
Q

What are the presenting symptoms of Alcoholic hepatitis?

A
May remain asymptomatic and undetected unless they present for other reasons
May be mild illness with: 
-Nausea
-Malaise
-Epigastric or right hypochondrial pain 
-Low-grade fever
May be more severe with:
-Jaundice
-Abdominal discomfort or swelling
-Swollen ankles
-GI bleeding

Women tend to present with more florid (fully complete) illness than men
There is a history of heavy alcohol intake (􏰀15–20 years of excessive intake necessary for development of alcoholic hepatitis)
There may be trigger events (e.g. aspiration pneumonia or injury)

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21
Q

What are the signs of Alcoholic hepatitis on physical examination?

A
Signs of alcohol excess: 
-Malnourished
-Palmar erythema
-Dupuytren’s contracture
-Facial telangiectasia
-Parotid enlargement
-Spider naevi
-Gynaecomastia
-Testicular atrophy
-Hepatomegaly
-Easy bruising
Signs of severe alcoholic hepatitis: 
-Febrile (50% of patients)
-Tachycardia
-Jaundice (>50% of patients)
-Bruising
-Encephalopathy (e.g. hepatic foetor-breath has a strong, musty smell, liver flap, drowsiness, unable to copy a five-pointed star, disoriented)
-Ascites (30–60% of patients)
-Hepatomegaly (may be tender on palpation)
-Splenomegaly
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22
Q

What are the appropriate investigations for Alcoholic hepatitis?

A

Bloods:
-FBC: reduced Hb, raised MCV, raised WCC, reduced platelets
-LFT (raised transminases, raised bilirubin, reduced albumin, raised AlkPhos, raised GGT)
-U&Es: Urea and K+ levels tend to be low, unless significant renal impairment
*Clotting: Prolonged PT is a sensitive marker of significant liver damage
Ultrasound scan: For other causes of liver impairment (e.g. malignancies)
Upper GI endoscopy: To investigate for varices
Liver biopsy: Percutaneous or transjugular (in the presence of coagulopathy) may be helpful
to distinguish from other causes of hepatitis
Electroencephalogram: For slow-wave activity indicative of encephalopathy

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23
Q

What is the management of Alcoholic hepatitis?

A

Acute:

  • Thiamine, Vitamin C and other multivitamins (initially parenterally)
  • Monitor and correct K+ , Mg2+ and glucose abnormalities
  • Ensure adequate urine output
  • Treat encephalopathy with oral lactulose and phosphate enemas
  • Ascites is managed by diuretics (spironolactone with or without furosemide) or therapeutic paracentesis
  • Glypressin and N-acetylcysteine for hepatorenal syndrome (treatment of bleeding oesophageal varices)

Nutrition:
-Nutritional support with oral or nasogastric feeding is important with increased caloric intake
-Protein restriction should be avoided unless the patient is encephalopathic
-Total enteral nutrition may also be considered as this improves mortality rate
Nutritional supplementation and vitamins (B group, thiamine, folic acid) should be started parenterally initially and then continued orally after

Steroid therapy: Meta-analyses show that steroids reduce short-term mortality for severe alcoholic hepatitis

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24
Q

What are the complications of Alcoholic hepatitis?

A

Acute liver decompensation
Hepatorenal syndrome (renal failure secondary to advanced liver disease)
Cirrhosis

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25
What is the prognosis of Alcoholic hepatitis?
Mortality in first month is about 10%; 40% in first year If alcohol intake continues, most progress to cirrhosis within 1–3 years Prognostic scores: -Maddrey’s discriminant function (MDF): MDF= (bilirubin/17) + (prolongation of PT x 4.6) If MDF > 32, this indicates >50% 30-day mortality -Glasgow alcoholic hepatitis score (GAHS): Age (years) WCC (109/L) Urea (mmol/L) PT ratio Bilirubin (mmol/L) If GAHS> 9 from Day 1 to 9, this indicates >50% 30-day mortality
26
What is amyloidosis?
A (heterogenous) group of diseases characterised by extracellular deposition of amyloid fibrils
27
What are the two main subtypes of amyloidosis?
Type AA: serum Amyloid A protein -non-familial secondary amyloidosis: inflammatory polyarthropathies account for 60% of cases Type AL: immunoglobulin light chain amyloidosis (primary amyloidosis)
28
Which are the main 2 organs affected by amyloidosis?
Kidneys | Heart
29
What is the epidemiology of amyloidosis?
In the UK, the age-adjusted incidence is between 5.1 and 12.8 per 1 million per year, with around 60 new cases annually- RARE
30
What are the presenting symptoms of amyloidosis?
``` PMH of inflammatory conditions (RF) Chronic infections (RF) Positive FH (RF) Fatigue Weight loss Dyspnoea on exertion ```
31
What are the signs of amyloidosis on physical examination?
Jugular venous distension- high right-sided filling pressure Lower extremity oedema (nephrotic syndrome) Macroglossia- most specific finding for AL Diffuse muscular weakness Shoulder pad sign- psudeohypertrophy of amyloid
32
What are the appropriate investigations for amyloidosis?
1st line: Serum/ urine immunofixation- presence of monoclonal protein Immunoglobulin free light chain assay- diagnosing AL Bone marrow biopsy- clonal plasma cells Others: Tissue biopsy, ECG (for conduction abnormalities)
33
What is an anal fissure?
A split in the skin of the distal anal canal characterised by pain on defecation and rectal bleeding
34
What is the aetiology of anal fissures?
Passage of a hard stool bolus may precipitate an anal fissure (however, only a minority of patients are constipated at the onset of symptoms) The fissure may begin during an episode of loose stool, or often occurs spontaneously with no obvious precipitating factor *Opiate analgesia is associated with constipation and a subsequent increased incidence of anal fissure
35
What are the presenting symptoms of an anal fissure?
``` Pain on defecation 'Tearing' sensation on passing stool Fresh blood on stool or on wiping Anal spasm These symptoms are intermittent ```
36
What are the appropriate investigations for an anal fissure?
*Clinical diagnosis Others: -Anal manometry: in patients with resistant fissures: low resting pressure -Anal ultrasound: patients with suspected anal sphincter deficits
37
What is the management for anal fissures?
1. Conservative measures: consisting of a - High-fibre diet - Increased fluid intake - Sitz baths (warm-water bath covering the hips and buttocks) - Stool softeners and analgesics (more severe cases) Additional treatment: - Topical nitrates or calcium channel blockers - Treatment with diltiazem - because of dose-limiting headaches following topical nitrates - Topical treatment must be continued for 6 to 8 weeks to allow re-epithelialisation of the fissure- otherwise early relapse If a fissure is resistant to topical treatments, diagnosis of primary idiopathic fissure should be confirmed
38
What is the management for anal fissures?
1. Conservative measures: consisting of a - High-fibre diet - Increased fluid intake - Sitz baths (warm-water bath covering the hips and buttocks) - Stool softeners and analgesics (more severe cases) Additional treatment: - Topical nitrates or calcium channel blockers - Treatment with diltiazem - because of dose-limiting headaches following topical nitrates - Topical treatment must be continued for 6 to 8 weeks to allow re-epithelialisation of the fissure- otherwise early relapse If a fissure is resistant to topical treatments, diagnosis of primary idiopathic fissure should be confirmed, treatment is surgery
39
What are the complications of an anal fissure?
Chronic anal fissures: while many acute anal fissures spontaneously heal, a proportion will become chronic if left untreated Recurrence: most likely if a patient stops treatment too early Incontinence after surgery
40
What is the prognosis for anal fissures?
Approximately 60% of patients will achieve healing of their fissure at 6 to 8 weeks A further 20% will heal after a course of topical diltiazem Some of these patients may subsequently relapse and may require a surgical option
41
What is Appendicectomy?
The removal of the appendix either laparoscopically (mainly) or open surgery with general anaesthesia
42
What are the indications for an Appendicectomy?
Appendicitis: indicated in all cases of suspected nonperforated appendicitis Carcinoid tumors are the most common malignancy of the appendix; most of these are small (<1 cm)
43
What are the possible complications of an Appendicectomy?
Wound infection- prophylactic antibiotics may be given Haematoma Scarring Abscess Hernia – at the site of incision Bowel obstruction *Laparascopic appendectomy has been shown to decrease the incidence of overall complications
44
What is Appendicitis?
An acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix
45
What is the aetiology of Appendicitis?
Obstruction of the lumen of the appendix is the main cause of acute appendicitis Faecolith (a hard mass of faecal matter),normal stool or lymphoid hyperplasia are the main causes for obstruction
46
What are the risk factors for Appendicitis?
WEAK Smoking <6 months of breastfeeding Low dietary fibre
47
What is the epidemiology of Appendicitis?
One of the most common acute surgical abdominal emergencies May occur at any age but is most commonly seen in early teens to late 40s Slight predominance for males however females have a greater risk for an appendectomy
48
What are the presenting symptoms of Appendicitis?
``` Abdominal pain: -Initially epigastric -Later right iliac fossa Nausea and vomiting Fever ```
49
What are the signs of Appendicitis on physical examination?
Diminished bowel sounds Fever Tachycardia *Rovsing's sign: Pressing the left side of the abdominal cavity elicits pain in right lower quadrant *Psoas sign: Extending the right thigh on left lateral position elicits pain in right lower quadrant *Obturator sign: Pain is elicited in the right lower quadrant of abdomen by internal rotation of the flexed right thigh
50
What are the appropriate investigations for Appendicitis?
Bloods: *FBC (mild leukocytosis), high discriminatory power when combined with history *Abdominal and pelvic CT scan: -Abnormal appendix (diameter >6 mm) identified or calcified appendicolith seen in association with peri-appendiceal inflammation, fat stranding -Wall thickening, wall enhancement, and inflammatory changes in the surrounding tissues are additional findings Urinary pregnancy test: if positive, the possibility of ectopic pregnancy should be considered Others: - Abdominal ultrasound: aperistaltic (Absence of peristalsis) or non-compressible structure with outer diameter >6 mm, fluid collection if perforated, fat stranding, appendicolith -preferred in children - Urinalysis: if abnormal could suggest renal colic or UTI cause - Abdominal and pelvic MRI in pregnancy: In pregnant women presenting with features of appendicitis, an abdominal sonogram should be performed to identify the appendix: abnormal appendix (diameter >6 mm)
51
What is the management for Appendicitis?
Uncomplicated presentation: - Once the diagnosis is made, patients should be nil by mouth - IV fluids, such as lactated Ringer's solution, should be started - Use of prophylactic intravenous broad-spectrum antibiotic such as cefoxitin is recommended for uncomplicated appendicitis to reduce the risk of wound infection - Prompt appendectomy remains the treatment of choice Complicated presentation: occur in 4% to 6% of patients and include gangrene with subsequent perforation or intra-abdominal abscess - IV fluids, such as lactated Ringer's solution, should be started - Antibiotics should be started immediately: e.g. cefoxitin and should be continued until patient becomes afebrile and the leukocytosis is corrected - Interval appendectomy is performed after 6 weeks if the symptoms are not completely resolved
52
What are the complications of Appendicitis?
Perforation generalised peritonitis Appendicular mass (usually due to delay in medical treatment) Appendicular abscess: usually occurs as a progression of the disease process, particularly after perforation Surgical wound infection
53
What is the prognosis of Appendicitis?
If patients are treated in a timely fashion, the prognosis is good Wound infection and intra-abdominal abscess are potential complications associated with appendectomy Laparascopic appendectomy has been shown to decrease the incidence of overall complications
54
What is Autoimmune Hepatitis?
A chronic inflammatory disease of the liver of unknown aetiology, characterized by autoimmune features, hyperglobulinaemia and the presence of circulating autoantibodies
55
What is the aetiology of Autoimmune Hepatitis?
In a genetically predisposed individual, an environmental agent (e.g. viruses or drugs) may lead to hepatocyte expression of HLA antigens which then become the focus of a principally T-cell-mediated autoimmune attack The chronic inflammatory changes are similar to those seen in chronic viral hepatitis with lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and, eventually, cirrhosis
56
What is the epidemiology of Autoimmune Hepatitis?
Type 1 autoimmune hepatitis occurs in all age groups (although mainly in young women) Type 2 is generally a disease of girls and young women. Type 1 is the most common form
57
What are the two types of Autoimmune Hepatitis?
``` Type I (classic): ANA, anti-smooth muscle antibodies (ASMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA) Type 2: Antibodies to liver/kidney microsomes (ALKM-1, directed at an epitope of CYP2D6), antibodies to a liver cytosol antigen (ALC-1) ```
58
What are the environmental factors that can cause Autoimmune Hepatitis in a genetically predisposed individual?
``` Measles Hepatitis viruses (A,C and D) Cytomegalovirus Epstein-Barr virus Drugs such as methyldopa, atorvastatin, interferon and infliximab ```
59
What are the presenting symptoms of Autoimmune Hepatitis?
``` Fatigue/malaise Anorexia Abdominal discomfort Pruritus Arthralgia Nausea Fever ```
60
What are the signs of Autoimmune Hepatitis on physical examination?
Hepatomegaly Jaundice Abdominal discomfort Spider angioma: dilation of vessels below the skin: central, red spot and reddish extensions which radiate outward like a spider's web
61
What are the appropriate investigations for Autoimmune Hepatitis?
*Liver function tests: -Aspartate transaminase (AST): 200 to 300 international units/L (indicator of inflammation) -Alanine transaminase (ALT): 200 to 300 international units/L (indicator of inflammation) -Bilirubin: mildly to moderately increased -GGT: mildly to moderately increased -Alkaline phosphatase: mildly to moderately increased -Serum albumin: decreased -Prothrombin time: prolonged Others: -Anti-nuclear antibodies (TYPE 1) -Smooth muscles antibodies (TYPE 1) -Other antibodies -Abdominal ultrasound: if extra-hepatic biliary obstruction is suspected *-Liver biopsy: Essential to establish the diagnosis, evaluate disease severity, and determine the need for treatment: plasma cell infiltration *When GGT and Alk Phosphate are markedly increased: bile duct injury should be suspected
62
What raises GGT levels (LFT)?
Alcohol abuse, intra-hepatic or extra-hepatic cholestasis and biliary obstruction, hepatocellular disease of other origin, and hepatic malignancies
63
What raises Alkaline phosphatase levels (LFT)?
Intra-hepatic or extra-hepatic cholestasis, hepatocellular disease of other origin, and some bone diseases
64
What decreases albumin level (LFT)?
Reduced in most forms of chronic liver disease, particularly cirrhosis. Decreased also in nephrotic syndrome, malnutrition and malabsorption, chronic infection, and loss from bloodstream (haemorrhage, burns, exudates) or gastrointestinal tract (protein-losing enteropathies)
65
What is Barrett’s oesophagus?
A change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia -associated with gastro-oesophageal reflux, even if the reflux is asymptomatic
66
What is the aetiology of Barrett’s oesophagus?
The primary aetiological factor involved in Barrett's oesophagus is gastro-oesophageal reflux Combined acid and bile reflux are the primary causative agents
67
What are the risk factors for Barrett’s oesophagus?
``` Acid/bile reflux or GORD Increased age White ethnicity Male sex FH Obesity Smoking ```
68
What is the epidemiology of Barrett’s oesophagus?
Between 0.5% and 2.0% of the general population due to the increased prevalence of GORD Becomes more prevalent with age and Men and white people seem to have a higher prevalence
69
What are the presenting symptoms/signs of Barrett’s oesophagus?
``` Heartburn Nausea Regurgitation: expulsion of material from the pharynx, or oesophagus Chest pain Dysphagia: difficulty swallowing ```
70
What are the appropriate investigations for Barrett’s oesophagus?
**Oesophago-gastroduodenoscopy (OGD): abnormal epithelium characteristic of Barrett's oesophagus proximal to the gastro-oesophageal junction (includes biopsy for histology) Others: -Barium oesophagogram: Cannot diagnose Barrett's oesophagus but can evaluate for a mass lesion or stricture before endoscopy -Chromoendoscopy: staining
71
What is the management for Barrett’s oesophagus?
Non-dysplastic Barrett's oesophagus: - Proton-pump inhibitors and surveillance: reduce acid exposure of the distal oesophagus - Anti-reflux surgery: such as laparoscopic Nissen fundoplication, eliminate acid and bile reflux in more than 90% of patients - Recommend AGAINST radiofrequency ablation (RFA) Barrett's oesophagus with low-grade dysplasia: - Endoscopic eradication therapies such as RFA - *Endoscopic mucosal resection (EMR) is the optimal diagnostic and therapeutic technique when mucosal nodularity is discovered Barrett's oesophagus with high-grade dysplasia: *High risk of adenocarcinoma! -Endoscopic mucosal resection -Endoscopic sub-mucosal dissection -radiofrequency ablation (RFA)* BEST OPTION* OR: Oesophagectomy is a definitive treatment option, related to significant procedure-related mortality and long-term morbidity
72
What are the complications of Barrett’s oesophagus?
Oesophageal stricture (abnormal narrowing ) Affect on quality of life Dysplasia and adenocarcinoma
73
What is the prognosis for Barrett’s oesophagus?
Patients are at a greater risk of developing adenocarcinoma Proton-pump inhibitor treatment does not lead to regression of Barrett’s oesophagus but anti-reflux surgery and surgery lowers the risk for progression to adenocarcinoma
74
What are cholangiocarcinomas?
Cancers arising from the bile duct epithelium. These can be divided depending on their location in the biliary tree: intrahepatic or extrahepatic (perihilar and distal)
75
What is the aetiology of cholangiocarcinomas?
There is a close association between infection, inflammation, and malignancy
76
What are the risk factors for cholangiocarcinomas?
Age > 50 years Cholangitis Choledocholithiasis (gall stones) Structural disorders of the biliary tract e.g. bile duct adenoma Ulcerative colitis Primary sclerosis cholangitis (high association with UC) Non-specific cirrhosis, alcoholic liver disease HIV Hepatitis B and C
77
What is the epidemiology of cholangiocarcinomas?
Slight male predominance Approximately 2/3rds of cholangiocarcinomas occur in patients between 50 and 70 years of age Highest rates in Thailand and South American Countries
78
What are the presenting symptoms of cholangiocarcinomas?
``` Painless jaundice (90% of patients) Others which are less common: -Weight loss -Abdominal pain -Itchiness -Dark urine and pale stools (obstructive jaundice) ```
79
What are the signs of cholangiocarcinomas on physical examination?
Jaundice Triad of: fever, jaundice and right upper quadrant pain (acute cholangitis- 10% of patients) Palpable gallbladder (RARE) Hepatomegaly (RARE)
80
What are the appropriate investigations for cholangiocarcinomas?
Bloods: -Serum bilirubin: Conjugated bilirubin is elevated in obstructive jaundice -Serum alkaline phosphate: Suggests obstructive (or cholestatic) pattern of elevated LFTs, along with GGT, AST and ALT -Serum prothrombin time: increased in prolonged obstruction of the common bile or hepatic duct *Tumour marker: Ca 19-9- elevated in up to 85% of patients with cholangiocarcinoma Imaging: -Abdominal ultrasound*: intrahepatic cholangiocarcinoma may be seen as a mass lesion -Abdominal CT: intrahepatic mass lesion, dilated intrahepatic ducts, and localised lymphadenopathy -Abdominal MRI/angiography: staging tool/extent of tumour -*ERCP (Endoscopic Retrograde Cholangiopancreatography) : a filling defect or area of narrowing will be seen if a tumour is present- INVASIVE Others: MRCP (extent of duct involvement) Percuatneous transhepatic cathertisation (invasive procedure that is used when the tumour causes complete obstruction of the biliary tree)
81
What is a Cholecystectomy?
The surgical removal of the gallbladder
82
What are the indications for a Cholecystectomy?
Gallbladder trauma Cholangiocarcinoma Acute cholecystitis Cholelithiasis- gallstones
83
What are the complications of a Cholecystectomy?
Bile leak Bleeding Infection Injury to nearby structures, specifically bile duct injury. Also liver and small intestine Greater risk of DVT Risks from general anaesthetic: allergic reaction, death Post-cholecystectomy syndrome: *thought to be due to bile leaking into areas such as the stomach, or by gallstones being left in the bile ducts* -tummy pain -indigestion -diarrhoea -yellowing of the eyes and skin (jaundice) -high temperature (fever) of 38C or above
84
What is Cholecystitis?
Acute gallbladder inflammation, and one of the major complications of cholelithiasis or gallstones
85
What is the aetiology of Cholecystitis?
At least 90% of patients have gallstones: - It develops in up to 10% of patients with symptomatic gallstones. - In most cases it is caused by complete cystic duct obstruction usually due to an impacted gallstone in the gallbladder neck or cystic duct, which leads to inflammation within the gallbladder wall In 5% of cases, acute cholecystitis occurs in the absence of gallstones, causing an acalculous cholecystitis. Predisposing factors are: -Starvation -Total parenteral nutrition -Narcotic analgesics -Immobility This leads to bile inspissation (due to dehydration) or bile stasis (due to trauma or severe systemic illness) which can block the cystic duct
86
What is the epidemiology of Cholecystitis?
The distribution and incidence of acute cholecystitis follow that of cholelithiasis because of the close relationship between the two - Cholelithiasis occurs in approximately 15% of adults - It is 3X more common in women than in men up to the age of 50 years, and is about 1.5 X more common in women than in men thereafter
87
What are the presenting symptoms of Cholecystitis?
``` Pina in the upper right quadrant Fever/rigors Nausea Right shoulder pain (referred pain) Anorexia (associated with biliary disease) ```
88
What are the signs of Cholecystitis on physical examination?
Tenderness in the right upper quadrant Palpable mass: distended, tender gallbladder may be palpable as a distinct mass Signs of infection: unwell, tachycardia, fever
89
What are the appropriate investigations for Cholecystitis?
If sepsis is suspected: CT or MRI of the abdomen: - Irregular thickening of the gallbladder wall - Poor contrast enhancement of the gallbladder wall (interrupted rim sign) - Increased density of fatty tissue around the gallbladder - Gas in the gallbladder lumen or wall - Membranous structures within the lumen (intraluminal flap or intraluminal membrane) - Peri‐gallbladder abscess * If sepsis is not suspected: Abdominal ultrasound (first line for suspected gallstones) - Pericholecystic fluid - Distended gallbladder - Thickened gallbladder wall (>3 mm) - Gallstones - Positive sonographic Murphy's sign Bloods: - FBC: WCC - CRP: inflammation - Bilirubin: elevated may indicate acute focal cholestasis in adjacent liver tissue or due to common bile duct stones - LFTs: if raised may indicate whether further imaging is required, such as MRCP - Serum lipase/amylase: exclude acute pancreatitis - Blood cultures/ bile cultures: infective organism suspected Others: - Magnetic resonance cholangiopancreatography (MRCP): if ultrasound has not detected common bile duct stones but the bile duct is dilated and/or liver function test results are abnormal - Endoscopic ultrasound: May detect stones not identified by MRCP or abdominal ultrasound
90
What is a positive Murphy's sign?
Firmly placing a hand at the costal margin in the right upper abdominal quadrant and asking the patient to breathe deeply If the gallbladder is inflamed, the patient will experience pain and catch their breath as the gallbladder descends and contacts the palpating hand A similar manoeuvre in the left upper quadrant should not elicit discomfort
91
What is the management for Cholecystitis?
Initial treatment: analgesia, fluid resuscitation, and antibiotics (if infection is suspected) Arrange urgent laparoscopic cholecystectomy (surgery within 72 hours of onset is preferable)
92
What are the possible complications of Cholecystitis?
- Gangrenous cholecystitis: Associated inflammation leads to ischaemic necrosis of the wall - Perforation of the gallbladder (10%) - Suppurative cholecystitis: Thickened gallbladder wall with white cell infiltration, intra-wall abscesses, and necrosis -may result in perforation of the gallbladder and a pericholecystic abscess formation - Bile duct injury due to surgery - Gallstone ileus: gallstone passing from the biliary tract into the intestinal tract (through a fistula), leading to small-intestinal obstruction. Treatment is with enterotomy and stone extraction - Cholecystoenteric fistulas: Decompression of the gallbladder because of a fistula may cause resolution of the acute cholecystitis (common sites duodenum and the hepatic flexure of the colon)
93
What is the prognosis of Cholecystitis?
Removing the gallbladder and the contained gallstones when biliary pain starts will prevent further biliary attacks and reduce the risk of developing cholecystitis If the gallbladder perforates, mortality is 30% *Untreated acute acalculous cholecystitis is life-threatening and is associated with up to 50% mortality
94
What is Cirrhosis?
End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes Decompensated when there are complications such as ascites, jaundice, encephalopathy or GI bleeding
95
What is the aetiology of Cirrhosis?
Cirrhosis can derive from any chronic liver disease: -Chronic alcohol misuse: Most common UK cause -Chronic viral hepatitis: Hepatitis B/C are the most common causes worldwide -Non-alcoholic fatty liver disease (NAFLD and associated steatohepatitis): associated with obesity, diabetes, total parenteral nutrition -Chronic biliary diseases: Primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), biliary atresia (condition in infants in which the bile ducts outside and inside the liver are scarred and blocked) -Autoimmune hepatitis Drugs: e.g. methotrexate, hepatotoxic drugs Inherited: a1-Antitrypsin deficiency, haemochromatosis, Wilson’s disease, galactosaemia, cystic fibrosis Vascular: Budd–Chiari syndrome (occlusion of the hepatic veins that drain the liver) or hepatic venous congestion.
96
What is the triad in Budd–Chiari syndrome?
Abdominal pain, ascites, and liver enlargement
97
What is the epidemiology of Cirrhosis?
Among the top 10 leading cause of deaths worldwide, liver disease is the third biggest cause of premature mortality in the UK
98
What are the precipitating factors of Decompensation?
``` Infection GI bleeding Constipation High-protein meal Electrolyte imbalances Alcohol and drugs Tumour development Portal vein thrombosis ```
99
What are the presenting symptoms of Cirrhosis?
``` Early non-specific symptoms: -Anorexia -Nausea -Fatigue -Weakness -Weight loss Symptoms caused by reduced liver synthetic function: -Easy bruising -Abdominal swelling -Ankle oedema Reduced detoxification function: -Jaundice -Personality change -Altered sleep pattern -Amenorrhoea Portal hypertension: -Abdominal swelling -Haematemesis -PR bleeding or melaena ```
100
What are the signs of Cirrhosis on physical examination?
``` Stigmata of chronic liver disease: Asterixis (‘liver flap’) Bruises Clubbing Dupuytren’s contracture Erythema (palmar) Others: -Jaundice -Gynaecomastia, -Leukonychia (hypoalbuminaemia) -Parotid enlargement -Spider naevi -Scratch marks (due to pruritus) -Ascites (‘shifting dullness’ and fluid thrill) -Enlarged liver (shrunken and small in later stage) -Testicular atrophy -Caput medusae (dilated superficial abdominal veins) -Splenomegaly (indicating portal hypertension) ```
101
What are the appropriate investigations for Cirrhosis?
* LFTs: - Deranged - AST and ALT levels increase with hepatocellular damage - Raised AlkPhos, GGT and bilirubin - Reduced Albumin (marker of hepatic synthetic dysfunction) - Clotting: Prolonged PT (reduced synthesis of clotting factors) - Serum alpha-fetoprotein (AFP): elevated in chronic liver disease, but high levels may suggest hepatocellular carcinoma* - FBC: low Hb, low platelets as a result of hypersplenism Others (to investigate cause): - Viral serology (HBsAg, HBsAb, HCV ab) - a1-antitrypsin (155 of patients can develop cirrhosis) - caeruloplasmin (Wilson’s disease) - Iron studies: serum ferritin, iron, total iron binding capacity (haemochromatosis) - Anti-mitochondrial antibody (PBC) - Anti-nuclear antibodies (ANA), SMA (autoimmune hepatitis) - Liver biopsy: architectural distortion of the liver parenchyma with formation of regenerative nodules (not always necessary) Imaging: - Abdominal ultrasound/CT: COMPLICATIONS: liver surface nodularity, small liver, possible hypertrophy of left/caudate lobe, ascites, splenomegaly, increased diameter of the portal vein (≥13 mm), or collateral vessels - OGD: presence of gastro-oesophageal varices or portal hypertensive gastropathy secondary to portal hypertension
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What is the management for Cirrhosis?
Treat the cause if possible such as such as hepatitis B and C virus infections Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver Nutrition is very important and if intake is poor, dietitian review and enteral supplements should be given; nasogastric feeding may be indicated Treatment of the complications *Liver transplantation is the only curative measure
103
What are the possible complications of Cirrhosis and their management?
Encephalopathy: -Treat infections -Exclude a GI bleed -Lactulose, phosphate enemas and avoid sedation Portal Hypertension-Ascites: -Diuretics (spironolactone/􏰃furosemide) -Dietary sodium restriction (88meq or 2g/day), -Therapeutic paracentesis (with human albumin replacement IV) -Monitor weight daily -Fluid restriction in patients with plasma sodium <120mmol/L -Avoid alcohol and NSAIDs. Spontaneous bacterial peritonitis: -Antibiotic treatment (e.g. cefuroxime and metronidazole), prophylaxis against recurrent SBP with ciprofloxacin Surgical: -Consider insertion of TIPS to relieve portal hypertension (if recurrent variceal bleeds or diuretic-resistant ascites) although it may precipitate encephalopathy Other complications include: Hepatocellular carcinoma, Renal failure (hepatorenal syndrome), Pulmonary hypertension (hepatopulmonary syndrome)
104
What is the prognosis of Cirrhosis?
Depends on the aetiology and complications Generally poor; overall 5-year survival is 􏰀50% In the presence of ascites, 2-year survival of 􏰀50%
105
What is Coeliac disease?
Inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption
106
What is the aetiology of Coeliac disease?
Systemic autoimmune disorder triggered by gluten peptides from grains including wheat, rye, and barley Almost all people with coeliac disease carry one of two major histocompatibility complex class-II molecules (HLA-DQ2 or -DQ8) that are required to present gluten peptides in a manner that activates an antigen-specific T cell response FH of coeliac disease is a RF as is PMH of autoimmune diseases such as TYPE 1 DM, autoimmune thyroid disease, IBD (UC and Crohn's disease)
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What is the epidemiology of Coeliac disease?
Coeliac disease is a common disorder in the US and in Europe Women are slightly more likely to be affected (2/3) Can present at any age
108
What are the presenting symptoms of Coeliac disease?
May be asymptomatic Abdominal discomfort, pain and distention (bloating) Steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away) Diarrhoea Tiredness, malaise, weight loss (despite normal diet) Failure to ‘thrive’ in children, amenorrhoea in young adults
109
What are the signs of Coeliac disease on physical examination?
Signs of anaemia: Pallor Signs of malnutrition: Short stature, abdominal distension (bloating) and wasted buttocks in children Triceps skinfold thickness gives an indication of fat stores Signs of vitamin or mineral deficiencies (e.g. osteomalacia, easy bruising) Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)-UNCOMMON
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What are the appropriate investigations for Coeliac disease?
``` FBC and blood smear: -Iron deficiency (microcytic) anaemia is the most common clinical presentation in adults -Folate (and rarely vitamin B12) deficiency may lead to a macrocytic anaemia *Immunoglobulin A- tissue transglutaminase (IgA-tTG): titre above normal range for laboratory Endomysial antibody (EMA): more expensive alternative to IgA-tTG Skin biopsy: patient with skin lesions suggestive of dermatitis herpetiformis: granular deposits of IgA IgG DGP or IgA/IgG DGP (deamidated gliadin peptide): test of choice for patients with IgA deficiency (common,1 in 50 with coeliac disease) Small bowel endoscopy and biopsy: -Direct visualization shows villous atrophy in the small intestine (particularly the jejunum and ileum) giving the mucosa a flat smooth appearance -Biopsy shows villous atrophy with crypt hyperplasia of the duodenum -The epithelium adopts a cuboidal appearance, and there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria ```
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What is the management of Coeliac disease?
Advice: -Strict lifelong gluten-free diet with avoidance of all wheat, rye and barley products -Education and expert dietary advice is essential- the Coeliac Society offers patient support and advice Medical: -Vitamin and mineral supplements -Oral corticosteroids may be used if the disease does not subside with gluten withdrawal
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What are the complications of Coeliac disease?
``` Iron, folate and Vitamin B12 deficiency Osteomalacia Ulcerative jejunoileitis Gastrointestinal lymphoma (particularly T cell) Bacterial overgrowth Rarely, can cause cerebellar ataxia ```
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What is the prognosis of Coeliac disease?
With strict adherence to gluten-free diet, most patients make a full recovery Symptoms usually resolve within weeks but histological changes may take longer to resolve A gluten-free diet needs to be followed for life
114
What is Colonoscopy?
A procedure that uses a long, narrow, flexible, telescopic camera called a colonoscope to look at the lining of your large bowel
115
What are the indications for a Colonoscopy?
``` Lower GI bleeding Screening and surveillance of colorectal polyps and cancers: -Colon cancer -Surveillance after polypectomy -Colorectal cancer post-resection surveillance -Inflammatory bowel diseases Acute and chronic diarrhoea Therapeutic indications for colonoscopy: -Excision and ablation of lesions -Treatment of lower GI bleeding -Colonic decompression -Dilation of colonic stenosis -Foreign body removal Miscellaneous indications: -Abnormal radiological examinations -Isolated unexplained abdominal pain -Chronic constipation -Preoperative and intraoperative localization of colonic lesions ```
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What are the possible complications for a Colonoscopy?
Intestinal perforations Bleeding Adverse reaction to anaesthetic Infection
117
What is colorectal cancer?
Malignancy of the large bowel - the majority of colorectal cancers are adenocarcinomas derived from epithelial cells
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What is the aetiology of colorectal cancer?
Colorectal cancer represents a complex interaction of genetic and environmental factors: Genetic: next to age, FH is the most common risk factor *Family cancer syndromes: familial adenomatous polyposis (FAP) and Lynch syndrome Environmental: Obesity, high energy intake, and physical inactivity are synergistic risk factors (low fibre diet) Also: inflammatory bowel disease, acromegaly
119
What is the epidemiology of colorectal cancer?
Second most common cause of cancer death in the West | Average age at diagnosis 60–65 years.
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What are the presenting symptoms of colorectal cancer?
Left-sided colon and rectum: - Change in bowel habit (increased frequency, looser stools) - Rectal bleeding or blood/mucous mixed in with stools - Rectal masses may also present as tenesmus (sensation of incomplete emptying after defecation) Right-sided colon: -Later presentation, with symptoms of anaemia, weight loss and non- specific malaise or, more rarely, lower abdominal pain Up to 20% of tumours will present as an emergency with pain and distension caused by large bowel obstruction, haemorrhage or peritonitis as a result of perforation
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What are the signs of colorectal cancer on physical examination?
Anaemia may be only sign, particularly in right-sided lesions Abdominal mass, low-lying rectal tumours may be palpable on rectal examination Metastatic disease: Hepatomegaly, ‘shifting dullness’ of ascites
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What are the appropriate investigations for colorectal cancer?
Blood: FBC (for anaemia), LFT (often normal), tumour markers (CEA to monitor treatment response or disease recurrence) Stool: Occult or frank blood in stool (screening test) Endoscopy: -Sigmoidoscopy, colonoscopy: may see ulcerating or exophytic (growing outward) mucosal lesion that may narrow the bowel lumen -Allows visualization and biopsy. Polypectomy can also be performed if isolated small carcinoma in situ Barium contrast studies: ‘Apple core’ stricture on barium enema Abdominal ultrasound scan for hepatic metastases Other staging investigations include: -CXR -CT: colonic wall thickening, enlarged lymph nodes, liver metastases, ascites, lung secondaries -MRI, endorectal ultrasound
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What is Crohn's disease?
Chronic granulomatous transmural inflammatory disease that can affect any part of the gastrointestinal tract Grouped with ulcerative colitis and together they are known as inflammatory bowel disease
124
What is the aetiology of Crohn's disease?
Cause has not yet been elucidated, but thought to involve an interplay between genetic and environmental factors Inflammation can occur anywhere along GI tract (40% involving the terminal ileum) and ‘skip’ lesions with inflamed segments of bowel interspersed with normal segments is not unusual
125
What is the epidemiology of Crohn's disease?
Annual UK incidence is 5–8 in 100,000 Prevalence is 50–80 in 100,000 The peak age of onset is between 15 and 40 years, and there is a smaller second peak between 60 and 80 years (*teens or twenties) CD is equally prevalent among men and women
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What are the presenting symptoms of Crohn's disease?
Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction) Diarrhoea (may be bloody or steatorrhoea) Fever, malaise, weight loss Symptoms of complications
127
What are the presenting symptoms of Crohn's disease?
Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction) (Prolonged) Diarrhoea (may be bloody or steatorrhoea) Fever, malaise, weight loss Symptoms of complications
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What are the signs of Crohn's disease on physical examination?
Weight loss Clubbing Signs of anaemia (pallor) Aphthous ulceration of the mouth Perianal skin tags, fistulae and abscesses Signs of complications (eye disease, joint disease, skin disease)
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What are the appropriate investigations for Crohn's disease?
Bloods: -FBC: due to chronic inflammation: anaemia, leukocytosis, may be thrombocytosis- marker of active inflammation -ESR/CRP: elevated -Iron studies: normal, or may demonstrate changes consistent with iron deficiency (GI bleeding or malabsorption of iron) -Serum B12/folate: may be low secondary to malabsorption -Metabolic profile: hypoalbuminaemia, hypocholesterolaemia, hypocalcaemia due to chronic or severe disease Stool microscopy and culture: To exclude infective colitis Plain abdominal x-ray: small bowel or colonic dilation; calcification; sacroiliitis; intra-abdominal abscesses *CT abdomen: skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae MRI/abdomen pelvis: superior to CT, used when contraindicated: same as CT findings Others: (helpful in differentiating with UC) -*Colonoscopy with intubation of the ileum is the definitive test to diagnose CD: aphthous ulcers (painful, clearly defined, round shallow), hyperaemia, oedema, *cobblestoning*, discontinuous-skip lesions -Tissue biopsy: confirmatory rather than diagnostic -faecal calprotectin: elevated (proteins released into faeces when neutrophils gather at the site of any GI tract inflammation)
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What are the histological findings for Crohn's disease?
Significant inflammation in the colonic wall, widening of submucosa, and dense lymphoid aggregates in the submucosa Cryptitis with morphological distortion of the crypts accompanied by inflammation and abundant lymphatic and plasma cells Inflammation of deeper layers and presence of non-caseating granulomas
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What is the long term management for Crohn's disease?
Symptomatic treatment: managing diarrhoea, abdominal pain, and malabsorption -Antidiarrhoeal agents should be avoided in patients with active colitis, given the risk of developing toxic megacolon Medical therapy: -Immunomodulators (azathioprine, mercaptopurine, methotrexate), reduce relapses- MYELOSUPPRESION, HEPATOOXICITY, LUNG FIBROSIS -TNF-alpha inhibitors (infliximab- Biosimilars), effective agents in achieving and maintaining remission- RISK OF TB -Severely active disease: Oral or intravenous corticosteroids and combination of immunomodulator therapy and TNF-alpha inhibitor therapy Advice: Stop smoking, dietician referral. Education and advice (e.g. from inflammatory bowel disease nurse specialists) Surgery: - Indicated for failure of medical treatment, failure to thrive in children or the presence of complications -This involves resection of affected bowel and stoma formation, although there is a risk of disease recurrence (due to discontinuous skip lesions)
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What is the management for an acute exacerbation of Crohn's disease?
Fluid resuscitation IV or oral corticosteroids Immunmodulators (azathioprine and methotrexate) may induce a remission in colonic Crohn’s disease Analgesia Elemental diet may induce remission (more often used in children) Parenteral nutrition may be necessary Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin) Assess for complications
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What are the complications of Crohn's disease?
GI: -Haemorrhage -Bowel strictures -Toxic megacolon (colon expands, dilates, and distends- high risk of rupture which is life threatening) -Perforation -Fistulae (between bowel, bladder, vagina) -Perianal fistulae and abscess -GI carcinoma (5% risk in 10 years) -Malabsorption Extraintestinal features: -Uveitis -Episcleritis -Gallstones -Kidney stones -Arthropathy -Sacroiliitis -Ankylosing spondylitis -Erythema nodosum -Pyoderma gangrenosum: painful pustules or nodules become ulcers that progressively grow -Amyloidosis
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What is the prognosis for Crohn's disease?
Chronic relapsing condition Two-thirds will require surgery at some stage and two-thirds of these >1 surgical procedure
135
What is Diverticular disease?
The presence of outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel (diverticulosis) associated with complications, e.g. haemorrhage, infection, fistulae
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What is Diverticulitis?
Acute inflammation and infection of colonic diverticulae
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What is the aetiology of Diverticular disease?
``` Multi-factorial aetiology- both genetic and environmental factors are described as causative, especially a *low dietary fibre intake*, which in Western populations is deemed as the predominant contributing factor Other predisposing factors include: -Decreased physical activity -Obesity -Increased red meat consumption -Tobacco smoking -Excessive alcohol and caffeine intake -Steroids -Non-steroidal anti-inflammatory drugs ```
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What is the pathogenesis of Diverticular disease?
1. A low-fibre diet leads to loss of stool bulk 2. Consequently, high colonic intraluminal pressures must be generated to propel the stool, leading to herniation of the mucosa and submucosa through the muscularis 3. Proposed diverticular obstruction by inspissated faeces can lead to bacterial overgrowth, toxin production and mucosal injury and diverticulitis- perforation, abscess, ulceration and fistulation or stricture formation - Diverticulae are most common in the sigmoid and descending colon but can be right sided
139
What is the epidemiology of Diverticular disease?
Common, 60% of people living in industrialized countries will develop colonic diverticula (can be difficult to determine because most patients are asymptomatic) Rare < 40years
140
What are the presenting symptoms of Diverticular disease?
Often asymptomatic (80–90%) Complications include: -PR bleeding -Diverticulitis: typically, left iliac fossa or lower abdominal pain -Fever -Diverticular fistulation into bladder: pneumaturia (passage of gas mixed with urine), faecaluria (presence of faeces in the urine) and recurrent UTI
141
What are the signs of Diverticular disease on physical examination?
``` Diverticulitis: -Tender abdomen -Signs of local or generalized peritonitis if perforation has occurred: Abdominal pain or tenderness Signs of ascites: flank dullness, shifting dullness, fluid wave, and auscultatory percussion Signs of sepsis may be present: -Hypothermia -Hypotension -Tachycardia ```
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What are the appropriate investigations for Diverticular disease?
*FBC: Polymorphonuclear leukocytosis is present in acute diverticulitis (elevated CRP), cross match if bleeding *CT abdomen: (imaging modality of choice), thickening of bowel wall, mass, abscess, streaky mesenteric fat; may show gas in the bladder in cases of fistula Others: -Abdominal x-ray: (considered when acute diverticulitis is suspected), pneumoperitoneum, ileus, soft tissue densities; free air in bowel perforation -Abdominal USS: if CT cannot be obtained, signs of abscess, perforation, obstruction -CXR: normal, or free air under diaphragm if perforation -Contrast enema: (when initial acute symptoms have resolved to confirm diagnosis), diverticuli, abscess, perforation, obstruction, fistula -Colonoscopy/Sigmoidoscopy: *when diagnosis is unclear and malignancy is suspected* Single, multiple, or scattered diverticula, with or without acute mucosal inflammation -Blood culture: patients with suspected sepsis -Angiogram/isotope labelled RBC nuclear scan: in acute bleeding
143
What is the management of Diverticular disease?
Asymptomatic: -Soluble high-fibre diet (20–30 g/day) GI bleed: -PR bleeding is often managed conservatively with IV rehydration, antibiotics, blood transfusion if necessary. -Angiography and embolization or surgery if severe Diverticulitis: -Uncomplicated: low-residue diet and oral antibiotics -Complicated: IV antibiotics and IV fluid rehydration and bowel rest, localised collections or abscesses may be treated by radiologically sited drains Surgery: 'Hartmanns procedure' -Individual basis depending on age, frequency, and severity of recurrent symptoms, previous complications (e.g. perforation and peritonitis) and presence of co-morbidities -Surgical treatment can be by open or laparoscopic approaches: **More recently, laparoscopic drainage, peritoneal lavage and drain placement can be effective
144
What are the complications of Diverticular disease?
``` Diverticulitis Pericolic abscess Perforation Faecal peritonitis Colonic obstruction Fistula formation (bladder, small intestine, vagina) Haemorrhage low risk: colorectal neoplasm ```
145
What is the prognosis for Diverticular disease?
Most patients with uncomplicated diverticulitis recover following medical treatment and do not require surgical intervention Diverticular disease recurs in 1/3 of patients following response to medical treatment, mostly within 5 years- risk is higher in young patients and those with abscess formation at diagnosis Recurrent disease is associated with high mortality
146
What is Endoscopic retrograde cholangiopancreatography (ERCP)?
A procedure that combines upper gastrointestinal (GI) endoscopy and x-rays to treat problems of the bile and pancreatic ducts During an ERCP, stents can be inserted into the bile ducts, to allow drainage of bile into the intestine and biopsies can be taken
147
What are the indications for Endoscopic retrograde cholangiopancreatography (ERCP)?
When your bile or pancreatic ducts have become narrowed or blocked: - Jaundice - Choledocholithiasis (gallstones) - Infection - Acute/chronic pancreatitis - Abnormal LFTs - Trauma or surgical complications in your bile or pancreatic ducts - Pancreatic pseudocysts - Suspected malignancy of the bile ducts or pancreas * More used as a treatment rather than diagnostic test as it is invasive (MRCP is preferred)
148
What are the possible complications of Endoscopic retrograde cholangiopancreatography (ERCP)?
Pancreatitis (most common) Infection Bleeding Perforation Prolonged pancreatic stenting is associated with stent occlusion, pancreatic duct obstruction and pseudocyst formation
149
What is Endoscopy?
A procedure to examine internal organs by placing an endoscope (camera) inside the body
150
What are the indications for Endoscopy?
Investigate symptoms such as: -Dysphagia -Abdominal pain that is persistent -Frequent diarrhoea, or nausea and vomiting -Unintentional weight loss -Frequent heartburn or indigestion -PR bleeding More effective at identifying inflammation, ulcers, and tumours than other imaging techniques Can also take biopsies and treat some conditions by surgical removal
151
What are the complications of Endoscopy?
Infection | Perforation/ bleeding
152
What are the different types of Endoscopy?
``` Gastroscopy Colonoscopy Bronchoscopy Hysteroscopy Cystoscopy Flexible sigmoidoscopy Endoscopic ultrasound Endoscopic retrograde cholangiopancreatography (ERCP) ```
153
What is Enteral feeding?
The administration of feed and/or fluid via a tube going into the gastrointestinal tract. Can also be used: - To administer medication - For gastric aspiration - For gastric decompression
154
What is Parenteral feeding?
The administration of specialist nutritional products to a person intravenously, bypassing the usual process of eating and digestion (GI tract)
155
What are the indications for Feeding (enteral & parenteral)?
Stroke, which may impair ability to swallow Malignancy which may cause fatigue, nausea, and vomiting that make it difficult to eat Critical illness or injury, which reduces energy or ability to eat Failure to thrive or inability to eat in young children or infants Serious illness, which places the body in a state of stress, making it difficult to take in enough nutrients Neurological or movement disorders that increase caloric requirements while making it more difficult to eat GI dysfunction or disease Parenteral feeding can be a life-saving option in many circumstances. However, it’s preferable to use enteral nutrition if at all possible
156
What are the possible complications of Feeding (enteral & parenteral)?
Aspiration Refeeding syndrome, dangerous electrolyte imbalances that may occur in people who are very malnourished and start receiving enteral feeds Infection of the tube or insertion site Nausea and vomiting that may result from feeds that are too large or fast, or from slowed emptying of the stomach Skin irritation at the tube insertion site Diarrhoea due to a liquid diet or possibly medications Tube dislodgement or blockage, which may occur if not flushed properly
157
What are the different types of Enteral Feeding?
Nasogastric tube (NGT) starts in the nose and ends in the stomach Orogastric tube (OGT) starts in the mouth and ends in the stomach Nasoenteric tube starts in the nose and ends in the intestines (subtypes include nasojejunal and nasoduodenal tubes) Oroenteric tube starts in the mouth and ends in the intestines Gastrostomy tube is placed through the skin of the abdomen straight to the stomach (subtypes include PEG, PRG, and button tubes) Jejunostomy tube is placed through the skin of the abdomen straight into the intestines (subtypes include PEJ and PRJ tubes)
158
What is Functional dyspepsia?
A term to describe a symptom or a combination of symptoms where UGI endoscopy did not reveal a potential cause for the dyspepsia (It is generally reserved for patients with a normal endoscopy whose symptoms do not suggest GORD)
159
What is the aetiology of Functional dyspepsia?
1. Post-prandial distress syndrome (PDS), which is characterised by meal-induced dyspeptic symptoms, such as discomfort, pain, nausea, and fullness 2. Epigastric pain syndrome (EPS), which refers to epigastric pain, or epigastric burning, that does not occur exclusively post-prandially, can occur during fasting, and can even be improved by meal ingestion 3. Overlapping PDS and EPS, which is characterised by meal-induced dyspeptic symptoms and epigastric pain or burning
160
What is the epidemiology of Functional dyspepsia & irritable bowel syndrome (IBS)?
There is much overlap between functional dyspepsia and IBS Patients who have both disorders have a substantially greater symptom burden and are more likely to consult a physician Women who have experienced emotional or physical abuse appear to be particularly vulnerable to developing functional dyspepsia and irritable bowel syndrome (IBS)
161
What is Irritable bowel syndrome (IBS)?
A chronic condition characterised by abdominal pain associated with bowel dysfunction, the pain is often relieved by defecation and is sometimes accompanied by abdominal bloating
162
What is the aetiology of Irritable bowel syndrome (IBS)?
No specific endoscopic, biochemical, anatomic, microbiological, or histological findings in IBS that make the aetiology clear Stress and emotional tension can frequently trigger bouts of IBS
163
What are the presenting symptoms/signs of Functional dyspepsia?
Epigastric pain or burning Early satiety and post-prandial fullness Belching Bloating Nausea Discomfort in the upper abdomen
164
What are the presenting symptoms/signs of Irritable bowel syndrome (IBS)?
Abdominal discomfort Altered bowel habits Abdominal bloating or distension *Normal abdominal examination*
165
What are the appropriate investigations for Functional dyspepsia & irritable bowel syndrome (IBS)?
Exclude other causes: - FBC: normal, anaemia may suggest another cause - Stool studies: normal - Anti-endomysial antibodies/anti-tissue transglutaminase: if coeliac disease is suspected - Plain abdominal x-ray: normal no abnormal bowel pattern to suggest obstruction - Endoscopy: colonoscopy/sigmoidoscopy or gastroscopy are normal
166
What are gallstones?
Also known as cholelithiasis is the presence of solid concretions in the gallbladder Gallstones form in the gallbladder but may exit into the bile ducts (choledocholithiasis)
167
What is biliary colic?
A dull pain in the middle to upper right quadrant of the abdomen and occurs when a gallstone blocks the bile duct
168
What is the aetiology of gallstones?
90% of gallstones are composed of cholesterol Different types: -Mixed stones: Contain cholesterol, calcium bilirubinate, phosphate and protein. Associated with older age, female, obesity, parenteral nutrition, drugs (OCP, octreotide), family history, ethnicity (e.g. Pima Indians), interruption of the enterohepatic recirculation of bile salts (e.g. Crohn’s disease), terminal ileal resection -Pure cholesterol stones: Similar associations as mixed stones -Approximately 2% of all gallstones are black pigment stones: Black stones made of calcium bilirubinate (elevated bilirubin secondary to haemolytic disorders, cirrhosis). Associated with haemolytic disorders (e.g. sickle cell, thalassemia, hereditary spherocytosis)
169
What is the epidemiology of gallstones?
Cholelithiasis occurs in approximately 10% to 15% of adults in the US and Europe The highest prevalence of cholelithiasis arises in American Indian populations Age, obesity, and female sex hormones are important aetiological factors
170
What are the presenting symptoms of gallstones?
Asymptomatic (90%): Found incidentally Biliary colic: -Sudden onset, severe RUQ or epigastric pain, constant in nature -May radiate to right scapula, often precipitated by a fatty meal -Can last hours, may be associated nausea and vomiting Acute cholecystitis: -Patient systemically unwell, fever, prolonged upper abdominal pain that may be referred to the right shoulder (due to diaphragmatic irritation) Ascending cholangitis: -Classical association between RUQ pain, jaundice and rigors/fever (Charcot’s triad) -If combined with hypotension and confusion, it is known as Reynold’s pentad
171
What are the signs of gallstones on physical examination?
Biliary colic: -RUQ or epigastric tenderness: typically increases in intensity and lasts for several hours Acute cholecystitis: -Tachycardia -Pyrexia -Right upper quadrant or epigastric tenderness. -There may be guarding with/without rebound -*Murphy’s sign is elicited by placing a hand at the costal margin in the RUQ and asking the patient to breathe deeply, patient stops breathing as the inflamed gallbladder descends and contacts the palpating fingers Ascending cholangitis: -Pyrexia -RUQ pain -Jaundice
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What are the appropriate investigations for gallstones?
Bloods: -FBC: elevated WBC in cholecystitis or cholangitis -LFTs: Normal in cholelithiasis, Elevated alkaline phosphatase (suggests obstruction of the cystic or bile duct) and elevated bilirubin in choledocholithiasis -Serum lipase and amylase: elevated (>3 times upper limit of normal) in acute pancreatitis -*Abdominal ultrasound: *best single diagnostic test for cholelithiasis: =cholelithiasis: stones in the gallbladder =choledocholithiasis: stones in the bile duct with or without bile duct dilation =assess increased thickness of gallbladder wall Others:for suspected choledocholithiasis that is not confirmed by abdominal ultrasound: -MRCP -Endoscopic USS -ERCP: preferred intervention for patients with high risk of bile duct stones (positive imaging, symptoms, and/or blood tests) as it offers both diagnosis and therapy, removing the stones -Abdominal CT: can be used to investigate suspected ascending cholangitis or gallstone pancreatitis
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What is the management of gallstones?
Asymptomatic cholelithiasis does not require any treatment (advice: avoidance of fat in diet) Laparoscopic cholecystectomy is the procedure of choice for symptomatic cholelithiasis For Choledocholithiasis: 1. ERCP stone extraction 2. Following this cholecystectomy represents definitive treatment to reduce the risk of recurrent biliary events, in particular cholangitis or pancreatitis For most patients with simultaneous gallbladder and bile duct stones, early laparoscopic cholecystectomy should generally follow within 72 hours after ERCP and stone extraction
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What is the management of severe biliary colic?
Admission, IV fluids, analgesia, antiemetics and antibiotics if there are signs of infection (cholecystitis or cholangitis) If symptoms fail to improve or worsen, a localized abscess or empyema should be suspected This can be drained percutaneously by cholecystostomy and pigtail catheter If there is evidence of obstruction, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram
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What are the complications of gallstones?
Stones within gallbladder: -Biliary colic, cholecystitis, mucocoele or gallbladder empyema, porcelain gallbladder, predisposition to gallbladder cancer (rare) Stones outside gallbladder: -Obstructive jaundice, pancreatitis, ascending cholangitis, perforation and pericholecystic abscess or bile peritonitis, cholecystenteric fistula, gallstone ileus -Mirizzi syndrome: large gallstone can become lodged in the cystic duct and compress or damage the common hepatic duct, resulting in biliary obstruction and jaundice Surgical complications: -ERCP associated pancreatitis -Cholecystectomy: Bleeding, infection, bile leak, bile duct injury (0.3% laparoscopic, 0.2% open), post-cholecystectomy syndrome (persistent dyspeptic symptoms), port-site hernias
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What is the prognosis for gallstones?
In most cases gallstones are (asymptomatic) benign and do not cause significant problems If they become symptomatic, surgery is an effective treatment Risk factors for recurrent choledochal problems are common: bile duct dilatation to >15mm, gallbladder being left intact, diverticulum, brown pigmented stones
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What is gastric cancer?
A neoplasm that can develop in any portion of the stomach and may spread to the lymph nodes and other organs, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma
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What is the aetiology of gastric cancer?
Most cases are probably caused by environmental insults in genetically predisposed individuals that lead to mutation and subsequent unregulated cell growth Risk factors include: -Helicobacter pylori infection -Atrophic gastritis -Diet high in smoked, processed foods and nitrosamines -Smoking -Alcohol
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What is the epidemiology of gastric cancer?
Common cause of cancer death worldwide, with highest incidence in Asia, especially Japan Sixth most common cancer in UK (annual incidence is 15 in 100000) M: W is 􏰄2:1 Age>50 years *Cancer of the antrum/body is becoming less common, while that of the cardia and gastro- oesophageal junction is increasing
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What are the presenting symptoms of gastric cancer?
In the early phases, it is often asymptomatic Early satiety or epigastric discomfort Weight loss, anorexia, nausea and vomiting Haematemesis, melaena, symptoms of anaemia Dysphagia (tumours of the cardia) Symptoms of metastases, particularly abdominal swelling (ascites) or jaundice (liver involvement)
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What are the signs of gastric cancer on physical examination?
``` Physical examination may be normal Epigastric mass Abdominal tenderness Ascites Signs of anaemia Many eponymous signs: **Virchow’s node/Troisier’s sign: Lymphadenopathy in left supraclavicular fossa Sister Mary Joseph node: Metastatic nodule on umbilicus Krukenberg’s tumour: Ovarian metastases ```
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What are the appropriate investigations for gastric cancer?
*Upper gastrointestinal endoscopy with biopsy: ulcer or mass or mucosal changes Bloods: FBC (for anaemia), LFT CT/MRI: Staging of tumour and planning of surgery (metastatic lesions) Ultrasound of liver: Staging of tumour (metastatic lesions) Bone scan: Staging of tumour (metastatic lesions) Endoscopic ultrasound: Assesses depth of invasion and lymph node spread (determines clinical tumour (T) and node (N) stage) Laparoscopy: May be needed to determine if tumour is resectable
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What is Gastro-oesophageal reflux disease (GORD)?
Inflammation of the oesophagus caused by reflux of gastric acid and/or bile
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What is the aetiology of Gastro-oesophageal reflux disease (GORD)?
The lower oesophageal sphincter (LOS) regulates food passage from the oesophagus to the stomach and contains both intrinsic smooth muscle and skeletal muscle Episodes of transient lower oesophageal sphincter relaxation are a normal phenomenon, but they occur *more frequently in GORD, causing reflux of gastric contents into the oesophagus It is more likely to occur if there is a hiatal sac containing acid- Patients with severe reflux often have a hiatus hernia and decreased resting lower oesophageal sphincter pressure (can have high/moderate pressure too) FH link
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What is the epidemiology of Gastro-oesophageal reflux disease (GORD)?
GORD is a common condition that affects between 10% and 30% of people in developed countries There is global variation, with less than 10% prevalence in East Asia All age groups are affected but risk increases with age and obesity
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What are the presenting symptoms of Gastro-oesophageal reflux disease (GORD)?
Substernal burning discomfort or ‘heartburn’ aggravated by lying supine, bending or large meals and drinking alcohol Regurgitation of gastric contents Dysphagia (caused by formation of peptic stricture after long-standing reflux) Bloating/ early satiety -Pain relieved by antacids Waterbrash: stomach acid gets into throat resulting in sudden flow of saliva RARE: Aspiration may result in voice hoarseness, laryngitis, nocturnal cough and wheeze with (out) pneumonia
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What are the signs of Gastro-oesophageal reflux disease (GORD) on physical examination?
Usually normal | Occasionally, epigastric tenderness, wheeze on chest auscultation, dysphonia (hoarse voice)
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What are the appropriate investigations for Gastro-oesophageal reflux disease (GORD)?
Diagnosis is clinical- a therapeutic trial of a proton-pump inhibitor (PPI) can serve for both diagnosis and initial treatment (e.g. omeprazole) Others: -OGD: indicated for alarm symptoms or symptoms suggesting complicated disease (atypical, persistent, or relapsing symptoms): may show oesophagitis (erosion, ulcerations, strictures) or Barrett's oesophagus -Ambulatory (24h) pH monitoring: can demonstrate abnormal exposure to oesophageal acid in the absence of oesophagitis, pH <4 more than 4% of the time is abnormal -Oesophageal manometry: may suggest achalasia, oesophageal spasm, or other motor disorders -Barium swallow: may be useful in patients with dysphagia for whom endoscopy is contraindicated or unavailable- To detect hiatus hernia, peptic stricture, extrinsic compression of the oesophagus can be visualized -Oesophageal capsule endoscopy: swallowing a capsule endoscope to visualise the oesophagus, may show oesophagitis or Barrett's oesophagus, less-invasive, safe alternative to upper endoscopy -CXR: finding of hiatus hernia (gastric bubble behind cardiac shadow)
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What is the management of Gastro-oesophageal reflux disease (GORD)?
Advice: Lifestyle changes, weight loss, elevating head of bed, avoid provoking factors, stopping smoking, lower fat meals, avoiding large meals late in the evening Medical: -Proton-pump inhibitors (PPIs) are the most effective drugs (adverse effects: increased risk of bone fracture, decreased efficacy of clopidogrel, hypomagnesaemia) -If there is absent or inadequate response, treatment can proceed to high-dose PPI and endoscopy (investigate cause) Endoscopy: Annual endoscopic surveillance for Barrett’s oesophagus; may be necessary for stricture dilation or stenting Surgery: -Antireflux surgery for those with symptoms despite optimal medical management or in those intolerant of medication (people who do not respond to PPIs will probably not respond to surgery) -Bariatric surgery: Patients with GORD who are obese may benefit
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What are the complications of Gastro-oesophageal reflux disease (GORD)?
Low risk: Oesophageal ulceration-anaemia if perforated Peptic stricture Barrett’s oesophagus (risk increases with positive smoking history or hiatus hernia) Oesophageal adenocarcinoma
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What is the prognosis of Gastro-oesophageal reflux disease (GORD)?
50% respond to lifestyle measures alone Most patients respond to treatment with proton-pump inhibitors (PPIs) Maintenance PPI therapy is recommended for those who have symptoms when the PPI is discontinued, as well as for those with erosive oesophagitis and Barrett's oesophagus Most patients relapse off PPI therapy however, there are risks associated with long-term use
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What is Gastroenteritis?
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort
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What is Infectious Colitis?
Inflammation of the colon due to a virus or bacteria
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What is the aetiology of Gastroenteritis and Infectious Colitis?
Can be caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water
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What are the common causative organisms of Gastroenteritis and Infectious Colitis?
Viral: Rotavirus, adenovirus, astrovirus Bacterial: Campylobacter jejuni, Escherichia coli, Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica Protozoal: Entamoeba histolytica Toxins: From Staphylococcus aureus, Clostridium botulinum, Bacillus cereus, mushrooms, heavy metals, seafood Commonly contaminated foods: Improperly cooked meat (S. aureus, C. perfringens), old rice (B. cereus, S. aureus), eggs and poultry (Salmonella), milk and cheeses (Listeria, Campylobacter), canned food (botulism)
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What is the epidemiology of Gastroenteritis and Infectious Colitis?
Common, and often under-reported, a serious cause of morbidity and mortality in the developing world
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What are the presenting symptoms of Gastroenteritis and Infectious Colitis?
Sudden onset nausea, vomiting, anorexia Diarrhoea (bloody or watery) Abdominal pain or discomfort Fever and malaise *Enquire about recent travel, antibiotic use and recent food intake (how cooked, source andwhether anyone else ill) Time of onset: -Toxins (early; 1–24 h) -Bacterial/viral/protozoal (12 h or later) Effect of toxin: -Botulinum causes paralysis -Mushrooms can cause fits, renal or liver failure
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What are the signs of Gastroenteritis and Infectious Colitis on physical examination?
Diffuse abdominal tenderness Abdominal distension Bowel sounds are often increased If severe: -Pyrexia -Dehydration -Hypotension -Peripheral shutdown
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What are the appropriate investigations for Gastroenteritis and Infectious Colitis?
Blood: -FBC -Blood culture (helps identification if bacteriaemia present) -U&Es: dehydration Stool: -Faecal microscopy for polymorphs, parasites, oocysts, culture, electron microscopy (used to diagnose viral infections) -Analysis for toxins, particularly for pseudomembranous colitis (Clostridium difficile toxin) AXR or ultrasound: -To exclude other causes of abdominal pain Sigmoidoscopy: -Often unnecessary unless inflammatory bowel disease needs to be excluded
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What is the management for Gastroenteritis and Infectious Colitis?
Bed rest Fluid and electrolyte replacement with oral rehydration solution (containing glucose and salt) IV rehydration may be necessary in those with severe vomiting *Most infections are self-limiting -Antibiotic treatment is only warranted if severe or the infective agent has been identified (e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter) Botulism: Botulinum antitoxin IM and manage in ITU. Public health: -Often a notifiable disease -Educate on basic hygiene and cooking
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What are the complications of Gastroenteritis and Infectious Colitis?
Dehydration Electrolyte imbalance Pre-renal failure Secondary lactose intolerance (particularly in infants) Sepsis and shock (particularly Salmonella and Shigella) Haemolytic uraemic syndrome is associated with toxins from E. coli Guillian–Barre syndrome may occur weeks after recovery from Campylobacter gastroenteritis *Botulism: Respiratory muscle weakness or paralysis
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What is the prognosis for Gastroenteritis and Infectious Colitis?
Generally good, as the majority of cases are self-limiting
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What is Gastrointestinal perforation?
Also known as ruptured bowel | May occur at any anatomical location from the upper oesophagus to the anorectal junction
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What is the aetiology of Gastrointestinal perforation?
The most common causes of GI perforation are peptic ulcers (gastric or duodenal) and sigmoid diverticulum
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What are the inflammatory or ischaemic causes of Gastrointestinal perforation?
Chemical: -Peptic ulcer disease -Foreign body Infection: -Diverticulitis -Cholecystitis Ischaemia: -Mesenteric ischaemia -Obstructing lesions (e.g. malignancy or faeces) resulting in bowel distension and subsequent ischaemia and necrosis Colitis: -Toxic Megacolon (e.g. Clostridum Difficile or IBD- UC)
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What are the traumatic causes of Gastrointestinal perforation?
Iatrogenic: -Recent surgery (including anastomotic leak) -Endoscopy or overzealous NG tube insertion Penetrating or blunt trauma: Shear forces Direct rupture: -Excessive vomiting leading to oesophageal perforation (Boerhaave Syndrome)
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What is the epidemiology of Gastrointestinal perforation?
In adults, ulcerative disease represents the most common cause of bowel perforation, with duodenal ulcers causing 2- to 3-times the rate of perforation than gastric ulcers do
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What are the presenting symptoms of Gastrointestinal perforation?
Main feature is pain: -Typically this is rapid onset and sharp in nature -Patients are systemically unwell therefore may also have associated malaise, vomiting, and lethargy Thoracic perforation: such as a oesophageal rupture -Pain, ranging from chest or neck pain to pain radiating to the back, typically worsening on inspiration There may be associated vomiting and respiratory symptoms
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What are the signs of Gastrointestinal perforation on physical examination?
Patients will look unwell and often have features of sepsis On examining their abdomen, they will have features of peritonism, which may be localised or generalised (a rigid abdomen) Thoracic perforation: auscultation and percussion may reveal signs of a pleural effusion
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What are the appropriate investigations for Gastrointestinal perforation?
Bloods: routinely: FBC may show high WCC and CRP, non-specific raised amylase Urinalysis: also routine to exclude renal or tubo-ovarian pathology *Imaging: demonstrating air outside the gastrointestinal tract -CT scan is gold standard: confirming any free air presence and suggesting a location -Also Abdominal X-ray and erect CXR (free air under the diaphragm) -Features of AXR: =Rigler’s sign – both sides of the bowel wall can be seen, due to free intra-abdominal air acting as an additional contrast =Psoas sign – loss of the sharp delineation of the psoas muscle border, secondary to fluid in the retroperitoneum
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What is the management of Gastrointestinal perforation?
Prophylactic brand spectrum antibiotics- particularly in patients requiring surgery Surgical: -Identification and (where possible) management of underlying cause -Appropriate management of perforation, such as: =Repairing perforated peptic ulcer with an omental patch =Resecting a perforated diverticulae (e.g. via a Hartmann’s procedure) Conservative: -For patients who have localised perforation (diverticular disease) or sealed upper GI perforation without generalised peritonism -Can also be for patients not suitable for surgery e.g. elderly patients with extensive co-morbidities
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What are the complications of Gastrointestinal perforation?
Infection (peritonitis and sepsis) | Haemorrhage
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What is the prognosis of Gastrointestinal perforation?
Most patients require urgent surgery | Prognosis is dependent on early recognition and prompt resuscitation
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What is Haemochromatosis?
A multisystem disorder of dysregulated (excessive) dietary iron absorption and increased iron release from macrophages resulting in body iron overload which may lead to organ damage (particularly liver, joints, pancreas, pituitary and heart)
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What is the aetiology of Haemochromatosis?
``` Hereditary haemochromatosis (HH) is caused by a mutation in the HFE gene on chromosome 6p Most common mutation (90%) is C282Y, less common is H63D ```
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What is the pathogenesis of Haemochromatosis?
1. Liver model: HFE deficiency causes reduced expression of the hepatic hormone ‘hepcidin’ which causes an increase in duodenal iron absorption through a lack of the inhibitory effect of hepcidin on ferroportin (the protein which exports iron from enterocytes into circulation) 2. Crypt cell model: The HFE protein interacts with the transferrin receptor 1 in duodenal crypt cells. Mutations in HFE may impair uptake of transferrin-bound iron into crypt cells, resulting in upregulation of the iron transporter DMT1 in the crypt cells as they migrate up the villus and mature into enterocytes. This leads to increased iron absorption
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What is the epidemiology of Haemochromatosis?
The most common form, type 1 (HFE-related) haemochromatosis, occurs primarily in people of northern European descent Carrier frequency is up to 1 in 10 but not all express disease Typical age of presentation: 40–60 years Females have a later onset and less severe presentation as a result of iron loss through menstruation
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What are the presenting symptoms of Haemochromatosis?
May be asymptomatic Non-specific symptoms of weakness, fatigue, lethargy, abdominal pain Later features include: -Small/large joint pains (most commonly second/third metacarpophalangeal joints) -Symptoms of liver disease -Diabetes mellitus -Hypogonadism -Cardiac failure Exclude causes of secondary iron overload (e.g. multiple transfusions)
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What are the signs of Haemochromatosis on physical examination?
May be normal, but with severe iron overload: Skin: Pigmentation (‘slate-grey’) resulting from increase in melanin deposits Liver: Hepatosplenomegaly Heart: Signs of heart failure, arrhythmias Hypogonadism: Testicular atrophy, loss of hair, gynaecomastia
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What are the appropriate investigations for Haemochromatosis?
Bloods: -*Serum transferrin saturation: first test to become abnormal, elevated, >45% -*Serum ferritin: raised (also raised in inflammation, alcoholism, chronic viral hepatitis, non-alcoholic fatty liver disease) Others: -HFE mutation analysis: C282Y mutation homozygosity, or less commonly H63D -MRI of liver: measure liver iron content (degree of iron loading) -*Liver biopsy: most sensitive and specific test for measuring liver iron content: iron content raised -LFTs: aminotransferase levels above normal -Pancreas: Fasting or random blood glucose to test for diabetes mellitus -Pituitary function tests: testosterone, FSH and LH assays- lower than normal Heart: ECG, echocardiography: mixed dilated-restrictive or dilated cardiomyopathy Joint X-ray/ bone densitometry: performed in patients with a raised ferritin level who have concomitant predisposing factors to osteoporosis (T score
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What is a Haemorrhoidectomy?
An operation to remove haemorrhoids-swollen blood vessels in the anal canal
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What are the indications for a Haemorrhoidectomy?
Relieve persistent discomfort/pain Prevent bleeding from the anus Surgically correct strangulated haemorrhoids, a condition when the anal sphincter squeezes the prolapsed haemorrhoids and interrupts blood flow
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What are the possible complications of a Haemorrhoidectomy?
From surgery: -Bleeding -Constipation -Infection -Excessive bleeding- seek advice Further complications: -Incontinence of stool: very rare (less than 1%) -Recurrent haemorrhoids
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What are Haemorrhoids?
Vascular-rich connective tissue cushions located within the anal canal Classified into internal (lie above the dentate line) and external (lie below the dentate line)
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What is the aetiology of Haemorrhoids?
Excessive straining due to either chronic constipation or diarrhoea -Repetitive or prolonged straining causes downward stress on the vascular haemorrhoidal cushions, leading to the disruption of the supporting tissue elements with subsequent elongation, dilation, and engorgement of the haemorrhoidal tissues Other causes include: -increase in intra-abdominal pressure by pregnancy or ascites -presence of space-occupying lesions within the pelvis may cause a concomitant decrease in vascular return and increase in anal vascular engorgement Degrees of haemorrhoids: -1st: do not prolapse -2nd: prolapse with defecation but reduce spontaneously -3rd: prolapse and require manual reduction -4th: prolapse that cannot be reduced
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What is the epidemiology of Haemorrhoids?
Prevalence is approximately 4% and is more common in white patients than in black patients, with presentation peaking between the ages of 45-65 years
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What are the presenting symptoms of Haemorrhoids?
Painless rectal bleeding or sudden onset of perianal pain/discomfort (acute thrombosis)
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What are the signs of Haemorrhoids on physical examination?
Tender palpable perianal lesion- can form adjacent to the anal canal on the anal margin when there is acute thrombosis Internal haemorrhoids are not usually palpable on DRE Anal mass: may be present with prolapsing haemorrhoids
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What are the appropriate investigations for Haemorrhoids?
*Anoscopic examination: -most specific and conclusive diagnostic test for haemorrhoids Colonoscopy/flexible sigmoidoscopy: exclude serious pathology such as inflammatory bowel disease or cancer FBC: -Ordered only if there is concern that the patient has experienced significant prolonged rectal bleeding and signs of anaemia are present -May demonstrate microcytic/hypochromic anaemia Stool of occult Haem: unnecessary unless no significant haemorrhoidal tissue is seen on examination
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What is the management for Haemorrhoids?
Mild intermittent bleeding: diet and lifestyle modifications to prevent constipation are usually all that are required, short term topical corticosteroids may be used Internal haemorrhoids: -Rubber band ligation (or Sclerotherapy and infrared photocoagulation) for lower grade haemorrhoids -For high grade haemorrhoids, surgical haemorrhoidectomy is the most effective first-line treatment
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What are the complications of Haemorrhoids?
Anaemia from continuous or excessive bleeding Acute thrombosis of a haemorrhoid: sudden onset of perianal pain and the appearance of a tender nodule adjacent to the anal canal Incarceration: prolapsing haemorrhoidal tissue can become incarcerated and be unable to be reduced into the anal canal, causing severe pain- urgent surgical haemorrhoidectomy Faecal incontinence Pelvic sepsis: rectal pain, urinary retention, abdominal pain, and pyrexia Anal stenosis: increased incidence with extensive, circumferential excision
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What is the prognosis of Haemorrhoids?
For patients following treatment of haemorrhoidal disease, the prognosis is good (resolution or improvement of symptoms with low rates of recurrence) Surgical haemorrhoidectomy has the best long-term effect (lower risk of recurrence)
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What is hepatocellular carcinoma?
Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver
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What is the aetiology of hepatocellular carcinoma?
- Chronic liver damage e.g. alcoholic liver disease, hepatitis B, hepatitis C, autoimmune disease - Metabolic disease e.g. haemochromatosis (inherited condition where iron levels accumulate) - Aflatoxins: Aspergillus flavus fungal toxin found on stored grains or biological weapons
235
What is the epidemiology of hepatocellular carcinoma?
Worldwide, HCC is the sixth most common cause of cancer and the second leading cause of cancer-related death Rare in West (1–2 in 100 000/year) Very common malignancy in areas where Hepatitis B and C are endemic, i.e. Asia and sub-Saharan Africa
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What are the presenting symptoms of hepatocellular carcinoma?
``` Symptoms of malignancy: -Malaise -Weight loss -Loss of appetite Symptoms of chronic liver disease: -Abdominal distension -Jaundice -Right upper quadrant pain History of carcinogen exposure: -High alcohol intake -PMH of Hepatitis B or C or Aflatoxins ```
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What are the signs of hepatocellular carcinoma on physical examination?
``` Signs of malignancy: -Cachexia -Lymphadenopathy Hepatomegaly: -Nodular (but may be smooth) Deep palpation may elicit tenderness *There may be bruit heard over the liver Signs of chronic liver disease: -Jaundice -Ascites -Palmar erythema Others: -Splenomegaly: indicative of portal hypertension secondary to cirrhosis of the liver -Decompensated cirrhosis- hepatic encephalopathy: asterixis, spider naevi ```
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What are the appropriate investigations for hepatocellular carcinoma?
Blood: -*Raised AFP (tumour marker with high sensitivity): elevated in 60% of patients with HCC -Vitamin B12-binding protein is a marker of fibrolamellar hepatocellular carcinoma -LFT has poor specificity and sensitivity but may show biliary obstruction (elevated aminotransferases, alkaline phosphatase, and bilirubin; low albumin) -Prothrombin time: normal or elevated Abdominal ultrasound: -Poorly defined margins and coarse, irregular internal echoes -Not sensitive for tumours <1 cm Duplex scan of liver: -May be used to demonstrate large vessel invasion (e.g. into hepatic or portal veins) *CT (thorax, abdomen, pelvis) with contrast: -Typical hypervascular pattern -To define structural lesion and spread -Hepatic angiography: Using lipiodol (an iodized oil). Liver biopsy: -Confirms histology of tumour: well-differentiated to poorly differentiated hepatocytes with large multinucleated giant cells having central necrosis -Small risk of tumour seeding along biopsy tract Staging: -CXR -Radionuclide bone scan: "hot" spots- bone mets *Screening: AFP and abdominal ultrasound in at-risk individuals
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What is a hernia?
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
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What are the different types of hernia and where do they lie?
*Femoral: located below the inguinal ligament, lateral and inferior to the pubic tubercle Inguinal: located in the line of the inguinal ligament between the anterior iliac spine and pubis (superior and medial to the pubic tubercle) Miscellaneous: include such types as lumbar, flank, obturator and interparietal hernias
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What is the epidemiology of Hernias?
Inguinal hernias are the most common type and mainly affects men, often associated with ageing and repeated strain on the bowel Femoral hernias are much less common than inguinal hernias and tend to affect more women than men
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What is an inguinal hernia?
The most common type of hernia The protrusion of abdominal or pelvic contents through a dilated internal inguinal ring or attenuated inguinal floor into the inguinal canal and out of the external inguinal ring, causing a visible or easily palpable bulge
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What is the aetiology of Hernias?
Mechanical; protrusion of contents through a weakness / defect in the abdominal wall Congenital and acquired forms Connective tissue disorders such as Marfan syndrome may predispose to hernia formation
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What are the types of inguinal hernia?
Direct: protrusion directly through a weakness in the posterior wall of the inguinal canal and emerge in the canal medial to the deep ring and inferior to the epigastric vessels- (through Hesselbach's triangle: lateral border of rectus abdomens, inferior epigastric vessels and inguinal ligament) Indirect: protrusion through the deep inguinal ring following the path of the inguinal canal *if they both coexist: pantaloon hernia
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What is the aetiology of Inguinal hernias?
Congenital: abdominal contents enter the inguinal canal through a patent processes vaginalis Acquired: due to increased intra-abdominal pressure along with muscle and transversalis fascia weakness RF: -Male -Prematurity -Family history -Old age -Obesity -Constipation -Smoking -Chronic bronchitis or emphysema (COPD)- raised intra-abdominal pressure
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What is the epidemiology of Inguinal hernias?
Common- predominantly affects men (male to female ratio is 7-9:1) Affects all ages, but the incidence increases with age
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What are the presenting symptoms of Inguinal hernias?
Groin discomfort Pain with a lump in the groin Visible and/or palpable mass or bulge in the groin that may or may not be reducible
248
What are the signs of Inguinal hernias on physical examination?
More common in R side- groin mass Extends to the scrotum (men) or labia (women) Exclude scrotal lump Distinguish between direct and indirect: -Reduce the hernia and occlude the deep internal ring with 2 fingers. Ask the patient to cough (or stand). If the hernia is restrained it is indirect. If not it is direct. -Surgery: direct hernias are medial to inferior epigastric vessels Auscultation: bowel sounds may be heard over the hernia Tenderness: strangulation Complications: bowel obstruction- systemic upset
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What are the appropriate investigations for Inguinal hernias?
``` *Clinical diagnosis In acute, painful irreducible hernias: -Bloods (FBC, U&Es, CRP, ABGs for lactic acidosis in bowel ischaemia) -Imaging: -USS -Erect CXR: perforation -AXR: obstruction ```
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What is the management of Inguinal hernias?
Surgical-potential for cure and role in preventing strangulation of hernias, and for treating hernias that are painful and difficult to reduce: - Minimally invasive laparoscopic mesh repair - Open-mesh repair It involves placing a large (approximately 12 cm diameter) mesh prosthesis in the preperitoneal space, extending from pubis to iliac spine and overlying the iliac vessels - Watchful waiting is a reasonable option in adults with minimally symptomatic or asymptomatic inguinal hernia
251
What is a femoral hernia?
Protrusion of abdominal contents through a naturally occurring weakness called the femoral canal presenting as a mass in the upper medial thigh
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What is the aetiology of femoral hernias?
Risk factors include: - Female - Increasing age - Pregnancy (higher intra-abdominal pressure) - Constipation, weight-lifting
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What is the epidemiology of femoral hernias?
Most common in women- middle aged and older Less common than inguinal hernias however are more likely to become incarcerated (when herniated tissue becomes trapped and cannot easily be moved back into place- risk of bowel obstruction and strangulation) due to the tighter location
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What are the presenting symptoms of femoral hernias?
Lump in the groin Can be asymptomatic on presentation Around 30% present as an emergency due to obstruction or strangulation (cutting off the blood supply to the bowel)- tender, warm
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What are the signs of femoral hernias on physical examination?
Location: infero-lateral to the pubic tubercle, medial to the femoral pulse Check cough impulse- exclude inguinal hernias Likely t be irreducible and to strangulate due to the rigidity of the canal's borders
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What are the appropriate investigations for femoral hernias?
Clinical diagnosis | Others include ultrasound scan
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What is the management of femoral hernias?
Surgical: - Herniotomy: ligation and excision of the sac - Herniorrhaphy: repair of the hernial defect
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What are the possible complications of hernias?
Incarceration Strangulation Bowel obstruction: -Maydl's hernia: strangutated 'w' shape loop of bowel -Richter's hernia: protrusion and/or strangulation of part of the intestine's antimesenteric border Surgery complications: -pain (chronic) -wound infections -haematoma -paraesthesias/numbness in the groin that dissipates over time -mesh infection -bowel resection -inguinal: penile/scrotal oedema or testicular ischaemia
259
What is the prognosis for hernias?
Prognosis is excellent after surgical repair and patients often report an improvement in their quality of life The incidence of recurrent hernia with mesh repair is reported to be less than 2%
260
What is a Hiatus hernia?
The protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm
261
What is the aetiology of Hiatus hernias?
1. During normal swallowing, the oesophagus shortens several cm secondary to contraction of its longitudinal muscular layer 2. This action, in combination with elevations in intra-abdominal pressure such as from coughing, sneezing, straining, and strenuous exercise, produces physiological movement of the distal oesophagus and possibly the gastro-oesophageal junction through the oesophageal hiatus and into the posterior mediastinum 3. This movement is countered by the resistance of the phreno-oesophageal ligaments, which run between the diaphragm and the gastro-oesophageal junction which are somewhat elastic in terms of their stretch and recoil 4. At some point, however, the physiolgical movement and stretching may enlarge the hiatus, leading to permanent residence of a portion of the stomach above the diaphragm
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What is the epidemiology of Hiatus hernias?
Most cause mild or no symptoms and diagnostic criteria may vary- so difficult to know exactly The incidence of symptomatic cases of hiatus hernia is closely related to the diagnosis of GORD, as these two conditions are closely (but not completely) correlated Higher risk in patients with obesity
263
What are the presenting symptoms of Hiatus hernias?
Can be asymptomatic | Mild symptoms include heartburn, regurgitation (GORD), dysphagia, dyspnoea
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What are the signs of Hiatus hernias on physical examination?
Normal | Bowel sounds may be heard in chest
265
What ar the appropriate investigations for Hiatus hernias?
CXR: symptomatic patients: retrocardiac air bubble or normal *Upper gastrointestinal series: -standard criterion test -Patients with moderate-to-severe symptoms from a suspected hiatus hernia should have this study -stomach is partially or completely intrathoracic Others: -OGD: moderate-to-severe reflux symptoms, exclude oesophagitis or oesophageal dysplasia -CT/MRI: when the diagnosis is not clear or other pathology is suspected: partial or complete intrathoracic stomach and herniation of other intra-abdominal organs into the chest -Oesophageal manometry: Double hump configuration seen due to gastric herniation above the high-pressure zone of the crura (lower pH seen in patients with larger hernias)
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What is the management for Hiatus hernias?
main goal of treatment for hiatus hernia is to alleviate the patient's symptoms 1. Lifestyle changes: -losing weight -elevating the head of the bed -avoiding large meals and meals just before bedtime -avoiding alcohol and acidic foods (and caffeine, nicotine) 2. Medical therapy: -Patients with symptoms of GORD are treated medically with a proton-pump inhibitor (PPI) 3. Surgical: -Laparoscopic procedure: reduction of hernia contents, excision of the hernia sac, lengthening of the intra-abdominal oesophagus, primary cruroplasty with mesh reinforcement, and an anti-reflux procedure or gastropexy Indications for surgery include: patients who have not had a satisfactory response to medical therapy, have a long-term risk of strangulation and mediastinitis or patients who have life-threatening complications of obstruction, volvulus, irreversible ischaemia of the stomach or upper gastrointestinal haemorrhage
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What are the complications of Hiatus hernias?
``` Gastric volvulus (stomach twists round) Obstruction (with suspected strangulation is a surgical emergency) GI bleeding from associated oeaphagitis Barret's oesophagus: associated with GORD Following surgery: -boating -dysphagia -haemorrhage -early mesh infection -recurrent hernia ```
268
What is the prognosis of Hiatus hernias?
Most patients with an uncomplicated sliding hiatus hernia will have adequate relief of symptoms (but not cure) with medical therapy Successful hiatus hernia repair in conjunction with an anti-reflux procedure can provide a long-term cure for both hiatus hernia and gastro-oesophageal reflux disease, but this is a major procedure (individual basis)
269
What is Intestinal Ischaemia?
Group of disorders which can be classified into three types: 1. acute mesenteric ischaemia 2. chronic mesenteric ischaemia 3. colonic ischaemia Result from decreased blood flow to the gastrointestinal tract
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What is the aetiology of Intestinal Ischaemia?
OCCLUSIVE ISCHAEMIA Arterial compromise: -Embolism (50% of acute mesenteric ischaemia events) -Thrombosis (15% to 20% of acute mesenteric ischaemia) -Vasculitis e.g. RA, SLE -External compression (tumours, masses) Venous compromise: -Venous thrombosis (5% of cases of acute mesenteric ischaemia), frequently involves the superior mesenteric vein, associated with cirrhosis or portal hypertension NON-OCCLUSIVE ISCHAEMIA: Hypoperfusion: (20% of cases of acute mesenteric ischaemia) Shock/ Hypotension caused by: -HF -Dialysis -Drug related (igitalis, oestrogen, contraceptives, vasopressin) -Recent surgery or trauma e.g. aortic aneurysm repair -Infection (cytomegalovirus, hepatitis B, Escherichia coli) -Other e.g. pancreatitis, polycythaemia vera, phaeochromocytoma, carcinoid syndrome
271
What is the epidemiology of Intestinal Ischaemia?
Colonic ischaemia frequently occurs in older people with co-existing morbidities, Irritable bowel syndrome, recent cardiovascular surgery, constipation increases this risk Acute mesenteric ischaemia accounts for approximately 0.1% of hospital admissions
272
What are the presenting symptoms of Intestinal Ischaemia?
``` Abdominal pain Diarrhoea Weight loss Blood in stool- fresh/mixed in Light headed (rare) ```
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What are the risk factors for Intestinal Ischaemia?
Old age History of smoking Hypercoaguable states e.g previous DVT, PE PMH of AF, MI, structural heart defects, vasculitis, atherosclerosis, IBD, colonic carcinoma
274
What are the signs of Intestinal Ischaemia on physical examination?
Abdominal tenderness Abdominal bruit: epigastric bruit in 48% to 63% of patients with bowel ischaemia, indicative of turbulent flow through an area of vascular narrowing Weight loss
275
What are the appropriate investigations for Intestinal Ischaemia?
Bloods: -FBC: leukocytosis, anaemia, metabolic acidaemia, evidence of haemoconcentration -Chemistry panel: Acidosis (elevated creatinine) and elevated serum amylase usually occur late in the course of ischaemic bowel -Coagulation profile: detect underlying prothrombotic disorder -ABG/Lactate level: acidosis, elevated lactate (degree of acidosis determine the severity of illness) ECG: detect aetiology such as atrial fibrillation, arrhythmia, acute myocardial infarction Erect CXR: identify whether perforation has occurred due to bowel necrosis, free air may be identified under the diaphragm= peri-operative resuscitation, empirical intravenous antibiotics and surgery AXR: demonstrate air-fluid levels or bowel dilation that may be the result of ischaemia or may indicate the aetiology of ischaemia, such as a distal obstruction **CT: first line if acute ischaemia is suspected: -bowel wall thickening -bowel dilation -pneumatosis intestinalis (gas cysts in the bowel wall) -portal venous gas -occlusion of the mesenteric vasculature -bowel wall thickening with thumb-printing sign suggestive of submucosal oedema or haemorrhage **Sigmoidoscopy/colonoscopy: best test to establish the diagnosis of colonic ischaemia, mucosal sloughing or friability; mucosal petechiae; submucosal haemorrhagic nodules, erosions, or ulcerations, necrosis, gangrene Others: -Mesenteric angiography: preceded by positive CT angiography in the acute setting -Mesenteric duplex ultrasound: reduced or lack of blood flow through proximal mesenteric vessels -CT angiography: for chronic mesenteric ischaemia
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What is Ileus?
The slowing of gastrointestinal (GI) motility accompanied by distention, in the absence of a mechanical intestinal obstruction *diagnosis of exclusion after bowel obstruction has been ruled out It usually occurs in response to physiological stress, including surgery, sepsis, metabolic derangements, and Gl diseases
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What is Intestinal obstruction?
A mechanical disruption in the patency of the gastrointestinal tract, resulting in a combination of emesis (that may be bilious), absolute constipation, and abdominal pain
278
What is the aetiology of Intestinal obstruction?
Common causes of SBO in adults include: - Previous surgery with the formation of intra-abdominal adhesions, including colorectal/gynaecological surgery, resection of intra-abdominal tumours, laparotomy for trauma - Inguinal hernia with incarceration; ventral, incisional, umbilical, and parastomal hernias - Crohn's disease - Intestinal malignancy - Appendicitis
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What is the epidemiology of Intestinal obstruction?
The lifetime incidence of SBO varies between 0.1% and 5% in patients who have not undergone previous surgery, yet may rise to over 60% in patients who have undergone previous surgery In patients with Crohn's disease, the incidence may be upwards of 25% *Can be a major cause of morbidity and mortality, and it can be fatal in untreated patients due to its progression to intestinal necrosis, perforation, sepsis, and multi-organ failure
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What are the presenting symptoms of Intestinal obstruction?
``` Failure to pass flatus or stool Abdominal pain Vomiting Abdominal distension (bloating) Constipation Fever Lethargy ```
281
What are the signs of Intestinal obstruction on physical examination?
Abdominal tenderness Peritonitis (more a complication) Tachycardia Hypotension
282
What are the appropriate investigations for Intestinal obstruction?
Abdominal XR: -Upright and supine x-rays of the abdomen -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: may indicate potential severe intestinal obstruction with necrosis or blood loss into obstructed bowel, increased WBC -Urea: increased in the setting of volume depletion (dehydration) -Electrolytes: imbalance in dehydration; hyponatraemia, hypokalaemia, metabolic alkalosis Abdominal CT: when AXR are inconclusive, help determine underlying cause- may visualise transition zone, mass, tumour, appendicitis Other: -Upper GI x-ray with contrast: detect presence and location of obstruction; In partial SBO, medium passes into rectum, in complete SBO, medium does not pass into rectum and is held up at site of obstruction, also extent of disease in patients with Crohn's disease -Laparotomy/ laparoscopy: when it is difficult to distinguish between partial and complete SBO
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What is the management for Intestinal obstruction?
MEDICAL EMERGENCY Diagnosis requires immediate resuscitation and occasionally urgent surgery depending on whether SBO is partial (some flatus) or complete (no flatus/no air in rectum on imaging), and whether it is simple (no peritonitis) or complicated (peritonitis present) In general: -Patients with complete SBO with or without peritonitis require surgery (exploratory laparotomy) -Patients with partial SBO may benefit from nasogastric decompression (and fluid resuscitation) and close observation- surgery will be required if there is a poor response to non-operative management after 48 to 72 hours
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What are the complications of Intestinal obstruction?
Intestinal necrosis Sepsis Multi-organ failure Intestinal perforation Low risk: -intra-abdominal abscess in cases of intestinal perforation -short bowel syndrome: extensive removal of small intestine during surgery resulting in inadequate absorption of enteral nutrition
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What is the prognosis of Intestinal obstruction?
SBO is 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
286
What is Laparoscopic abdominal surgery?
Also known as “minimally invasive” surgery is a specialized technique for performing surgery using a laparoscope to view into the abdominal cavity but is less invasive Compared to traditional open surgery, patients often experience less pain, a shorter recovery, and less scarring with laparoscopic surgery *at the beginning the abdomen is inflated with carbon dioxide gas to provide a working and viewing space
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What are the indications for Laparoscopic abdominal surgery?
Most intestinal surgeries can be performed using the laparoscopic technique. These include surgery for Crohn’s disease, ulcerative colitis, diverticulitis, cancer, rectal prolapse and severe constipation
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What are the possible complications of Laparoscopic abdominal surgery?
As safe as traditional open surgery- carries the same risks such as complications related to anaesthesia and bleeding or infection
289
What are Liver abscesses?
Localised infections in the liver parenchyma resulting in a walled off collection of pus
290
What is the aetiology of Liver abscesses?
May be may be bacterial, fungal, or parasitic in origin: - Pyogenic liver abscess is often a polymicrobial infection - The most commonly isolated organisms are Escherichia coli, Klebsiella species, Streptococcus constellatus - In immunocompromised hosts, fungal abscess of the liver may occur and amoebic abscess may occur following infection with the parasite Entamoeba histolytica. E histolytica infection which are endemic in Central and South America, Africa, and Asia
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What is the epidemiology of Liver abscesses?
Liver abscess is an uncommon disease, and the incidence of liver abscess increases with age, occurring slightly more often in men than in women
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What are the presenting symptoms of a Liver abscess?
Non-specific symptoms: fever, malaise, nausea, anorexia, night sweats, weight loss RUQ or epigastric pain, which may be referred to shoulder (diaphragmatic irritation) Jaundice- uncommon Diarrhoea 1/3 of patients have chest symptoms, including cough, shortness of breath, and chest pain *Ask about foreign travel
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What are the signs of a Liver abscess on physical examination?
Fever (continuous or spiking) Jaundice Hepatomegaly (right lobe affected more commonly than left) UNCOMMON: -Dullness to percussion and reduced breath sounds at right base of lung, caused by reactive pleural effusion
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What are the appropriate investigations for Liver abscesses?
Bloods: -FBC: demonstrate infectious process but are non-specific; leukocytosis, elevated neutrophil count, anaemia (CRP-non-specific) -Serum LFTs: Elevated serum alkaline phosphatase most common finding, falling albumin level (aminotransferases and bilirubin levels are only mildly elevated except in severe disease or with concomitant biliary obstruction) -Prothrombin time: Indicated to check that blood clotting is within normal limits before aspiration is performed Blood cultures: pyogenic: may be positive for causative bacterial organism; fungal: may be positive for Candida species Liver ultrasound: -can be used to guide aspiration of the abscess -gram stain and culture of aspirated abscess fluid Non-contrast CT: demonstrates hypodense liver lesions, gas within the lesion is highly suggestive of a pyogenic abscess Others: -CXR: indicated only if there are any chest symptoms or signs on examination - plural effusion -serum antibody for amoebiasis if suspected -stool Enzyme-linked immunosorbent assay (ELISA) performed in people with suspected amoebiasis with diarrhoea -PCR of aspiration of the lesion confirms the diagnosis of amoebic abscess (may not be needed) -Liver MRI: more sensitive than abdominal CT for detecting small abscesses but less available
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What are Liver cysts?
Fluid filled sacs in the liver, that can be congenital
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What is the aetiology of Liver cysts?
Inherited disorders can cause cysts, including polycystic liver disease, congenital hepatic fibrosis and Caroli’s syndrome (rare-cystic dilatation (or ectasia) of the bile ducts within the liver) Majority of cystic disease is caused by simple cysts- caused from a malformation of your bile ducts Although rare in the UK, hydatid cysts are caused by a parasitic infection- Tapeworm Echinococcus granulosis
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What is the epidemiology of Liver cysts?
Congenital causes are present at birth Simple cysts are estimated to affect between 1% and 2.5% of the population- they affect all ages, but occur more frequently in the population as age increases
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What are the presenting symptoms/signs of Liver cysts?
Usually have no symptoms Larger cysts may occasionally cause some dull pain and/ or swelling RUQ- hepatomegaly Jaundice (often caused by bile duct obstruction) is rare
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What are the appropriate investigations for Liver cysts?
FBC: lack of signs of inefction- abscess CRP: elevated if inflamed LFTs: elevated AlkPhos and bilirubin if bile duct is obstructed Ultrasound or CT scan- localise structure of mass, exclude abscess Aspiration of fluid- exclude infection
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What is the management of Liver cysts?
Simple liver cysts generally do not require treatment unless they become large enough to cause pain- aspirated and then stick the walls together using sclerosant or remove part of the wall of the cyst, called laparoscopic de-roofing
301
What is Liver failure?
Syndrome defined by a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy
302
What are the classifications of Liver failure?
Hyperacute liver failure: -Jaundice with encephalopathy occurring in <7 days Acute: -The interval from the onset of jaundice to the development of encephalopathy occurs within 24 to 26 weeks (BMJ) - Jaundice with encephalopathy occurring from 1 to 4 weeks of onset (rapid) Subacute: -Jaundice with encephalopathy occurring within 4–12 weeks of onset Acute-on-chronic: -Acute deterioration (decompensation) in patients with chronic liver disease
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What is the aetiology of Liver failure?
Most common cause is Paracetamol overdose Other causes include idiosyncratic drug-induced liver injury (e.g. anti-TB therapy), hepatitis B and A and autoimmune hepatitis Less commonly: Budd-Chiari syndrome, pregnancy-related, malignancy (e.g. lymphoma), haemochromatosis, mushroom poisoning (Amanita phalloides), Wilson’s disease
304
What is Budd-Chiari syndrome?
A very rare condition involving the occlusion of the hepatic veins that drain the liver It presents with the classical triad of abdominal pain, ascites, and liver enlargement
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What is the pathogenesis of the manifestation in Liver failure?
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) or platelet functional abnormalities associated with jaundice or renal failure
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What is the epidemiology of Liver failure?
Paracetamol overdose accounts for 50% of acute liver failure in the UK
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What are the presenting symptoms of Liver failure?
May be asymptomatic Jaundice Fever, nausea, malaise Abdominal pain
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What are the signs of Liver failure on physical examination?
Jaundice Signs of encephalopathy: time of onset of encephalopathy in relation to jaundice is important; -Grade 1: sleep reversal, mild lack of awareness, shortened attention span, and impaired computations -Grade 2: lethargy, poor memory, personality change, development of asterixis on physical exam -Grade 3 : somnolence (strong desire to sleep), confusion, disorientation, and physical findings that include hyper-reflexia, nystagmus, clonus, and rigidity Grade 4 is characterised by stupor (near unconsciousness) and coma Fetor hepaticus (smell of ‘pear drops’). Ascites and splenomegaly (less common in acute or hyperacute) Bruising or bleeding from puncture sites or GI tract
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What are the appropriate investigations for Liver failure?
LFTs: hyperbilirubinaemia (associated with jaundice), elevated liver enzymes Prothrombin time/INR: elevated INR (>1.5)- coagulopathy Basic metabolic profile: renal failure is a common complication-elevated urea and creatinine, metabolic derangements FBC: leukocytosis (infectious cause), anaemia, thrombocytopenia Blood type and screen: pre-emptively in case a blood transfusion is required ABG: metabolic acidosis. elevated lactate- presence of acidosis is an important prognostic indicator, particularly in paracetamol overdose Paracetamol level/Urine toxicology screen: may be elevated: N-Acetylcysteine therapy should be administered in all suspected cases Factor V level: low result (<20% to 30% of normal) in the presence of hepatic encephalopathy may be predictive of mortality Viral hepatitis serologies/autoimmune markers/ ceruloplasmin (Wilson's disease) Pregnancy test: increased risk of acute viral hepatitis, acute fatty liver of pregnancy CXR: possible aspiration pneumonia Abdominal ultrasound with doppler: may assess vessel patency and evidence of hepatic vein thrombosis associated with Budd-Chiari syndrome Others: -HIV etst, EEG: monitor encpehalopathy, liver biopsy: hepatocellular necrosis, microvesicular steatosis, viral inclusions/ inflammatory presence -CT head: considered once grade 3 to 4 hepatic encephalopathy develops to assess for presence of cerebral oedema or haemorrhage
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What is the management for Liver failure?
Resuscitation (ABC approach): ITU care and specialist unit support essential Treat the cause if possible: N-acetylcysteine for paracetamol overdose Invasive ventilatory support often required plus coagulopathy treatment: IV Vitamin K, FFP, platelet infusions if required, gastric mucosa protection (PPI) Antiviral therapy should be considered *Avoid: Sedatives or drugs metabolized by the liver Liver transplantation should be considered in all patients with ALF who fulfil prognostic criteria for a high risk of mortality
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What is the prognostic criteria for a high risk of mortality in Liver failure?
According to the United Network for Organ Sharing (UNOS): Age >18 years, life expectancy without a liver transplant of <7 days, onset of encephalopathy within 8 weeks of the first symptoms of liver disease, absence of pre-existing liver disease, admission to an intensive care unit, and 1 of the following: -Ventilator dependence -Requirement of renal replacement therapy -INR >2.0
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What are the contraindications of Liver transplantation?
Severe infection or septic shock Brain death Severe cardiopulmonary disease or ARDS Multi-organ failure Extrahepatic malignancy Other factors that may preclude liver transplant candidacy are ongoing alcohol or illicit drug abuse, inadequate social support, or a history of repeated suicide attempts
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What are the complications of Liver failure?
Rapidly progressing hepatic encephalopathy Coagulopathy Infection Hepatorenal syndrome (concurrent hepatic and renal failure) Metabolic disorders: hypoglycaemia, acid–base and electrolyte disturbances Cerebral oedema GI bleeding due to coagulopathy
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What is the prognosis of Liver failure?
Depends on the severity and aetiology: - secondary to paracetamol overdose, acute hepatitis A, or shock liver is associated with a favourable prognosis - in contrast, resulting from idiosyncratic drug-induced liver injury, acute hepatitis B, or indeterminate cause has a much lower rate of spontaneous recovery
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What is Mallory-Weiss tear?
A syndrome characterised by a tear or laceration often along the right border of, or near, the gastro-oesophageal junction
316
What is the aetiology of a Mallory-Weiss tear?
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 Causes include: -Coughing (chronic e.g. COPD, bronchiectasis) -Retching, vomiting and straining -Closed-chest pressure or cardiopulmonary resuscitation -Acute abdominal blunt trauma -Alcohol and medications (aspirin or other NSAIDs) -Chemotherapeutic agents *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
317
What is the epidemiology of Mallory-Weiss tears?
Admission to hospital for non-variceal upper gastrointestinal (GI) bleeding is common Age of presentation may vary but is most common in people aged between 30- 50 years More common in men than in women in a ratio of 3:1 In women of childbearing age, the most common cause is hyperemesis gravidarum (severe nausea and vomiting)
318
What are the presenting symptoms and signs of a Mallory-Weiss tear?
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 Light headedness/dizziness Postural/orthostatic hypotension
319
What are the appropriate investigations for a Mallory-Weiss tear?
Bloods: -FBC: Hb, Hct, and platelets are usually unremarkable in an acute setting; however, anaemia may range from mild to severe in rare cases -Urea: important parameter to evaluate the severity of bleeding, elevated in patient with ongoing bleeding -LFTs/prothrombin time: exclude liver disease which may predispose a patient to oesophageal varices, gastric varices -Cross matching: patient presenting with haemorrhage CXR: may be an initial test diagnosis in patients with suspected oesophageal perforation, typically normal in uncomplicated MWT **OGD: -diagnostic test of choice and should be performed in all patients with upper GI bleed after stabilisation -tear or laceration typically appears as a red longitudinal defect with normal surrounding mucosa; the lesions vary from mm to cm Others: -Creatinine kinase (troponin and other cardiac enzymes)/ECG : for patients with CAD or with symptoms of cardiac ischaemia, massive bleeding, or multiple comorbidities- usually normal -Angiography: indicated for massive haemorrhages in which visualisation of the lesion is not possible on OGD
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What is the management for Mallory-Weiss tears?
Patients who are actively bleeding and/or with multiple medical comorbidities should be attended to as an emergency During investigations: blood should be transfused when Hb is <8 g/dL or <100 g/L (<10 g/dL) in patients with CAD or multiple comorbidities Medical: -Treatment includes anti-secretory drug therapy with (IV) PPIs or H2 antagonists and anti-emetics- it should be given before endoscopic procedure Endoscopic: -First line and the procedure of choice for patients with non-variceal upper GI bleeding -It is usually performed after medical treatment is given -Injection therapy (adrenaline) is commonly used alongside thermal or mechanical (haemoclip) Surgical: -reserved for situations where endoscopic haemostasis of bleeding has failed or transmural oesophageal perforation has occurred -Laparoscopic over-sewing of the laceration at the gastro-oesophageal junction Other: -Angiography therapy: when endoscopy or surgery is contraindicated or not available- infusion of a vasoconstrictor (vasopressin) or transcatheter embolisation -Compression by Sengstaken-Blakemore tube is a last resort
321
What are the complications of Mallory-Weiss tears?
MI or infraction: usually related to the acuity, severity of bleeding, and associated CAD Hypovolaemic shock/death: usually related to acuity and severity of bleeding; however, it is rare in patients with early stabilisation and prompt treatment Oesophageal perforation: Gastric ischaemia Metabolic disturbance: intractable vomiting
322
What is the prognosis of Mallory-Weiss tears?
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 about 8% to 15% of patients and usually occurs within the first 24 hours and most often in patients with high-risk factors for re-bleeding (old age > 65, alcoholism/NSAID use, co-morbidities)
323
What is Nasogastric tube insertion?
The insertion of a tube from the patients nose into their stomach for either feeding or aspiration
324
What are the indications of Nasogastric tube insertion?
To empty the upper gastrointestinal tract or for feeding- insertion may be for prophylactic or therapeutic reasons Possible contraindications: -Ear, nose and throat abnormalities or infections -Facial/neck fractures -Possible strictures of the oesophagus -Oesophageal varices -Anatomical abnormalities (oesophageal diverticulae) -Risk of aspiration
325
What are the possible complications of Nasogastric tube insertion?
Main: aspiration and tissue trauma- if placed incorrectly into the trachea and lung it can cause pneumonia and death *Correct follow up procedure should be followed- pH test (NG tube is aspirated and the contents are checked using pH paper) and CXR
326
What is Non-alcoholic steatohepatitis (NASH)?
The most common cause of chronic liver disease in the Western world It includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis in those who do not consume alcohol in amounts generally considered harmful to the live
327
What is the aetiology of Non-alcoholic steatohepatitis (NASH)?
Associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia, hypertension and (hepatotoxic) drugs, e.g. amiodarone, tamoxifen
328
What is the epidemiology of Non-alcoholic steatohepatitis (NASH)?
Estimated that NASH affects 20% to 40% of the Western world, with the Asian and Pacific regions being less affected The majority of cases occur in people between the ages of 40-60 years
329
What are the presenting symptoms/signs of Non-alcoholic steatohepatitis (NASH)?
``` Fatigue and malaise Hepatosplenomegaly Obesity RUQ abdominal discomfort Absence of significant alcohol use: spider naevi, palmar erythema, dupuytren's contracture, gynaecomsastia, parotid gland enlargement, asterixis ```
330
What are the appropriate investigations for Non-alcoholic steatohepatitis (NASH)?
Bloods: LFTs: -AST and ALT: usually mildly elevated at 1-4 times upper limit of normal values- the AST:ALT ratio (AAR) in NASH is typically <1 (acute alcoholic hepatitis: >2) -Bilirubin: elevates with decompensated disease -Alkaline phosphatase: elevated -GGT: elevated -Prothrombin time/INR: elevated- impaired or decompensated liver synthetic function/ iron studies show elevated iron indices with elevated transferrin saturation and ferritin -Serum albumin: LOW FBC: Anaemia and thrombocytopenia due to hypersplenism usually seen after the development of cirrhosis and portal hypertension Metabolic profile: Mild hyponatraemia is commonly seen in patients with cirrhosis Anti-nuclear antibody: positive, relatively common Serum ammonia: marker of encephalopathy Portal venous pressure: end stage liver disease (transjugular approach) Test for aetiology: - Insulin (elevated in diabetics) - Alpha fetoprotein: exclude hepatocellular carcinoma - Lipid panel: Fasting lipid panel shows -hypertriglyceridaemia in 20% to 80% of patients Imaging: - Liver ultrasound: 1) diffuse hyperechoic echotexture (bright liver) 2) increased liver echotexture compared with kidney 3) vascular blurring 4) deep attenuation - Abdominal CT/MRI: low attenuation liver/ increased liver fat content respectively - OGD: surveillance of portal hypertensive gastropathy and oesophageal and gastric varices which can precede cirrhosis *Liver biopsy: ultimately required for the diagnosis; ballooning degeneration of the hepatocytes and spotty lobular inflammation in addition to mixed micro- and macrovesicular steatosis
331
What is the management of Non-alcoholic steatohepatitis (NASH)?
1.Weight loss through lifestyle modification/ pharmacological agents or surgery (Orlistat is an enteric lipase inhibitor that prevents the absorption of fats from the gastrointestinal tract/ bariatric surgery) Treatment of insulin resistance and diabetes (metformin) Presence of end-stage liver failure: -Transjugular intrahepatic portosystemic shunt (TIPS) -Liver transplantation
332
What are the complications of Non-alcoholic steatohepatitis (NASH)?
``` Ascites Cirrhosis Variceal haemorrhagae Portosystemic encephalopathy Hepatocellular carinome (seen in patients with cirrhosis) Hepatorenal syndrome Hepatopulmonary syndrome Death: result of the increased risk of coronary artery disease ```
333
What is the prognosis of Non-alcoholic steatohepatitis (NASH)?
Independent predictors of fibrosis progression include: -Diabetes mellitus -A low initial fibrosis stage -Higher body mass index *At a mean follow-up of 14 years, NASH is associated with increased overall mortality, which was primarily a result of cardiovascular disease and to a lesser extent liver-related causes Patients who have NASH progress to cirrhosis 9% to 20% of the time- Up to 1/3 of these patients will die from complications from liver failure or require liver transplantation Recurrent NAFLD following liver transplantation is now a well-recognised phenomenon
334
What is oesophageal cancer?
Malignant tumour arising in the oesophageal mucosa. There are two major histological types: - Squamous cell carcinoma - Adenocarcinoma
335
What is the aetiology of oesophageal cancer?
Squamous cell carcinomas are more common in the mid-upper oesophagus Adenocarcinoma usually develops in the lower oesophagus or, increasingly, the gastro- oesophageal junction *Barrett's oesophagus (metaplasia of the mucosal lining of the distal oesophagus) is caused by long-standing gastro-oesophageal reflux, and is considered a pre-malignant condition for the development of adenocarcinoma
336
What are the risk factors for oesophageal cancer?
``` Male sex (7:1) Squamous cell carcinoma: -Alcohol -Tobacco -FH of oesophageal, stomach, oral or pharyngeal cancer -Certain nutritional deficiencies (vitamins, trace elements) -HPV infection -Achalasia Adenocarcinoma: -GORD -Barrett’s oesophagus -Obesity ```
337
What is the epidemiology of oesophageal cancer?
Eighth most common malignancy (UK 7000–8000 per year) 3/4:1 male : female Worldwide squamous carcinoma is more common (95%) but in the West Adenocarcinoma is more common (65% cases in the UK)- INCIDENCE IS INCREASING Peak incidence 60–70 years
338
What are the presenting symptoms of oesophageal cancer?
``` Early: symptomatic/symptoms of reflux Later: -Dysphagia, initially worse for solids -Regurgitation -Cough or choking after food -Pain on swallowing (odynophagia) -Weight loss, fatigue -Voice hoarseness (may indicate recurrent laryngeal nerve palsy) ```
339
What are the signs of oesophageal cancer on physical examination?
No physical signs may be evident Signs of weight loss With metastatic disease there may be supraclavicular lymphadenopathy, hepatomegaly Respiratory signs may be due to aspiration or direct tracheobronchial involvement
340
What are the appropriate investigations for oesophageal cancer?
Endoscopy: - *First test- Oesophagogastrodueodenoscopy (OGD) with biopsy: mucosal lesion; histology shows squamous carcinoma or adenocarcinoma - Early high-grade dysplasia and cancer detection is improved by endoscopic techniques such as narrow band imaging or magnification, staging Imaging: - Barium swallow -exclude differentials - CT (chest, abdomen, pelvis): size of primary tumour, local invasion, and presence or absence of metastases - PET: hyperactivity 'hot' spot, can detect previously occult distant metastases Other: - Bronchoscopy (if risk of trancheobronchial invasion) - Bone scan if symptoms of bony involvement - Laparoscopy and peritoneal washings * Careful cardiac and respiratory assessment if surgery planned
341
What is Open abdominal surgery (incl. laparotomy)?
A way of performing operations by making an incision (cut) across the front of the abdomen
342
What are the indications for Open abdominal surgery (incl. laparotomy)?
Was the most common way of performing abdominal surgery until the key hole (Laparoscopic surgery) surgery was developed However, it is still used for some operations, such as: -Removing the womb (Hysterectomy), if it is too large to be removed with keyhole surgery -Removing large fibroids or large ovarian cysts -Some types of surgery for cancer -When it is not possible to stop bleeding or repair damaged structures by keyhole surgery
343
What are the complications of Open abdominal surgery (incl. laparotomy)?
Problems that frequently occur after this type of surgery include: - Pain - Wound infection - Bruising and thickened scar (Keloid scar) formation - Numbness, tingling or burning sensation around the scar- usually resolves over time - UTI and polyuria - Early menopause if you have had a hysterectomy - Damage to the bladder and /or ureter - Damage to the bowel - Heavy bleeding which requires blood transfusion, return to theatre after surgery because of bleeding or problems with the wound - Infection in the pelvis - DVT or PE - Risk of death within 6 weeks of surgery (rare) - Anaesthetic complications
344
What is pancreatic cancer?
Malignancy arising from the exocrine or endocrine tissues of the pancreas Refers to primary pancreatic ductal adenocarcinoma, which accounts for >85% of all pancreatic neoplasms
345
What is the aetiology of pancreatic cancer?
Pancreatic cancer is a disease of older people, with a peak incidence in people 65 to 75 years of age The only consistently reported exogenous risk factor for pancreatic cancer is cigarette smoking 5-10% have a familial component Other risk factors(weak): -Obesity -Diabetes Mellitus -Dietary factors ( high in meats and fat, and low serum folate)
346
What is the epidemiology of pancreatic cancer?
Increasing in incidence (8–12/100000), worldwide sixth cause of cancer deaths (poor prognosis) Peak age 60–80 years
347
What are the presenting symptoms of pancreatic cancer?
``` Initial symptoms (often non-specific): -Anorexia -Malaise -Weight loss -Nausea Later symptoms: jaundice, epigastric pain ```
348
What are the signs of pancreatic cancer of physical examination?
Signs of: -Weight loss -Epigastric tenderness -Mass Courvoisier’s law: Jaundice and a painless palpable gallbladder - UNLIKELY TO BE GALLSTONES (rather carcinoma of the pancreas or the lower biliary tree) In patients with metastatic spread: there may be hepatomegaly Trousseau’s sign is an associated superficial thrombophlebitis (sign in hypocalcaemia): increased risk of thromboembolic disease
349
What are the appropriate investigations for pancreatic cancer?
Bloods: -Tumour marker CA19-9 can be elevated (specific, but not diagnostic) -If causing obstructive jaundice: bilirubin, alkaline phosphatase, and gamma glutamyl transpeptidase elevated Imaging: -*(without delay)Abdominal ultrasound: pancreatic mass, dilated bile ducts, liver metastases -Pancreatic protocol CT: may demonstrate a mass in the pancreas and the extent of local or distant spread -ERCP: ampullary tumour may be seen; all other pancreatic tumours are only detectable if there is pancreatic duct involvement, may allow biopsy/bile cytology with stenting -PET scan: may demonstrate a mass in the pancreas -MRI: detailed duct involvement -Endoscopic ultrasound: detect small tumours in the pancreas -Laparoscopy: useful in staging the disease (peritoneum, liver)
350
What is acute pancreatitis?
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 ) The severity of the disease ranges from mild pancreatic oedema with full recuperation to severe systemic inflammatory response with pancreatic/peripancreatic necrosis, multiple organ failure, and death
351
What is the aetiology of acute pancreatitis?
Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation *Most common: Gallstones, alcohol (80% cases) Other causes include: -Hypertriglyceridemia -Hypercalcemia -Pancreatic malignancy -Post-ERCP(2% to 3%) -Trauma -Drugs (furosemide, azathioprine, thiazide diuretics, sulfonamides, tetracyclines, valproic acid, oestrogen) -Infection (mumps, mycoplasma, Epstein-Barr virus) -Autoimmune conditions (collagen vascular diseases)
352
What is the epidemiology of acute pancreatitis?
Common- the most common cause worldwide is alcohol consumption Peak age is 60 years In males, alcohol-induced is more common while in females, principal cause is gallstones
353
What are the presenting symptoms of acute pancreatitis?
Severe epigastric or abdominal pain (radiating to back, relieved by sitting forward, aggravated by movement) Associated with anorexia, nausea and vomiting
354
What are the signs of acute pancreatitis on physical examination?
``` Epigastric tenderness Fever Shock, tachycardia, tachypnoea Reduced bowel sounds (due to ileus) If severe and haemorrhagic, Turner’s sign (bilateral flank bruising) or Cullen’s sign (periumbilical bruising) ```
355
What are the appropriate investigations for acute pancreatitis?
Serum lipase/amylase: 3 times the upper limit of the normal range For gallstones: aspartate and alanine transaminase: if >3 times the upper normal limit FBC: leukocytosis CRP/haematocrit: if >150 mg/L, is associated with pancreatic necrosis ABG: monitor the arterial oxygenation since patients may be hypoxemic Abdominal imaging is not needed for diagnosis in most patients: -Abdominal plain film: Abnormal in two-thirds of patients -Transabdominal ultrasound: may show pancreatic inflammation, peripancreatic stranding, calcifications, or fluid collections -CXR: exclude other causes -CT scan with intravenous contrast: *the most sensitive and specific study for confirming diagnosis of pancreatitis; diffuse or segmental enlargement of the pancreas with irregular contour and obliteration of the peripancreatic fat, necrosis, or pseudocysts -MRCP: advantage of not requiring intravenous contrast or radiation-allows better visualization of common bile duct stones and the pancreatic duct; findings may include stones, diffuse or segmental enlargement (Endoscopic ultrasound is used as an alternative)
356
What is the Glasgow criteria scoring system for assessing the severity of pancreatitis?
``` Modified Glasgow criteria (􏰂3 or > 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 ```
357
What is the management of acute pancreatitis?
Medical: - Fluid and electrolyte resuscitation - Urinary catheter and NG tube if vomiting (enteral) - Analgesia and blood sugar control - Early HDU or intensive care support For gallstone pancreatitis (and cholangitis): -If the presence of stones in the common bile duct is confirmed, cholecystectomy with common bile duct exploration -ERCP for patients with persistent choledocholithiasis that can obstruct the common bile duct (within 24h) For alcoholic pancreatitis: -Patients may need pharmacological treatment for alcohol withdrawal For severe cases of pancreatitis: - Hypocalcemia should be identified and treated because it may lead to cardiac dysrhythmias - Blood glucose control and insulin administration to keep glucose <150 mg/dL has been associated with reductions in morbidity and mortality (reduce risk of infection) Indications to intervene on pancreatic collections include: - Infection (systemic signs of sepsis or evidence of gas in the collection on cross-sectional imaging) - Clinical deterioration - Symptomatic sterile necrosis (may include abdominal pain, anorexia, early satiety, nausea, vomiting, biliary obstruction, or persistent nonspecific systemic symptoms [i.e., malaise, fatigue, and low-grade fever]) For highly suspected infected necrosis should receive immediate intravenous antibiotics; If the patient fails to improve: - image-guided catheter drainage - Necrosectomy is typically reserved for those patients who do not respond to drainage (drainage and debridement of all necrotic tissue)
358
What are the complications of acute pancreatitis?
Local: -Pancreatic necrosis -Pseudocyst (peripancreatic fluid collection persisting >4 weeks) -Abscess -Ascites -Pseudoaneurysm or venous thrombosis Systemic: Multiorgan dysfunction, sepsis, renal failure, ARDS, DIC, hypocalcemia, diabetes Long term: Chronic pancreatitis (with diabetes and malabsorption)
359
What is the prognosis of acute pancreatitis?
The majority of patients with acute pancreatitis will improve within 3 to 7 days of conservative management The cause of pancreatitis should be identified and a plan to prevent recurrence should be initiated before the patient is discharged from hospital (e.g. cholecystectomy)
360
What is chronic pancreatitis?
Chronic inflammatory disease of the pancreas characterized by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain
361
What are the classifications of pancreatitis?
(1) Recurrent acute pancreatitis: there is an identifiable cause of acute pancreatitis that does not lead to chronic pancreatitis (e.g., gallstones, drugs, hypercalcaemia, etc.) (2) Idiopathic pancreatitis: exhaustive evaluation identifies no cause. Most commonly this represents chronic relapsing pancreatitis or definite chronic pancreatitis (3) Chronic relapsing pancreatitis: patients have relapsing pain not recognised clinically as chronic pancreatitis (no hallmark features) but have pathological changes in tissue specimens (4) Established chronic pancreatitis: hallmark features of chronic pancreatitis are present, including reduced pancreatic exocrine function, malabsorption, diabetes, and pancreatic calcifications
362
What is the aetiology of chronic pancreatitis?
Alcohol (70%) Idiopathic in 20% Others: Recurrent acute pancreatitis, ductal obstruction, autoimmune pancreatitis, hyperparathryroidism, hypertriglyceridemia
363
What is the epidemiology of chronic pancreatitis?
Annual UK incidence 􏰀1/100 000 | Mean age 40–50 years in alcohol-associated disease
364
What are the presenting symptoms of chronic pancreatitis?
Recurrent severe epigastric pain, radiating to back, relieved by sitting forward, can be exacerbated by eating or drinking alcohol Nausea and vomiting Over many years, weight loss, malnutrition, bloating and pale offensive stools (steatorrhoea)
365
What are the signs of chronic pancreatitis on physical examination?
Epigastric tenderness | Signs of complications, e.g. weight loss, malnutrition
366
What is the pathogenesis of chronic pancreatitis?
Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atropy, ductal dilatation, cyst and stone formation
367
What are the appropriate investigations for chronic pancreatitis?
Blood glucose: Glucose intolerance occurs early due to insulin resistance, and diabetes mellitus occurs late due to insulinopenia (elevated) Bloods: increased immunoglobulins, especially IgG4 in autoimmune pancreatitis *CT abdomen: pancreatic calcifications, focal or diffuse enlargement of the pancreas, ductal dilation, and/or vascular complications Abdominal ultrasound (done if CT is unavailable): structural/anatomical changes including cavities; duct irregularity; contour irregularity of head/body; calcification Abdominal XR: Pancreatic calcification is present on the x-ray in 30% to 70% of patients at their initial presentation Others: -Endoscopic ultrasound: more detailed evaluation of the pancreatic parenchyma and ducts compared with A USS and CT, and less invasive than ERCP -ERCP*: Commonly considered the most accurate test- characteristically shows beading of the main pancreatic duct (from alternating dilation and stenosis) as well as irregularities in the side branches -MRCP can also be used -Faecal elastase-1: indirect function test;reduced in severe disease to <200 micrograms/g -Increased faecal fat/ steatocrit *Amylase and lipase are usually normal
368
What is the management of chronic pancreatitis?
Lifestyle changes: -Both alcohol and smoking cessation are likely to be beneficial -consuming small, frequent meals, receiving adequate pancreatic enzyme therapy, monitoring blood glucose, avoiding alcohol Analgesia: consisting of paracetamol and ibuprofen in combination with tramadol Management of pancreatic insufficiency: -Pancreatin is a recommended first-line supplement Surgical: -3 general strategies: decompression (drainage), denervation, and resection -New predictors of surgical pain relief: Onset of symptoms less than 3 years, no pre-operative use of opioidsand 5 or < endoscopic procedures pre-operatively
369
What are the complications of chronic pancreatitis?
Local: Pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites, pancreatic carcinoma Systemic: Diabetes, steatorrhoea, reduced quality of life, chronic pain syndromes and dependence on strong analgesics
370
What is the prognosis of chronic pancreatitis?
Difficult to predict as pain may improve, stabilize or worsen (generally, pain decreases or disappears over time, regardless of aetiology) Surgery improves symptoms in 60–70% but results are often not sustained Life expectancy can be reduced by 10–20 years
371
What is Peptic ulcer disease?
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
372
What is the aetiology of Peptic ulcer disease?
Peptic ulcers result from an imbalance between: - Factors promoting mucosal damage (gastric acid, pepsin, Helicobacter pylori infection, NSAID drug use) - Mechanisms promoting gastroduodenal defense (prostaglandins, mucus, bicarbonate, mucosal blood flow) * Common: Very strong association with H. pylori (present in 95% of duodenal and 70–80% of gastric ulcers), NSAID use
373
What is the epidemiology of Peptic ulcer disease?
Common-annual incidence is about 1–4/10,00 More common in males Duodenal ulcers have a mean age in 30s while gastric ulcers have a mean age in 50s H. pylori is usually acquired in childhood and the prevalence is roughly equivalent to age in years
374
What are the presenting symptoms of Peptic ulcer disease?
Epigastric abdominal pain (relieved by antacids) Symptoms have a variable relationship to food: - if worse soon after eating, more likely to be gastric ulcers; - if worse several hours later, more likely to be duodenal
375
What are the signs of Peptic ulcer disease on physical examination?
May be no physical findings Epigastric tenderness Signs of complications (e.g. anaemia, succussion splash also known as a gastric splash, is a sloshing sound heard on auscultation during sudden movement of the patient on abdominal auscultation due to pyloric stenosis)
376
What are the appropriate investigations for Peptic ulcer disease?
*Helicobacter pylori urea breath test or stool antigen: positive result if H pylori present *OGD: most specific and sensitive test; peptic ulcer; may also detect cause, for example, H pylori through urease testing, histology can determine if NSAID use is the cause FBC: only ordered if clinically anaemic or has evidence of gastrointestinal bleeding; microcytic anaemia Fasting serum gastrin level: Ordered if there are multiple duodenal ulcers (especially postbulbar) or in patient with ulcers and diarrhoea; hypergastrinaemia in Zollinger-Ellison syndrome *Rockall scoring: For severity after a GI bleed. Less than 3 carries good prognosis, >8 have a high risk of mortality
377
What is the management for Peptic ulcer disease?
Acute: -Resuscitation if perforated or bleeding (IV colloids/crystalloids), close monitoring of vital signs, and proceeding endoscopic or surgical treatment -Patients with upper GI bleeding should be treated with IV PPI (e.g. omeprazole or pantoprazole) at presentation until the cause of bleeding is confirmed -Patients with actively bleeding peptic ulcers or ulcers with high-risk stigmata (e.g. visible vessel or adherent clot) should continue IV PPI -Switch to oral PPI If there is no re-bleeding within 24 hours H. pylori eradication with ‘triple therapy’ for 1–2 weeks: -one PPI and two antibiotics (e.g. clarithromycin + amoxicillin, metronidazole + tetracycline) If not associated with H. pylori: -Treat with PPIs or H2-antagonists -Stop NSAID use (especially diclofenac), use misoprostol (prostaglandin E1 analogue), if NSAID use is necessary
378
What are the complications of Peptic ulcer disease?
Medium risk of upper GI bleeding Rate of major complication is 1% per year including haemorrhage (haematemesis, melaena, iron-deficiency anaemia), perforation, obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)
379
What is the prognosis of Peptic ulcer disease?
Overall lifetime risk 􏰀10%. Generally good as peptic ulcers associated with H. pylori can be cured by eradication (or NSAID discontinuation) With proton-pump inhibitor (PPI) therapy, duodenal ulcers typically heal within 4 weeks and gastric ulcers within 8 weeks
380
What is Gastritis?
The histological presence of gastric mucosal inflammation
381
What is the aetiology of Gastritis?
Acute non-erosive gastritis is most commonly due to Helicobacter pylori infection- Chronic H pylori infection predisposes to atrophic gastritis and autoimmune gastritis Acute erosive gastritis may be caused by chronic NSAID or alcohol use/misuse (increased risk of NSAID complications include prior history of a GI event (peptic ulcer, haemorrhage), age >60 years, high dosage of NSAIDs, and concurrent use of corticosteroids or anticoagulants) Erosive gastritis may also be due to reflux of bile salts into the stomach as a result of compromised pyloric function (e.g., following gastric surgery) Critically ill patients are at risk of developing stress-induced GI bleeding (RF: mechanical ventilation for >48 hours and coagulopathy)
382
What is the epidemiology of Gastritis?
Helicobacter pylori infection and use of non-steroidal anti-inflammatory drugs (NSAIDs) or alcohol are the most common causes- exact epidemiology is unknown
383
What are the presenting symptoms/signs of Gastritis?
Dyspepsia (indigestion)/epigastric discomfort Nausea and vomiting Loss of appetite Absence of malignancy features
384
What are the appropriate investigations for Gastritis?
*Helicobacter pylori urea breath test or stool antigen: positive result if H pylori present FBC: may show reduced Hb and HCT and increased MCV in autoimmune gastritis; leukocytosis in phlegmonous gastritis (caused by numerous bacterial agents) Others: -Endoscopy: for patients 60 years of age or older presenting with dyspepsia, and only on a case-by-case basis in younger patients with dyspepsia who have alarm features (weight loss, anaemia, dysphagia and persistent vomiting); may be evidence of gastric erosions and/or atrophy- rapid urease test for H.pylori/ histology -Vitamin B₁₂/parietal cell antibodies: Check in patients presenting with dyspeptic symptoms with signs and symptoms consistent with clinical deficiency (autoimmune gastritis) along with parietal cell antibodies in atrophic gastritis -Intrinsic factor antibodies: pernicious anaemia
385
What is the management of Gastritis?
Helicobacter pylori gastritis: -Triple therapy’ for 1–2 weeks -One PPI and two antibiotics (e.g. clarithromycin + amoxicillin, metronidazole + tetracycline) Erosive gastritis: -Reducing exposure to the associated agent is essential e.g. alcohol and NSAID discontinuation -Symptomatic therapy with either H₂ antagonists or a PPI Autoimmune gastritis: -Risk of, or have, an established vitamin B₁₂ malabsorption state so should be treated with intramuscular cyanocobalamin (vitamin B₁₂) Bile reflux gastritis: -Symptomatic therapy with rabeprazole or sucralfate as an initial therapy is preferred to surgical intervention Phlegmonous gastritis: -Rare but life-threatening infection of the gastric submucosa and muscularis propria seen in debilitated patients- vigorous fluid resuscitation and early empirical parenteral antibiotic therapy -In many cases subtotal/total gastrectomy is necessary
386
What are the complications of Gastritis?
Gastric malignancy (carcinoma, carcinoid, lymphoma) Vitamin B12 deficiency Peptic ulcer disease Achlorhydria (decreased/absent production of hydrochloric acid)
387
What is the prognosis of Gastritis?
Prognosis is dependent upon underlying aetiology and type of gastritis- generally good with treatment except for phlegmonous gastritis (mortality rate for surgically treated patients was 20% and medically was 50%)
388
What are Perineal abscesses and fistulae?
Perineal abscess: is a collection of pus resulting from an infection in the perineum Perineal fistula: an abnormally chronically infected tract communication between the perineal skin and the anal canal or rectum
389
What is the aetiology of Perineal abscesses and fistulae?
``` Bacterial infection Fistulae are often a complication of an abscess RF for fistulae: -IBD (especially Crohn's) -DM -Malignancy ```
390
What is the epidemiology of Perineal abscesses and fistulae?
Common
391
What are the presenting symptoms of Perineal abscesses and fistulae?
Throbbing pain in the perineum Intermittent discharge near the anal region (mucus or faecal) PMH or FH of IBD
392
What are the signs of Perineal abscesses and fistulae on physical examination?
Localised tender perineal mass Small skin lesion near the anus - opening of the fistula DRE: thickened area over the abscess or fistula may be felt Goodsall'slaw: correlate the location of the internal fistula opening based on the location of the external fistula opening -if external opening is anterior to anal canal, the fistula runs radially and directly into anal canal -If external opening lies posterior to the transverse anal line, it will follow a curved path and open internally in the posterior midline
393
What are the appropriate investigations for Perineal abscesses and fistulae?
Bloods: -FBC: leukocytosis -CRP/ESR: inflammation Blood culture: positive for causative organism Imaging: MRI (endoanal ultrasound is less useful)
394
What is the management of Perineal abscesses and fistulae?
Medical: antibiotics Surgical treatment: -Open drainage of abscess -Laying open if fistula, investigate via probe or dye LOW fistula: fistulotomy, care taken to prevent damage to anal sphincter HIGH fistula: seton- non-absorbable suture that is threaded through the fistula and allows drainage (fistulotomy would cause incontinence)
395
What are the complications of Perineal abscesses and fistulae?
Recurrence Damage to internal anal sphincter Incontinence Persisting pain
396
What is the prognosis of Perineal abscesses and fistulae?
High recurrence rate without complete excision
397
What is Peritonitis?
Inflammation of the peritoneum usually caused by infection from bacteria or fungi Left untreated, peritonitis can rapidly spread into the blood (sepsis) and to other organs, resulting in multiple organ failure and death
398
What is the aetiology of Peritonitis?
The two main types: - Primary spontaneous peritonitis, an infection that develops in the peritoneum - Secondary peritonitis, which usually develops when an injury or infection in the abdominal cavity allows infectious organisms into the peritoneum
399
What is the epidemiology of Peritonitis?
Both types of peritonitis are life-threatening The death rate from peritonitis depends on many factors, but can be as high as 40% in those who also have cirrhosis As many as 10% may die from secondary peritonitis
400
What are the risk factors for Peritonitis?
The most common risk factors for primary spontaneous peritonitis include: - Liver disease with cirrhosis: buildup of abdominal fluid (ascites) that can become infected - Kidney failure getting peritoneal dialysis Common causes of secondary peritonitis include: - A ruptured appendix, diverticulum, or stomach ulcer - Digestive diseases such as Crohn's disease and diverticulitis - Pancreatitis - Pelvic inflammatory disease - Perforations of the bowel, stomach, intestine, gallbladder, or appendix - Surgery - Trauma to the abdomen
401
What are the presenting symptoms of Peritonitis?
Abdominal pain or tenderness Rigors Fever Not passing any urine (or passing less volume than usual) Difficulty passing gas or having a bowel movement Vomiting *may have fluid in the abdominal cavity= ascites
402
What is Spontaneous bacterial peritonitis?
An infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition It is one of the most frequently encountered bacterial infections in patients with cirrhosis
403
What are the signs of Peritonitis on physical examination?
``` Abdominal pain or tenderness Signs of ascites: flank dullness, shifting dullness, fluid wave, and auscultatory percussion Signs of sepsis may be present: -Hypothermia -Hypotension -Tachycardia ```
404
What are the appropriate investigations for Peritonitis?
Bloods: -FBC: leukocytosis, anaemia (if worsens may be a GI bleed) -Creatinine: elevated hepatorenal syndrome may be present -LFTs: May be useful in determining if patient has liver disease: liver enzymes and bilirubin elevated; albumin decreased Blood cultures: growth of causative organism Peritoneal fluid analysis: - culture - pH - WCC CT scan of abdomen: demonstrates diffuse ascites; excludes pneumoperitoneum in patients with secondary peritonitis
405
What is the management for Peritonitis?
Patients who appear otherwise well with no signs of sepsis, encephalopathy, or GI bleeding may be started on oral antibiotics: quinolone or a cephalosporin such as cefixime- continue for 5 to 10 days Patients who have signs of sepsis, encephalopathy, or GI bleeding should be started on empirical broad-spectrum antibiotics active against both gram-negative and gram-positive organisms Typical choice of antibiotic would be: -cephalosporin, ciprofloxacin -or a broad-spectrum penicillin with a beta-lactamase inhibitor, such as ampicillin/sulbactam 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
406
What are the possible complications of Peritonitis?
HIGH RISK: sepsis/septic shock HIGH RISK: renal dysfunction/impairment Medium: worsening ascites Risk of paracentesis: -Bleeding e.g. intraperitoneal haemorrhage -Persistent leak at the site of the paracentesis -Bowel perforation
407
What is the prognosis of Peritonitis?
One year reoccurrence in primary spontaneous peritonitis however the mortality rate has decreased *renal dysfunction was found to be the most important independent predictor of mortality
408
What is Pilonidal sinus?
Caused by the forceful insertion of hairs into the skin of the natal cleft in the sacrococcygeal area This promotes a chronic inflammatory reaction, causing an epithelialised sinus which can be multiple and communicate via a deep cavity- if infected it can lead to an abscess
409
What is the aetiology of a Pilonidal sinus?
Caused by hair in the natal cleft (deep groove which runs between the two buttocks) and is more common in hirsute (hairy) people
410
What is the epidemiology of Pilonidal sinus?
Pilonidal sinus is common and affects men more often than women; 80% of patients are male he mean age at presentation is about 20 years (16-40), and patients are often hirsute (hairy)
411
What are the presenting symptoms/ signs of a Pilonidal sinus?
Sacrococccygeal discharge/ pain and swelling/ visible sinus tracts Acutely increased natal cleft pain and swelling Maceration of the skin: defined as the softening and breaking down of skin resulting from prolonged exposure to moisture (sinus discharge)
412
What are the appropriate investigations for Pilonidal sinus?
Clinical diagnosis
413
What is the management of a Pilonidal sinus?
Asymptomatic disease: Conservative treatment can be attempted for asymptomatic disease using either shaving or laser hair depilation, along with local hygiene Symptomatic: primary disease without abscess: -Sinus excision can be performed either under local or general anaesthesia (aims to remove all of the sinus tissue) -Post-surgical laser hair removal has been shown to decrease recurrence Symptomatic: primary disease with abscess: -Incision and drainage, followed by healing by secondary intention (left open to heal) Symptomatic: recurrent disease: surgical
414
What are the possible complications of a Pilonidal sinus?
Necrotising fasciitisL Presence of fever and toxaemia should raise suspicion for severe skin infection Pilonidal abscesses- post operative collection below the sutures
415
What is the prognosis of Pilonidal sinus?
Depending on the surgical technique chosen, recurrence rates are variable and average 6.9%- less likely to occur after healing by secondary intention
416
What is Portal Hypertension?
Increase in the pressure within the portal vein (carries blood from the bowel to the liver)
417
What is the aetiology of Portal Hypertension?
The most common cause is liver cirrhosis where the scar (fibrotic) tissue blocks the flow of blood through the liver Other causes include thromboembolic events, schistosomiasis and HIV related conditions
418
What is the epidemiology of Portal Hypertension?
Common complication of cirrhosis, can result in liver failure
419
What are the presenting symptoms and signs of Portal Hypertension?
``` Abdominal swelling- ascites Haematemesis PR bleeding or melaena Signs of encephalopathy Caput medusae (dilated superficial abdominal veins) Splenomegaly ```
420
What are the appropriate investigations for Portal Hypertension?
Clinical diagnosis based on the presence of ascites or of dilated veins (caput medusae) or varices Others: -FBC: thrombocytopaenia ± anaemia, leukopaenia -LFTs: deranged (low albumin, raised others, pronged prothrombin time) -Endoscsopy (oeshgeal varices) -Imaging- CT scan
421
What is the management of Portal Hypertension?
b-Blockers and endoscopic banding of varices if present Transjugular intrahepatic portosystemic shunt (TIPS): -A radiological procedure whereby a vascular tract is created in the liver from hepatic to portal veins allowing decompression of the portal hypertension -HOWEVER :TIPS increases risk of hepatic encephalopathy Ascites: Diuretics (spironolactone/􏰃furosemide), dietary sodium restriction (2g/day), therapeutic paracentesis (with human albumin replacement IV)- Monitor weight daily and fluid restriction in patients with plasma sodium <120mmol/L- Avoid alcohol and NSAIDs Liver transplantation is the only curative measure for cirrhosis
422
What are the complications of Portal Hypertension?
Cirrhosis and associated complications: Jaundice, encephalopathy, ascites, variceal bleeding, hepatocellular carcinoma, osteoporosis, hyperlipidaemia and malabsorption of fat-soluble vitamins
423
What is the prognosis for Portal Hypertension?
Depends on the severity and aetiology of portal hypertension | For cirrhosis: Generally poor, in the presence of ascites, 2-year survival of 􏰀50%
424
What is Primary biliary cirrhosis?
A chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis (decrease in bile flow) and, ultimately, cirrhosis Also known as Primary biliary cholangitis
425
What is the aetiology of Primary biliary cirrhosis?
PBC is conventionally thought to be an autoimmune disease There is a very high incidence of autoantibodies, most characteristically directed against mitochondrial antigens (antimitochondrial antibody)
426
What is the epidemiology of Primary biliary cirrhosis?
The prevalence of PBC is approximately 35 per 100,000 It is significantly more common in women than in men (up to a 10-fold difference) The peak age for the diagnosis of PBC is between 55-65 years, although patients can present from their 20s onwards
427
What are the presenting symptoms of Primary biliary cirrhosis?
May be an incidental finding on blood tests (e.g. elevated AlkPhos, elevated cholesterol) Insidious onset Fatigue Weight loss Pruritus Dry eyes and mouth* Sleep disturbance Postural dizziness/blackouts May present with a complication of liver decompensation (e.g. jaundice, ascites, variceal haemorrhage) Symptoms of associated conditions, e.g. Sjogren’s syndrome* (dry eyes and mouth), arthritis, Raynaud phenomenon
428
What are the signs of Primary biliary cirrhosis on physical examination?
Early: May be no signs Late: -Jaundice -Skin pigmentation -Scratch marks -Xanthomas (secondary to hypercholesterolaemia) -Hepatomegaly, ascites and other signs of liver disease may be present (RARE) signs of chronic liver disease, e.g. palmar erythema, clubbing and spider naevi
429
What are the appropriate investigations for Primary biliary cirrhosis?
LFTs: -Alkaline phosphatase: elevated- presence of cholestasis -Co-elevation of gamma-GT: presence of cholestasis -Bilirubin: elevation suggestive of impaired liver synthetic function -ALT: elevated -Serum albumin: decreased *Anti-mitochondrial antibody immunofluorescence and ELISA: positive : -antipyruvate dehydrogenase: Indicates presence of antimitochondrial antibody -Also: anti-nuclear antibody positive Abdominal ultrasound: excludes obstructive lesion within visible bile ducts MRCP: alternative to ultrasound; excludes obstructive lesion within visible bile ducts Others: -Prothrombin time: prolonged- suggestive of impaired liver synthetic function compatible with the presence of advanced liver disease -Serum immunoglobulin: Polyclonal elevation of IgM and IgG is supportive of the diagnosis of primary biliary cholangitis -Liver biopsy: only carried out when there is uncertainty: -bile duct lesions (biliary ductular cell disruption within inflamed portal tracts) and granulomata formation -later: bile duct loss (ductopenia) with progressive biliary fibrosis -Upper GI endoscopy: excludes the presence of oesophageal varices -Serum alpha fetoprotein: exclusion of hepatocellular carcinoma in patients at risk of the presence of advanced disease
430
What is Primary sclerosing cholangitis?
A chronic progressive cholestatic liver disease, characterised by inflammation and fibrosis of the intrahepatic and/or extrahepatic bile ducts, resulting in diffuse, multi-focal stricture formatio It is often associated with inflammatory bowel disease, particularly Ulcerative Colitis
431
What is the aetiology of Primary sclerosing cholangitis?
Unknown Postulated immune and genetic predisposition and toxic or infective triggers Close association with IBD, especially UC (present in around 2/3rds)
432
What is the epidemiology of Primary sclerosing cholangitis?
PSC is relatively rare and is more common in men than in women, with a male-to-female ratio of 2:1 It can occur at any age (including childhood), but typically presents during the fourth or fifth decade of life, with a mean age of 40 years at the time of diagnosis Large-duct (classic) PSC is more common
433
What are the presenting symptoms of Primary sclerosing cholangitis?
May be asymptomatic (diagnosed after persistently raised AlkPhos) RUQ pain or epigastric Intermittent pruritus and jaundice Weight loss and fatigue Episodes of fever and rigors caused by acute cholangitis are less common PMH of ulcerative colitis
434
What are the signs of Primary sclerosing cholangitis on physical examination?
May have no signs | May have have of jaundice, splenomegaly and ascites (rarely encephalopathy)
435
What are the appropriate investigations for Primary sclerosing cholangitis?
LFTs: -Alkaline phosphatase: normal or elevated (>3x upper limit of normal), presence of cholestasis -Gamma-GT: elevation, presence of cholestasis -Serum aminotransferases: mild to moderate elevation (typically <300 international units/L), indication of hepatocellular injury -Bilirubin: normal or elevated (30/40%) suggestive of impaired liver synthetic function -Serum albumin: normal or low -Prothrombin time: normal or prolonged FBC: normal or thrombocytopaenia ± anaemia, leukopaenia *no auto-antibodies specific to PSC; however, a number of serum auto-antibodies are often present in PSC patients (atypical antineutrophil cytoplasmic auto-antibody) Abdominal ultrasound: -non-invasive initial test -abnormal bile ducts (± cirrhotic liver, ascites, splenomegaly) MRCP (*preferred*): normal or multi-focal intrahepatic and/or extrahepatic strictures (often both) and dilations ± dominant biliary stricture ERCP: when MRCP is not diagnostic Others: -seum immunoglobulins: IgG normal or elevated; IgM elevated -Elevated levels of IgG4 have been associated with a multi-organ lymphoplasmocytic sclerosing disease -Hepatic/urine copper concentration: elevated (although also elevated in other liver disease e.g. Wilson's) -Ceruloplasmin: elevated (low in Wilson's) -Anti-nucelar/SM antibody: exclude autoimmune hepatitis -CT abdomen: may reveal bile duct thickening -Liver biopsy: wide ranging and non-specific -Bone mineral density scan: normal or may show hepatic osteodystrophy -Colonoscopy: normal (patients with PMH of IBD)
436
What is Rectal Prolapse?
The abnormal protrusion of the full thickness (or only the mucosal layer) of the rectum through the anus
437
What is the aetiology of Rectal Prolapse?
Triggered by: - Pregnancy - Constipation or chronic straining - Diarrhoea (15%) - Chronic cough - Neurological conditions: MS, cauda equina syndrome
438
What are the different types of Rectal Prolapse?
*Full-thickness: The full thickness of the wall of the rectum sticks out through the anus. This is the most common type of rectal prolapse. There can be a partial or complete protrusion Mucosal: Only the lining of the anus (known as the mucosa) sticks out through the anus Internal: The rectum folds in on itself but does not stick out through the anus
439
What is the epidemiology of Rectal Prolapse?
More common in adults than children, and it is particularly prevalent in women aged 50 years or older, who are six times more likely to be affected than men In older women, rectal prolapse will often occur at the same time as a prolapsed uterus or bladder because of general weakness in the pelvic floor muscles
440
What are the presenting symptoms/signs of Rectal Prolapse?
``` Patients may notice a mass protruding which is associated with defection (initially this is reducible however overtime it becomes permanent) Usually does not cause pain Faecal incontinence (75%) PR mucus or bleeding Discomfort Further constipation Symptoms of complication: -Strangulated prolapse: ischaemia of the rectum which can become gangrenous (can become ulcerated or necrotic) -Reduced anal sphincter tone ```
441
What are the appropriate investigations for a Rectal Prolapse?
Proctography: A type of X-ray that shows the rectum and anal canal during a bowel movement Colonoscopy/sigmoidoscopy Endoanal ultrasound: A thin ultrasound probe looks at the muscles used to control the bowels Others: -anal manometry: asess anal sphincter tone -pudendal nerve studies
442
What is Ulcerative Colitis?
A type of chronic relapsing and remittining flammatory bowel disease that characteristically involves the rectum and extends proximally to affect a variable length of the colon (large bowel)
443
What is the aetiology of Ulcerative Colitis?
The cause of inflammatory bowel disease (IBD) in general and of UC in particular is unclear, but it seems to occur in genetically susceptible people in response to environmental triggers (HLA-B27) Thought to be autoimmune, strong association with elevated serum pANCA (anti-neutrophil cytoplasmic autoantibodies) and primary sclerosing cholangitis
444
What is the epidemiology of Ulcerative Colitis?
In the Western world the incidence rate ranges from 1 to 24 cases per 100,000 It is slightly more common in men than in women Most patients are aged 20 -40 years at diagnosis with another peak at 60 years UC is uncommon in children <10 years of age
445
What are the presenting symptoms of Ulcerative Colitis?
Bloody or mucous diarrhoea (stool frequency related to severity of disease) Abdominal pain (crampy before passing stool) Tenesmus (recurrent inclination to evacuate the bowels) and urgency Less common: weight loss, fever Extra-articualr mainfestations e.g. ankylosing spondylitis, (psoriatic) arthritis, uveitis
446
What are the signs of Ulcerative Colitis on physical examination?
Signs of iron-deficiency anaemia, dehydration Abdominal tenderness Tachycardia Blood, mucus and tenderness on PR examination Signs of extra GI manifestations: ankylosing spondylitis, (psoriatic) arthritis, uveitis
447
What are the appropriate investigations for Ulcerative Colitis?
Stool studies: elevated feacal calprotectin and WBC present, negative culture and Clostridium difficile toxins Bloods: -FBC: may show anaemia, leukocytosis, or thrombocytosis -LFTs: hypokalaemic metabolic acidosis, elevated liver enzymes and bilirubin, low albumin (surveillance of primary sclerosing cholangitis) -ESR/CRP: elevated, persistent elevation may suggest flare-up Imaging: -Plain abdominal x-ray: estimate extent of disease, ulcerated colon usually contains no solid faeces, severe: dilated loops with air-fluid level secondary to ileus; free air is consistent with perforation; in toxic megacolon, the transverse colon is dilated to ≥6 cm in diameter -*Endoscopy: sigmoid and colonoscopy with obtained biopsies to assess the extent of inflammation- continuous distal inflammation with rectal involvement Others: -Differentiate IBD: about 70% of patients with UC have positive pANCA (Perinuclear anti-neutrophil cytoplasmic antibodies); about 70% of patients with CD have positive ASCA (anti-Saccharomyces cerevisiae antibodies) -Barium enema and radionuclide studies: assess extent of disease (used when the other is contraindicated)
448
What is the management of Ulcerative Colitis?
Distal disease (proctitis and left-sided disease, below splenic flexure) is generally amenable to topical therapies: -Acute: topical mesalazine or topical corticosteroids and oral mesalazine (5-aminosalicylic acid [5-ASA]) -Maintenance therapy: combination of topical mesalazine suppositories in proctitis or enemas in left-sided disease and oral mesalazine Extensive disease (pancolitis, beyond splenic flexure) requires systemic therapy: -Acute: oral 5-ASA is the first-line treatment option (Sulfasalazine and mesalazine), complete remission within 4 weeks is seen in 80% of patients who receive a high daily dose -Maintenance: Oral 5-ASA therapy with corticosteroid-sparing agents for refractory disease Refracatory disease: -Thiopurines (azathioprine and mercaptopurine) are recommended in corticosteroid-dependent patients and are effective agents for relapse prevention -Tumor necrosis factor (TNF)-alpha inhibitors e.g. Infliximab -Tofacitinib is an oral small molecule Janus kinase (JAK) inhibitor -Ciclosporin (immunosuppressant) can be used to induce or maintain remission but requires very careful monitoring Colectomy Any patients with severe intractable symptoms or intolerable medicine adverse effects should be considered for colectomy
449
What is the requirement of severe disease in Ulcerative Colitis?
Passage of ≥6 bloody stools daily Pulse rate of at least 90 bpm Temperature of at least 37.5°C (99.5°F) Haemoglobin level of <105 g/L (10.5 g/dL) Erythrocyte sedimentation rate of at least 30 mm/hour
450
What is the management of severe disease in Ulcerative Colitis?
Topical therapy and oral 5-ASA at maximal doses, and systemic corticosteroids Immunosuppression with azathioprine If patients do not improve after 3 days, treatment with ciclosporin or infliximab should be considered, or referral for surgery *Colectomy is indicated if the patient does not respond to, or worsens despite, aggressive medical therapy within 24 to 48 hours
451
What are the possible complications of Ulcerative Colitis?
``` From high to low risk: Inflammatory pseudopolyps Primary sclerosing cholangitis Benign stricture Colonic adenocarcinoma Massive lower GI bleed (haemorrhage) Infection Perforation Toxic megacolon ```
452
What is the prognosis of Ulcerative Colitis?
Overall mortality does not appear to be increased in patients with UC compared with the general population, however it is more in patients with associated complications The most common cause of death remains toxic megacolon Colonic adenocarcinoma develops in 3% to 5% of patients
453
What is Viral hepatitis?
An infection with the RNA viruses, hepatitis A (HAV) or hepatitis E virus (HEV), that is not associated with chronic liver disease
454
What is the aetiology of Viral hepatitis?
Both are small non-enveloped single-stranded linear RNA viruses of 􏰀7500 nucleotides, with transmission by the faecal–oral route Both viruses replicate in hepatocytes and are secreted into bile (resistant to bile lysis due to lack of a lipid envelope) Liver inflammation and hepatocyte necrosis is caused by the immune response, with targeting of infected cells by CD8+ T cells and natural killer cells Transmitted via close contact with an infected person or by contact with contaminated food or water products
455
What is the epidemiology of Viral hepatitis?
HAV is endemic in Asia, Africa and Central America, infection often occurs sub-clinically In the developed world, better sanitation means that seroprevalence is lower, age of exposure is older and hence is more likely to be symptomatic
456
What are the presenting symptoms of Viral hepatitis?
Incubation period for HAV or HEV is 3–6 weeks Prodromal period: -Malaise, anorexia (distaste for cigarettes in smokers), fever, nausea and vomiting Hepatitis: -Prodrome followed by dark urine, pale stools and jaundice lasting 􏰀3 weeks -Occasionally, itching and jaundice last several weeks in HAV infection (owing to cholestatic hepatitis)
457
What are the signs of Viral hepatitis on physical examination?
Pyrexia Jaundice Tender hepatomegaly- spleen may be palpable (20%) *Absence of stigmata of chronic liver disease, although a few spider naevi may appear, transiently
458
What are the appropriate investigations for Viral hepatitis?
Bloods: -LFTs: SIGNIFCANTLY ELEVATED AST and ALT, raised bilirubin, raised AlkPhos) -Elevated ESR -In severe cases, reduced albumin and elevated platelets Viral serology: -Hepatitis A: Anti-HAV IgM (during acute illness, disappearing after 3–5 months) -Anti-HAV IgG (recovery phase and lifelong persistence) -Hepatitis E: Anti-HEV IgM (" 1–4 weeks after onset of illness) -Anti-HEV IgG. Hepatitis B and C viral serology is also necessary to rule out these infections Urinalysis: Positive for bilirubin, raised urobilinogen
459
What is the management for Viral hepatitis?
No specific management but there is post prophylactic exposure: -Active or passive immunisation is available for protection following exposure to hepatitis A virus Bed rest and symptomatic treatment (e.g. antipyretics, antiemetics) Colestyramine for severe pruritus
460
What are the prevention measures for Viral hepatitis?
Public health: -Safe water -Sanitation -Food hygiene standards *Both are notifiable diseases -Personal hygiene and sensible dietary precautions when travelling Immunization (HAV only): -Passive immunization with IM human immunoglobulin is only effective for a short period -Active immunization with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas, high-risk individuals (e.g. residents of institutions)
461
What are the complications of Viral hepatitis?
Fulminant hepatic failure develops in 0.1% cases of HAV, 1 or 2% of HEV but up to 20% in pregnant women Cholestatic hepatitis with prolonged jaundice and pruritus may develop after HAV infection Post-hepatitis syndrome: Continued malaise for weeks to months
462
What is the prognosis of Viral hepatitis?
Recovery is usual within 3–6 weeks Occasionally, a relapse during recovery There are no chronic sequelae *Fulminant hepatic failure carries an 80% mortality (greater risk in pregnant women)
463
What is Vitamin B12 deficiency?
A common condition that can manifest with neurological, psychiatric, and haematological disorders
464
What is the aetiology of Vitamin B12 deficiency?
Vitamin B12 is an essential vitamin obtained only from diet or by supplementation Dietary sources include animal and dairy products such as meat, poultry, milk, and eggs Stores of vitamin B12 in the liver remain in the body for years, so vitamin B12 deficiency depends on chronic, long-term deficiency Anything that decreases the intake or the absorption of vitamin B12 places people at risk of vitamin B12 deficiency. In general: -Decreased dietary intake -Diminished gastric breakdown of vitamin B12 from food -Malabsorption from the gastrointestinal tract
465
What is the epidemiology of Vitamin B12 deficiency?
Prevalence increases with advancing age May be more prevalent in vegans and strict vegetarians who don't get enough dietary supplementation
466
What are the presenting symptoms of Vitamin B12 deficiency?
Symptoms of anaemia: dyspnoea, fatigue *Paraesthesias: tingling, early and subtle symptom of neurological damage Ataxia- uncommon
467
What are the signs of Vitamin B12 deficiency on physical examination?
Decreased vibration sense | Neurological findings
468
What are the appropriate investigations for Vitamin B12 deficiency?
Bloods: -Serum Vitamin B12: <148 picomols/L (<200 picograms/mL) indicates probable vitamin B12 deficiency -FBC: elevated MCV, low haematocrit, low Hb -Reticulocyte count: Low reticulocyte index indicates decreased production, unlike in haemolytic anaemia, in which reticulocyte index would be increased Blood film: megalocytes, hypersegmented polymorphonucleated cells- causing megaloblastic anaemia
469
What is Folate deficiency?
Classically presents as megaloblastic anaemia, with absence of neurological signs
470
What is the aetiology of Folate deficiency?
Folate is present in dietary sources such as green leafy vegetables, legumes, and fruits. In addition, it is present in synthetic form, as folic acid, in fortified cereal-grain products Can be due to decreased intake or intestinal malabsorption of folate (such as coeliac disease) Increased demand in pregnancy, lactation, and prematurity can lead to folate deficiency Increased loss of folate occurs in patients undergoing chronic dialysis, and decreased folate is seen in disorders of increased cell turnover, such as chronic haemolytic disease
471
What is the epidemiology of Folate deficiency?
``` The primary age groups affected: -Pre-school children -Pregnant women -Older people Thought to be a low prevalence in high income countries and high in low income countries ```
472
What are the presenting symptoms of Folate deficiency?
``` Symptoms of anaemia: dyspnoea, fatigue Prolonged diarrhoea Headache Loss of appetite Weight loss ```
473
What are the signs of Folate deficiency on physical examination?
Pallor | Other signs of anaemia
474
What are the appropriate investigations for Folate deficiency?
Bloods: -FBC: low Hb, elevated MCV and MCH -Reticulocytes: low corrected reticulocyte count (decreased production) -Serum folate: low -Red blood cell folate: Low-better indicator of tissue folate status than serum folate -Serum Vitamin B12: IMPORTANT TO EXCLUDE (can co-exist) Blood film: Macrocytic anaemia, macrocytosis, anisocytosis, poikilocytosis, hypersegmented neutrophils
475
What can Vitamin A deficiency cause?
Xerophthalmia is a progressive eye disease where there is abnormal dryness of the conjunctiva and cornea of the eye, with inflammation and ridge formation
476
What are the aetiology and epidemiology of Vitamin A deficiency?
Vitamin A is required for the formation of rhodopsin, a photoreceptor pigment in the retina Deficiency can be due to inadequate intake, fat malabsorption or liver disorders (liver stores vit A) In xerophthalmia, there is dryness of the conjunctiva and cornea due to keratinisation of the eyes- conjunctivae develop oval/triangular spots (Bitots spots), and cornea becomes cloudy and soft Rare in UK but common in southern and eastern Asia where rice is the staple food
477
What are the presenting symptoms and signs of Vitamin A deficiency?
Initially presents with with night blindness (may cause injuries) As diseases progresses, cornea becomes hazy and can develop erosions which can lead to its destruction- complete blindness (dry conjunctiva): -Bitots spots on conjunctiva -Corneal xerosis – cornea appears dry and dull -Corneal ulcerations -Keratomalacia – last stage of xerophthalmia - softening of cornea, followed by perforation of eyeball and blindness Can also get drying, scaling and follicular thickening of the skin due to keratinisation of skin (dry skin and hair) More prone to infection: respiratory infections due to keratinisation of mucous membranes in respiratory tract
478
What are the appropriate investigations for Vitamin A deficiency?
Check sight in darkness Serum retinol binding protein Zinc levels – zinc deficiency can interfere with production of retinol-binding protein Iron studies – can affect metabolism of vitamin A FBC: for anaemia or infection
479
What is Vitamin B1 deficiency?
Known as thiamin deficiency, severe and chronic form is known as beriberi Can lead to Wernicke's encephalopathy
480
What are the aetiology and epidemiology of Vitamin B1 deficiency?
There are two main types: 1. Dry Beriberi: Thiamine deficiency with nervous system involvement -Usually occurs with poor caloric intake and physical inactivity -Involves peripheral neuropathy -Wernicke encephalopathy and Korsakoff syndrome are forms of dry beriberi 2. Wet Beriberi: Thiamine deficiency with cardiovascular involvement -First, peripheral vasodilation occurs causing high CO -This leads to salt and water retention via RAAS -As vasodilation progresses, kidneys detect relative loss of volume and therefore conserve salt -Salt retention causes fluid absorption into vessels, hence oedema- the high cardiac workload results in heart failure with general oedema Common in alcoholics and in developing countries due to malnutrition
481
What are the risk factors for Vitamin B1 deficiency?
Diets consisting of high levels of milled rice and raw freshwater fish High consumption of tea, coffee and betel nuts Alcoholic state Starvation state Prolonged vomiting Gastric bypass surgery – due to limited caloric intake post surgery Parental nutrition without adequate thiamine supplementation
482
What are the presenting symptoms and signs of Vitamin B1 deficiency?
Dry: numbness of peripheries, confusion, trouble moving legs, pain Wet: palpitations, SOB, leg swelling (oedema) Tachycardia Ankle oedema Peripheral neuropathy
483
What are the appropriate investigations for Vitamin B1 deficiency?
Clinical diagnosis Rare tests: thiamine loading test is the best indicator of thiamine deficiency, red cell transketolase activity is decreased
484
What can Vitamin C deficiency lead to?
Scurvy (severe deficiency)
485
What are the aetiology and epidemiology of Vitamin C deficiency?
Vitamin C is important for wound healing and immune function and iron absorption Usually due to inadequate diet or increased demand such as in pregnancy
486
What are the presenting symptoms and signs of Vitamin C deficiency?
``` Fatigue Depression Rash Internal bleeding, Petechiae Gingivitis, loose teeth, foul breath Impaired wound healing Bleeding from gums, nose, hair follciles or into joints In children, bone growth may be impaired Anorexia, cachexia Muscle pain and weakness Oedema ```
487
What are the appropriate investigations for Vitamin C deficiency?
Clinical diagnosis No test is completely satisfactory WBC ascorbic acid is low
488
What can Vitamin D deficiency cause and what is the aetiology of it?
Vitamin D deficiency is the primary cause of osteomalacia (metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix) in the Western world, resulting from inadequate endogenous production of vitamin D3 in the skin, caused by: -Lack of sunlight exposure -Dietary deficiency -Malabsorption (small bowel disease e.g. coeliac disease/inflammatory bowel disease) Other causes of Vitamin D deficiency include: -Chronic kidney disease -Hypoparathyroidism
489
What is the epidemiology of Vitamin D deficiency?
Common, more so in women
490
What are the presenting symptoms and signs of Vitamin D deficiency?
Osteomalacia (adults): -Malaise -Bone tenderness (mainly in the axial skeleton) -Proximal muscle weakness -Waddling gait -Signs of hypocalcaemia: =Trousseau's sign - inflation of a blood pressure cuff to above the systolic pressure for > 3 mins causes tetanic spasm of the wrist and fingers =Chvostek's sign - tapping over the facial nerve causes twitching of the ipsilateral facial muscles Rickets (children): - Bossing of frontal and parietal bones - Swelling of costochondral junctions (rickety rosary) - Bow legs in early childhood - 'Knock knees' in later childhood - Short stature - Hypotonia - Growth retardation - Skeletal deformities
491
What are the appropriate investigations for Vitamin D deficiency?
Bloods: -Low or normal Ca2+ -Low phosphate -High ALP -Low 25-hydroxy vitamin D -High PTH (secondary hyperparathyroidism) -Check U&Es -Check ABGs (for renal tubular acidosis) -Increased phosphate excreting (in renal phosphate wasting) Radiographs: -May appear normal -May show osteopaenia (T-1) -Looser's zones = wide, transverse lucencies traversing part way through a bone, usually at right angles to the involved cortex and are associated most frequently with osteomalacia and rickets (AKA pseudofractures) Bone biopsy after double tetracycline labelling: -Tetracycline is deposited at the mineralisation front as a band -After two course of tetracycline (separated by a few days), the distance between the bands of deposited tetracycline is reduced in osteomalacia -Not usually necessary (invasive nature)
492
What are the aetiology and epidemiology of Vitamin E deficiency?
Can be caused by cystic fibrosis affecting absorption, abetalipoproteinaemia, chronic cholestatic hepatobiliary disease, short bowel syndrome Causes haemolysis and neurological deficit Very rare
493
What are the presenting symptoms and signs of Vitamin E deficiency?
``` Weakness Loss of vibration sense Decline in visual field Hyporeflexia Decreaed proprioception Distal muscle weakness Loss of vibration sense Ataxia Dysarthria Retinopathy Compromise immune system ```
494
What are the aetiology and epidemiology of Vitamin E deficiency?
Vitamin K is important for coagulopathy so main symptom is excessive bleeding Risk Factors: -Anticoagulants -Lack of vitamin K in diet -Antibiotics which interfere with vitamin K absorption -Fat malabsorption e.g. in coeliac disease, CF -Infants at risk of breast milk low in vitamin K Rare in adults, more common in infants
495
What are the presenting symptoms and signs of Vitamin K deficiency?
Easily bruising Dark black, tar like stool Nose bleeds (epistaxis- haemorrhage)
496
What are the appropriate investigations for Vitamin K deficiency?
Clinical diagnosis | Prothrombin time: prolonged due to lack of coagulation factor synthesis
497
What is the management of Vitamin deficiency (A, B, C, D, E, K)?
``` Vitamin A: -Treat with vitamin A supplements -Re-educate and monitor diet -High vit A: chicken, eggs, leafy green veg Vitamin B1: -Thiamine (Pabrinex) IV -Oral supplementation to continue after IV -If there is coexisting hypoglycaemia, ensure thiamine given before glucose Vitamin C: -Dietary education -Ascorbic acid >250mg/24h oral Vitamin D: -Vitamin D and calcium replacement -Monitor 24 hr urinary calcium Also monitor: Serum calcium, Phosphate, ALP, PTH, Vitamin D levels -Treat the underlying cause Vitamin E: supplements Vitamin K: Vitamin K supplement ```
498
What are the possible complications of Vitamin deficiency (A, B, C, D, E, K)?
Vitamin A: Blindness and respiratory infections Vitamin B: Wernicke's encephalopathy and Korsakoff's psychosis Vitamin C: Scurvy; easy bruising, easy bleeding and joint and muscle pains Vitamin D: -Bone deformities -Depression -Hypocalcaemia symptoms = CATs go NUMB *Convulsions *Arrhythmias *Tetany *NUMBness/paraesthesia Vitamin K: Excessive bleeding and anaemia
499
What is the prognosis of Vitamin deficiency (A, B, C, D, E, K)?
Generally good if treated early Korsakoff psychosis is chronic Bone deformities in children are permanent
500
What is a Volvulus?
When a loop of intestine twists around itself and the mesentery that supports it, resulting in bowel obstruction Most volvuli occur at the sigmoid colon and are a common cause of large bowel obstruction
501
What are the risk factors for a Volvulus?
``` Increasing age Neuropsychiatric disorders Resident in a nursing home Chronic constipation or laxative use Male gender Previous abdominal operations ```
502
What are the presenting symptoms and signs of a Volvulus?
Present with the clinical features of bowel obstruction Rapid onset Colicky pain, abdominal distension, and absolute constipation Abdomen is often very tympanic to percussion Absent or tinkling bowel sounds (intestinal obstruction) Fever Tachycardia Signs of dehydration If there is suspicion of ischaemia or perforation (peritonitis)- surgical emergency
503
What are the appropriate investigations for a Volvulus?
AXR: bowel obstruction- classic ‘coffee bean sign’, as seen in sigmoid volvulus Erect CXR - if perforation is suspected Water-soluble contrast enema: shows site of obstruction CT Scan
504
What is Wilson's disease?
An autosomal-recessive disease of copper accumulation and copper toxicity caused by mutations in the ATP7B gene, which is part of the biliary excretion of copper pathway
505
What is the aetiology of Wilson's disease?
Autosomal-recessive disease caused by mutations in the ATP7B gene Copper accumulation leads to higher than normal levels of free copper resulting in cell injury, inflammation, and cell death In Wilson's disease: excess copper is initially stored in the liver, where inflammation and cell injury results in hepatitis- with continued exposure to high levels of copper, fibrosis (cirrhosis) occurs *Clinically this progresses to end-stage liver disease and hepatic failure The basal ganglia and areas of the brain that coordinate movement are most sensitive to copper accumulation
506
What is the epidemiology of Wilson's disease?
The worldwide incidence of Wilson's disease is in the order of 30 cases per million Clinical disease usually appears from about the age of 10 to 40 years
507
What are the presenting symptoms and signs of Wilson's disease?
``` Neurological: -Dyskinesia -Dysdiadochokinesia -Rigidity -Tremor -Dystonia -Dysarthria -Dysphagia -Drooling -Dementia -Ataxia Hepatic: May present with: hepatitis, liver failure, cirrhosis Symptoms: -RUQ tenderness -Jaundice -Easy bruising -Variceal bleeding -Encephalopathy Behavioural abnormalities (psychiatric): Can vary from loss of control of emotions to depression, delusions, loss of memory, inability to focus on tasks, impulsiveness, sexual disinhibition *Eyes: Kayser-Fleischer Rings – visible to naked eye in late stages, early stages seen by slit lamp Sunflower cataract (copper accumulation in the lens, seen with a slit lamp) ```
508
What are the appropriate investigations for Wilson's disease?
1st: LFTs: always abnormal in hepatic presentation 24h urine copper: >100 micrograms FBC: low platetelet count and low WBC count, caused by portal hypertension and splenic sequestration *Slit lamp examination: Kayser-Fleischer (KF) rings (99%) Blood Ceruloplasmin: low <180 mg/L Liver biopsy: liver copper (>200 micrograms/g for neurological/psychiatric presentation), >250 micrograms/g indicates liver disease MRI head: Only useful in neurological presentation; involvement of basal ganglia Blood free copper: elevated at least 6-fold DNA testing: ATP7B mutation found on both genes (one indicates carrier)- haplotype testing in siblings