1
Q
Define:
- Diverticulosis
- Diverticulitis
- Diverticular disease
A
- Diverticulosis (usually no symptoms although may be bleeding): the presence of diverticula (pouches that form in a hallow structure in the body, colonic diverticula = pouch formation in large intestine)
- Diveticulitis: the inflammation of diverticula
- Diverticular disease: symptomatic diverticula
2
Q
Outline the theories on the aetiology of diverticulosis of the colon
A
- There is thickening of the muscle layer and because of high intraluminal pressures, pouches of mucosa extrude through the muscular wall through weakened areas near blood vessels to form diverticula
- Cholinergic denervation with increasing age will lead to hypersensitivity and increased uncoordinated muscular contraction, which may lead to pouch formation
- It may be related to low-fibre diet, which induces a muscular hypertrophy, and an increase in intraluminal pressure
- Diverticulitis occurs when faeces obstruct the neck of the diverticulum causing stagnation and allowing bacteria to multiply
- This can then lead to perforation, abscess formation, fistulae or generalized peritonitis.
3
Q
Describe the morphology and pathological consequences of diverticulosis of the colon
A
- 95% of diverticulae are asymptomatic
- Diverticulosis takes the form of outpouchings of mucosa, which are weak. They have a peritoneal surrounding.
- Impaction of faecolith (faecal matter) within the diverticulum, similar to in appendicitis, will cause irritation, and may eventually lead to rupture
- Inflammation and ulceration may result in abscess formation, fistulae and haemorrhage
- Repeated attacks of diverticulitis trigger fibro-muscular thickening, and stenosis
- All inflammatory pathologies may stimulate carcinoma.
4
Q
Where does diverticula most commonly occur? Why?
A
The sigmoid colon with 95% of complications arising at this site. This is because it is the narrowest point and therefore has highest pressure
5
Q
What are the clinical features of diverticular disease?
A
- Left sided colic, relieved by defecation
- Altered bowel habit (including blood and mucus passage)
- Nausea
- Flatulence
- Severe pain and constipation if severe (causing luminal narrowing)
6
Q
Describe the clinical features of diverticulosis of the colon
A
Diverticulosis
- asymptomatic in 95% of cases and found incidentally on barium enema.
- If symptomatic they exactly mimic carcinoma colon (diverticular disease).
7
Q
Describe the signs and symptoms of diverticulitis
A
Infection occurs due to stagnation of the contents of the diverticula
Symptoms:
- Severe left sided colic
- Constipation (or overflow diarrhoea)
- Symptoms mimicking appendicitis but on the left
Signs:
- Fever & tachycardia
- Tenderness, guarding & rigidity on the left hand side
- Can be palpable mass in the LIF
- Raised WCC and inflammatory markers
8
Q
Outline the complications of diverticulosis
A
Diverticula may complicate to perforation (in association with acute diverticulosis), fistula formation (into bladder or vagina), intestinal obstruction, and bleeding with mucosal inflammation.
9
Q
Primary differential diagnosis for left iliac fossa pain?
A
diverticulitis as not many other causes of LIF pain
10
Q
What are the risk factors and protective factors for carcinoma of the large bowel.
A
Risk factors:
- Family history
- age
- western diet (low in fibre, high in fats)
- ulcerative colitis
- smoking
Protective factors:
- Fruit & vegetables
- exercise
- hormone replacement therapy
- aspirin/NSAIDs
11
Q
Carcinoma of the large bowel. Go into more depth about the genetic factors? What genes ect.?
A
Genetic aetiology:
- Familial adenomatous polyposis (FAP) is responsible for <1% of cancers, and occurs due to tumour suppressor gene APC mutations
- Hereditary non-polyposis colorectal cancer (HNPCC) is responsible for <5% of all cancers, and arises from germline mutations in mismatch repair genes
- Most cancer are sporadic however, occurring without family history
12
Q
Describe the morphology/natural history of carcinomas of the large bowel
A
- Adenocarcinoma, with characteristic ‘singlet ring cells’ on histology.
- The vast majority of colorectal cancers occur in the recto-sigmoid region
- Caecum & Ascending colon: 15%
- Transverse colon: 10%
- Descending colon: 5%
- Sigmoid colon: 25%
- Rectum: 45%
- They usually appear as a polypoid mass with ulceration, spreading initially by direct inflitration through the bowel wall.
- It then involves the lymphatics and blood vessels, metastasising primarily to the liver. Transcoelomic spread can also occur
13
Q
What are the main two types of carcinomas of the large bowel?
A
Many carcinomas develop sporadically, and originate from benign adenomas (polyps). Tubular adenomas (90%) start off as smaller swellings but develop into pedunculated structures, with hyperchromatic dysplastic glands. Villous adenomas (1%) most commonly occur in the rectum. They form a smaller mass which may be quite large and have a delicate frond-like structure, with a broad base and no pedicle. The fronds are formed of dysplastic epithelium.
14
Q
What are the common symptoms/signs suggestive of carcinoma of the colon, rectum and anus?
A
Any colorectal tumour may present with an abdominal mass, abdominal pain, haemorrhage, perforation or fistula
- Right sided (proximal) tumours are more often asymptomatic, and may present with iron deficency anaemia/weight loss
- Left-sided tumours more commonly present with PR (rectal) blood/mucus, altered bowel habit, tenesmus (crampling rectal pain), obstruction and a mass on PR examination
- Anal tumours may be present with bleeding, pain, changes in bowel habit, pruritis ani, masses or a stricture
15
Q
What is the staging system used for colorectal cancers?
A
Duke’s Staging:
- Duke’s A: Tumours invade submucosa +/- muscularis propria
- Duke’s B: Tumours invade past the muscularis propria (into subserosa/directly into other organs, but no nodal involvement)
- Duke’s C: Regional lymph node involvement
- Duke’s D: Distant metastases
16
Q
What are haemorrhoids?
A
They are vascular structures in the anal canal. In their normal state, they are cushions that help with stool control.
They become a disease when swollen or inflamed; the unqualified term “hemorrhoid” is often used to refer to the disease
17
Q
Describe the pathology of haemorrhoids?
Where are they? (anatomy)
A
- The anal cusions are highly vascular areas, formed of smooth muscle with subepithelial anastomoses of the rectal arteries/veins
- The anal cushions contribute to continence along with the anal sphincter, and are at 3, 7 and 11 o’clock when viewed from the lithotomy position
- Haemorrhoids (piles) are prolapses of these cushions, containing the normally dilated rectal venous plexus covered by rectal muscosa
- They are though to arise due to a breakdown of the smooth muscle layer, the muscularis mucosae
18
Q
Where is the anal canal?
Where are the anal sphincters?
How do they work?
What are their roles?
A
- The anal canal runs from the superior aspect of the pelvic diaphragm to the anus, and is normally collapsed
- The internal sphincter is an involuntary sphichter surrounding the upper 2/3rd of the anal canal
- Tonic contraction is stimulated by sympathetic fibres from the superior rectal/hypogastric plexus
- Parasympathetic fibres inhibit this tonic contraction, thus requiring contraction of puborectalis/the external anal sphincter to maintain continence
- The external anal sphincter surrounds the lower 2/3rd of the anal canal, and is under voluntary control, mediated by the inferior rectal nerve (S4)
- Aside from sphincter function, they provide important sensory information, allowing differentiation between solid, liquid and gas
19
Q
How can you differentiate between internal and external haemorrhoids?
A
Internal haemorrhoids
- originate from above the dentate (pectinate) line, therefore are covered with columnar epithelium (endoderm), and are not painful.
- They drain via the superior rectal vein into the portal venous system.
- The cushions make up internal haemorrhoids.
External haemorrhoids
- originate from below the dentate line, therefore are lined with epithelium (ectoderm) and innervated by cutaneous branches of the pudendal nerve – and become painful
- They drain via the middle and inferior rectal veins into the systemic circulation
- External haemorrhoids may cause problems around the entire circumference of the anus.
20
Q
What are the symptoms of haemorrhoids?
A
- Rectal bleeding (bright red on the paper)
- Prolapse
- Mucous discharge
- Pruritis ani
- Pain if the piles become thrombosed
21
Q
What are complications of haemorrhoids?
A
- Anaemia
- If severe/continued bleeding
- Thrombosis
- If prola[sing piles are gripped by the anal sphicter (‘stangulated piles’) then venous return is occluded, leading to thrombosis
- The haemorrhoids swell, become purple and tense, causing significant pain/distress
- the thrombosed piles often fibrose within 2-3 weeks, giving spontaneous cure
22
Q
What examinations would you do for a patient with haemorrhoids?
Why? What might you find?
A
- Abdominal examination
- Palpable masses, enlarged liver
- Rectal examination
- Prolapsing haemorrhoids are obvious
- Inspection of the perineum may show large external haemorrhoids at 3, 7 and 11 (left lateral, right posterior, right anterior) and will disclude other DDxs, but anal cancer may look similar
- Proctoscopy/rigid sigmoidoscopy
- Can visualize teh haemorrhoids/piles and assess for a lesion higher in the rectum
- Colonoscopy/Flexi-sigmoidoscopy
- If symptoms suggest a more sinister pathology
23
Q
What are the differential diagnosis for rectal bleeding?
(not an objective but useful to know)
A
- Haemorrhoids (most common cause)
- Anal fissure (exquiste tenderness, skin tag)
- Diverticulitis (bloody ‘splash’ in the pan, LIF symptoms)
- Rectal cancer (tenesmus [cramping rectal pain/need to have a bowel movement], PR bleeding with defecation)
- Colon cancer (red blood mixed with the stool, change in bowel habit)
- Ulcerative colitis (abdominal pain, urgency to defecate)
- Crohn’s disease (weight loss, chronic diarrhoea)
- Massive upper GI bleed (usually melena, but frank blood if very large, usually haematemesis also)
- Trauma
- ischaemic/infective colitis
- Angiodysplasia
24
Q
What are the symptoms of patients with perianal infections?
A
Patients may experience:
- pain, swelling (95%)
- fever (18%)
- discharge (12%)
- a mass (abscess)
25
What are the different types of perianal infections?
* Anorectal abscesses - caused by gut organaisms, 45% are perianal, 30% ischiorectal, 20% intersphincteric and 5% supralevator
* Pilonidal sinus - obstruction of natal cleft hair follicles around 6cm above the anus, with ingrowing of hair leading to a foreign body reaction
* Perianal warts
26
Describe the physical examination of patients with perianal infections
* Diagnosis is usually straightforward, however sepsis higher up the anal canal may require examination under anaesthetic or imaging
* Any discharging area near the anus should be assumed to communicate with the anorectum until proven otherwise
* Operative exploration is often the first diagnostic test, although MRI can be used
27
Define fissure in ano
* An anal fissure is a tear in the sensitive anal canal distal to the dentate line, producing pain on defecation, most commonly in males
* Most are due to hard faeces
28
Describe the symptoms and signs of patients with fissure-in-ano
**Symptoms:**
* ****Pain, worse on defecation, lasting for hours afterwards
* Associated constipation
* Pruritis ani (irritation of anal skin - itching)
* Bleeding on defecation
**Signs (O/E):**
* Midline longitudinal tear in the rectal muscosa
* 'Sentinal pile' (skin tag outside edge of anus) or muscosal tag at the external aspect
* PR may not be possible due to pain and sphicter spasm
29
List the common causes of acute hepatits
* Viral infection (Hepatitis A-E/Non A-E infections)
* Hep A may cause infection in childhood, though 80% of those infections are asymptomatic
* Hep D & E are rare in UK
* Hep B and C infection is usually astmptomatic except in IV drug users, in whom 30% develop jaundice
* Autoimmune
* Drug reactions
* Alcohol
30
What are risk factors for acute hepatitis?
* Use of needles
* Risky sexual behaviour
* Poor hygeine
* Blood transfusion
* Travel
31
Describe the types of liver damage that may be caused by drug therapy
* Intrinsic hepatotoxins cause type A reactions
* Augmented pharmacologic effects - Dose dependant & predictable
* Extrinsic hepatoxins cause idiosyncratic type B reactions
* Unpredictable
* Appear not to be concentration dependent
32
Describe the common causes of chronic hepatitis
* Hepatitis B +/- Hepatitis D virus - most common
* Hep B: Hepa-DNA virus, transmitted in the blood, semen and saliva via skin breaks or mucous membranes
* Hep D: can only cause infection in presence of Hep B as it is an incomplete RNA virus so needs Hep B for its own assembly
* Hepatitis C virus - most common
* RNA flavivirus, transmitted via bodily fluids, and is particuarly common in IV drug users
* Autoimmune hepatitis
* It is a cell-mediated auto-immunity and may be triggered by infection
* Alcohol
* Hyperlipidaemia (Non-acholic fatty liver disease - NAFLD)
* Drugs (methyldopa/nitrofuranroin)
* Metabolic disorders (Wilson's disease, alpha-1-antitrypsin deficiency, haemochromatosis)
## Footnote
**NOT HEPATITIS A & E!! (ONLY ACUTE)**
33
Describe the morphology and pathological consequences of acute hepatitis
* Patholigical changes are the same regardless of the cause
* Hepatocytes undergo degenerative changes (swelling & vaculoation) before necrosis and rapid removal
* Necrosis is usually maximal in zone 3, as this is centrilobular and thus receives the least oxygenated blood
* Extent can vary from scattered necrosis to multiacinal necrosis leading to fulminant hepatic failure
34
Describe the morphology and pathological consequences of chronic hepatitis
* Defined as any hepatitis lasting more than 6 months, and is the principle cause of chronic liver disease, cirrhosis and hepatocellular carcinoma
* Chronic inflammatory cell infiltrates are present in the portal tracts
* They may also be loss of definition of the portal/periportal limiting plate, confluent necrosis and fibrosis
* This eventually leads to cirrhosis
* The overall severity is judged by the degree of inflammation (grading), and the extent of fibrosis/cirrhosis (staging), using various scoring systems such as the Child Pugh score
35
Discuss the diagnosis of a patient with jaundice including relevant history, blood tests and radiological investigations
**Full history**
* Risk factors for viral hepatitis
* Acholol intake
* Nutrional status
* Establish extra-jaundice features
**Blood tests**
* FBC
* Reticulocytes
* LFTs
* U&Es
* bilirubin levels
* Albumin and clotting
* Toxins (paracetamol)
* Viral load
* Immunogloblin - paraproteinaemia (identify what virus)
**Urinalysis**
* Urobilinogen in urine --\> gives dark urine
**Imaging**
* An ultrasound of the liver may exclude alternative diagnoses.
* MRCP and ERCP may display abnormalities of the biliary system.
Biopsy is able to histologically confirm diagnoses of intra-hepatic pathology.
36
How will LFTs, virology, immunology and radiology help for a patient with jaundice?
Help find if the jaundice is: Pre-hepatic, Hepatic, Post-hepatic…
* LFTs – will show a hepatodestructive or obstructive pattern
* Virology – will guide to diagnosis of viral cause
* Immunology – will guide to diagnosis of autoimmune cause
* Radiology – USS and MRCP may exclude pancreaticobiliary cause.
37
What are the common primary sites for metastatic tumour to the liver?
* 90% of liver tumours are secondary metastases
* The primary sites are commonly the:
* **Lung**
* **Stomach**
* **Colon**
* **Breast**
* **Uterus**
38
List risk factors/causes for the development of primary hepatocellular carcinoma
Hepatocellular carcinoma is the most common malignant tumour worldwide - Common in China/sub-saharan africa although rare in west
* Causes:
* Chronic hepatitis
* Cirrhosis
* Metabolic liver diseases
* Aspergillus alfatoxin
* Parasites
* Anabolic steroids
* Greater risk in males
39
# Define cirrhosis
Give its key characteristics
Cirrhosis of the liver is an irreversible consequence of chronic hepatic injury, and has 3 key characteristics:
1. Destruction of liver cells
2. Associated chronic inflammation, stimulating fibrosis
3. Regeneration of hepatocytes to form nodules
40
Describe the pathology of cirrhosis of the liver
(What happens to cells in the liver?)
* Fibrosis is due to growth factors released from inflammatory cells, Kupffer cells and hepatocytes
* The inflammatory cells may be due to the disease process itself (hepatitis), or recruited in response to liver cell necrosis (chronic alcoholism)
* Stellate cels are activated to form myofibroblasts and secrete collagen, and nodules form due to the natural capacity of heptocytes to divide and regenerate in response to damage, but these nodules lack normal vascular and bile drainage connections
* Micronodular cirrhosis (nodules \<3mm) occurs as a result of alcoholic liver damage or biliary tract disease
* Macronodular cirrhosis (nodules \>3mm) occurs due to previous hepatitis
* Biliary cirrhosis is less common (fibrosis centred around intrahepatic bile ducts), and can be primary biliary cirrhosis or secondary (primary sclerosing cholangitis)
41
What are the common causes of cirrhosis of the liver?
* Alcholic liver disease
* Cryptogenic liver disease (no cause found on investigation)
* Non-alcoholic fatty liver disease (NAFLD)
* Chronic viral hepatitis
42
What initial investigations would you do for a patient with suspected cirrhosis?
**History & abdominal examination**
**Bloods** to determine severity of disease:
* Liver function: albumin & INR are the best indicators
* Liver damage: LFTs (ALT & AST enzymes)
* Complications: U&Es/ABG (hepatorenal/hepatopulmonary syndrome)
**Liver screen** to determine type of disease:
* Viral serology, serum antibodies/Immunogloblins, AFP, iron studies, serum copper, aplha1-antitrypsin level
**Imaging** to determine type of disease:
* Ultrasound & duplex:
* Liver can be shrunken or enlarged
* Splenomegaly may be present
* Portal system flow may be reversed
* Can also show focal lesions or portal vein thrombosis
* Endoscopy:
* Detection and treatment of suspected varices, should be undertaken in anyone with suspected cirrhosis
* CT/MRI if indicated
Further investigations: Ascitic tap (for MCS if infection suspected), Liver biopsy (to confirm severity and type of liver disease)
43
Describe the classic history of chronic liver disease?
* Fatigue
* Weight loss/anorexia
* Due to early satiety with hepatomegaly
* Patient often may notice central 'weight gain' of ascites
* Jaundice
* Leg swelling
* Due to: Increased intra-abdominal pressure & low oncotic pressure
* Bleeding/bruising
* Due to decreased synthetic function
* Itching
* Due to bile salt accumulation in peripheral nerves
44
What are signs of chronic liver disease seen on abdominal examination?
* Nails:
* Leuconychia due to low albumin
* Clubbing
* Hands:
* Palmar erythema
* Duyputren's contracture
* Liver flap
* Skin
* Pigmentation
* Spider naevi
* Striae
* Feminization - due to hyperaldosteronism
* Gynaecomastia
* Testicular atrophy
* Loss of body hair
* Signs of portal hypertension
* Caput medusae
* Heprosplenomegaly
* Ascites
* Signs of hepatocellular failure
* Bruising
* Prolonged clotting
45
Why to the underlying clinical features of cirrhosis such as hypoproteinanaemia, abnormal clotting, secondary hyperaldosteronism and portal hypertension occur?
**Hypoproteinanaemia:**
* Damage to hepatocytes results in reduced albumin synthesis (the major protein in blood)
**Abnormal clotting:**
* The liver is responsible for production of vitamin K dependent clotting factors (also factor 5)
**Secondary hyperaldosteronism**
* The liver is responsible for metabolism (degradation) of steroids, importantly aldosterone and oestrogen, which accumulate in chronic liver disease
* Also due to activation of the RAAS because hypoalbuminaemia leads to a lower circulating volume
**Portal hypertension**
* Damage to liver architecture results in disturbed blood flow through the liver, and portal hypertension
46
What are the complications of chronic liver disease?
* Hepatocellular failure
* Portal hypertension
* Malignant change
* Renal Failure (hepatorenal syndrome)
* Respiratory failure (hepatopulmonary syndrome)
47
What are the complications of cirrhosis and portal hypertension that may occur?
Patients with portal hypertension are often asympotmatic, or just show hepatosplenomegaly
Complications that may occur:
* Ruptured gastro-oesophageal varices
* Ascites
* Encephalopathy
48
Explain what the following complications of cirrhosis and portal hypertension are
1. Ruptured gastro-oesophageal varices
2. Ascites
3. Encephalopathy
1. **Ruptured gastro-oesophageal varices**
* Gasto-oesophageal varices are extremely dilated sub-mucosal veins in the lower third of the esophagus or stomach
* ****The gastro-oesophageal varies develop due to the cirrhosis (90% of cirrhosis pts get them)
* 1/3 of patient with gasto-oesophageal varies will suffer a bleed
1. **Ascites**
* ****Fluid in the peritoneal cavity, which can accumulate slowly or rapidly
* Mild abdominal pain is common
1. **Encephalopathy**
* ****Caused by nitrogenous waste building up in the circulation, leading to cerebral oedema when astrocytes attempt to clear it
* Grade I: Altered mood/behaviour, sleep disturbances
* Grade II: Increasing drowsiness and confusion
* Grade III: Stupor (state of near-unconsciousness), incoherence, restlessness
* Grade IV: Coma
*
49
Describe portal venous anatomy
(where do the porto-systemic anastomososes come from)
The portal vein collects nutrient rich blood from the abdominal part of the alimentary tract, carries it into the liver, where its branches divide and end in expanded capillaries - the venous sinusoids of the liver
Porto-systemic anastomososes exist in several locations;
* Cardia of the stomach: gastric/oesophageal varices (left gastric vein)
* Anus: rectal varices
* Retroperitoneal organs: stomal varices
* Paraumbilical veins of the anterior abdominal wall: caput medusae
50
Define portal hypertension
Pressure in the portal vein \>10mmHg
| (normal pressure is 2-5mmHg)
51
What are the causes of portal hypertension?
**Pre-hepatic:**
* Portal vein thrombosis (often due to portal pyaemia - a type of septicaemia or prothrombotic states)
* Extrinsic compression
**Hepatic:**
* Cirrhosis (90%)
* Hepatitis (e.g. alcohol)
* Idiopathic non-cirrhotic portal hypertension
* Schistosomiasis
* Congenital hepatic fibrosis
* Drugs
**Post-hepatic:**
* Budd-Chairi syndrome (obstruction of the hepatic veins, most commonly due to thrombosis, or obstruction due to external mass)
52
What are the clinical manifestations of portal hypertension?
* Variceal bleeding
* Haemorrhoids/caput medusae
* Ascites
* Splenomegaly (portal congestion)
* Porto systemic encephalopathy (toxins bypass liver)
* Fetor hepaticus (breath smells like pear drops)
53
What is the function of the spleen?
List the common causes of splenomegaly
The spleen is the largest lymphoid organ in the body, which functions to breakdown erytrocytes and for immunological defence
**Common causes of splenomegaly:**
* Infection
* Infective endocarditis
* Bacterial sepsis
* EBV
* TB
* Malaria
* Schistosomiasis
* Inflammation
* Rhuematoid arthitis
* SLE
* Sarcoidisis
* Portal hypertension
* Haematological disease
* Haemolytic anaemia
* Leukaemia
* Lymphoma
* Myeloproliferative disorders
54
When can massive splenomegaly be seen?
| (palpable in the RIF)
* Myelofibrosis
* Chronic myeloid leukaemia
* Lymphoma
* Malaria
* Lieshmaniasis (parasitic)
* Gaucher's disease (genetic disorder)
55
Describe the bilirubin metablism
| (not an objective)
* When r.b.c reach the end of their life (120 days), they are destroyed in the reticuloendothelial system of the spleen
* The haem is converted to biliverdin and then to bilirubin (insoluble/indirect bilirubin), which is bound by albumin in the plasma
* Bilirubin can then be taken up by hepatocytes as it is protein bound, and it is conjugated by glucuronyl transferase to bilirubin glucuronide (solube/direct bilirubin)
* This soluble bilirubin is excreted in the bile into the bowel lumen, where it is transformed by bacteria to urobilinogen
* Most urobilinogen is excreted in the stools to give it the dark colour (aka stercobilinogen)
* A small amount of urobilinogn is reabsorbed from the intestine into the portal venous tributaries and passes back to the liver, wheremost of it is excreted once more into the gut
* Some of this reabsorbed urobilinogen reaches the systemic circulation, and this is excreted by the kidney into the urine
* When the urobilinogen in the urine is exposed to air, it is oxidized to urobilin to give urine a dark colour
56
What is jaundice?
clinically
Yellowing of the skin, usually visible when the bilirubin level reaches 50 micromol/L, with the upper limit of normal being 25 micromol/L
57
How is jaundice classified?
* Pre-hepatic
* Hepatocellular (Hepatic)
* Obstructive/cholestatic (Post-hepatic)
58
What cause pre-hepatic jaundice?
* Occurs secondary to increased erytrocyte (RBC) breakdown, e.g. in haemolysis or reabsorption of a large haematoma
* The bilirubn has not yet been processed by the liver, thus is mainly unconjugated in the blood
59
Why does cholestatic jaundice occur? (Give an overview)
* There is an obstruction to bile outflow from the liver, leading to 'cholestasis'
60
How is cholestatic (obstructive) jaundice classified? (what is it?)
Give the causes for each
**Intra hepatic obstruction:**
* Obstruction of the hepatic bile canniliculi (failure of bile secretion)
* Can occur secondary to multiple different causes:
* Hepatitis
* Cirrhosis
* Neoplasm
* Drugs
* Pregancy
**Extra hepatic obstruction:**
* Obstruction of the hepatic ducts, or biliary tree
* Causes within lumen:
* Gallstones
* Causes within the wall:
* Cholangiocarcinoma
* Primary sclerosing cholangitis
* Congenital atresia of the common bile duct
* External causes:
* Pancreatitis
* Tumour of pancreatic head
61
What are the clinical features of obstructive jaundice?
Why do they occur?
* Jaundice of skin and sclera - high bilirubin
* Pruritus (itching) - bilirubin deposition
* Dark urine
* As the bilirubin has been processed by the liver, it is mainly conjugated in the blood, and thus can also enter the urine giving dark urine
* Pale stools
* The bilirubin cannot enter the GI tract and thus is not excreted in faeces, giving pale stools
* Steatorrhoea
* reduced fat soluble vitamin absorption
62
What investigations would you do for a patient presenting with obstruction jaundice?
(laboratory and radiological)
**Urine and stools investigation:**
* Very little bile can enter the gut, thus stercobilinogen low, giving _pale stools_
* As the bilirubin is conjugated in the blood, urinary bilirubin is present, giving _dark urine_
__**Bloods:**
* FBC, reticulocytes, LFTs, U&Es, clotting, glucose, bilirubin levels
* Transaminases most raised in intrahepatic jaundice
* ALP most raised in extrahepatic cholestasis
* Glucose may be low in liver failure, or raised in pancreatic disease
**Imaging:**
* Ultrasound
* Will show dilated duct system to confirm obstruction
* Gallstones within the gall bladder can be demonstrated accurately
* MRCP
* Gives non-invasive high resolution imaging of the biliary tress
63
What is bile made of?
How is it released into the duodenum?
* Bile usually conatins cholesterol, phospholipids, bile salts, water and conjugated bilirubin
* Bile salts act to break up and emulsify fats in the gut, and are enterohepatically recycled to be secreted once more into the bile
* Bile flows into the gallbladder if the sphincter of oddi is closed, where it becomes more concentrated as water is absorbed
* Presence of fatty acids or amino acids in the duodenum will lead to release of cholecystokinin (CCK), which causes the gall bladder to contract and bile to be released
64
What are the common types of gallstones?
How are they formed? (pathophysiology)
**Cholesterol gallstones:**
* Cholesterol crystallization within gall bladder bile, due to excess cholesterol secretion into the bile, or loss of bile salt content
**Bile pigment stones:**
* Both black and brown bile pigment gallstones contain calcium bilirubinate, and form independently of cholesterol stones
* Black pigment gallstones are associated with haemolytic conditions
* Brown pigment gallstones occur due to biliary stasis/infection, and are a common cause of recurrent bile stones following cholecystectomy
65
What are risk factors for cholesterol gallstones?
(not an objective)
* Increasing age
* Obesity, high fat diet, rapid weight loss
* Female sex, multiparity (multiple children e.g. twins), pregnancy, oral contraceptive pill
* Diabetes mellitus
* Ileal disease (e.g. Crohn's)/resection
* Disease of the ileum prevents bile salt re-absorption
* Liver cirrhosis
66
Describe the biliary system anatomy
67
What is biliary colic?
Describe the symptoms of biliary colic
Pain associated with the temporary obstruction of the cystic duct or common bile duct by a stone migrating from the gall bladder
* Severe **_constant_** epigastic/RUQ pain, with a crescendo characteristic (peaks around 2 hours after eating, due to CCK peak at this time)
* May radiate to back, or right shoulder/subscapular region
* Can be associated with nausea and vomiting
* Worse upon food consumption, especially fatty foods
* Worst mid-evening, lasting until the early hours (often wakes patient)
* Cessation may be spontaneous, or terminated by opiate analgesia
* Patient will be systemically well
68
What is acute cholecystitis?
* An obstruction of the gall bladder emptying (due to a gallstone in 95% of cases), leading to gall bladder distension
* There is ongoing water reabsorption from the retained bile, which becomes highly concentrated, leading to a secondary inflammatory response in the wall of the gall bladder (chemical cholecystitis)
* 30% will also get a superadded infection
69
Describe the symptoms and signs of acute cholecystitis
Initial features are similar to biliary colic until the inflammatory component develops, leading to:
* Severe localized RUQ pain (as inflammed gallbladder touches peritoneum) with guarding and rigidity
* Vomiting & systemic upset (_fever_ and leukocytosis)
* Palpable gall bladder - Murphy's sign positive
* Rarely the gall bladder can become ganrenous and perforate, leading to generalized peritonitis
70
What is Murphy's sign?
Continous pressure over the gall bladder whilst the patient is inhaling will cause the patient to catch their breath at the point of maximum inhalation due to pain of the inflammed gall bladder
71
What are the common tests used in the diagnosis of calculus biliary tract disease?
**Bloods:**
* WBC/Inflammatory markers raised in cholecystitis
* LFTs may be marginally deranged in cholecystitis, significant derangement and obstructive jaundice type picture in common bile duct obstruction
* Amylase to assess for pancreatitis (often mildly elevated in gallstone disease, large elevations in acut ston-related pancreatitis)
**Imaging: Ultrasound**
* Will show stones in gall bladder
* Thickened gall bladder of acute/chronic inflammation
* Increased diameter of the common bile duct in obstruction
72
Describe the natural history of a young patient with asymptomatic gallstones
* The majority of gallstones are asymptomatic and remain so during a person's lifetime (People with asymptomatic gall stones come across problems at a rate of 1-4% per year)
* Thus, prophylactic cholecystectomy is not favoured to a "watch and wait approach"
* However, a younger patient will have more time over which to encounter problems, and so treatment may be favoured
* Small stones may be more dangerous
73
What is choledocohlithiasis?
What can it cause and predispose to?
* Stone impaction in the common bile duct, which can cause biliary colic if temporary, or painful obstructive jaundice if more prolonged
* This can predispose to ascending cholangitis or acute pancreatitis
74
What is Mirizzi's syndrome?
What does it cause?
* Gallstone impacted in the cystic duct/Hartmann's pouch (at neck of gall bladder) causes extrinsic compression of the common hepatic duct
* This leads to obstuctive jaundice, without dilation of the cystic/common bile duct
75
What is gallstone ileus?
What may it cause?
* An uncommon condition where a large gallstone erodes through to the gall bladder lumen to create a fistula into the adjacent duodenum
* This can then produce an obstruction if it impacts in a narrow segment of bowel (usually terminal ileum)
* Characteristically on AXR there will be signs of small bowel obstruction, the gallstone may be visible and there will be air in the biliary tree (aerobilia)
76
What is ascending cholangitis?
How is it most commonly caused?
What are signs and symptoms?
* It is an infection of the bile duct
* Usually caused by bacteria ascending from its junction with the duodenum (first part of the small intestine)
* It tends to occur if the bile duct is already partially obstructed by gallstones
**Signs and symptoms:**
* Charcot’s triad will be present in severe disease:
* High fever (+/- rigors and chills)
* RUQ pain
* jaundice.
77
Describe the management of symptomatic gallstones in the bile ducts
* Initial management is with fluids and analgesia. (keep NBM)
* Antibiotics will be administered if patients are septic. (septic 6 bundle)
* Surgery is offered to all patients suffering recurrent painful attacks, eventually.
* Emergency surgery is indicated if disease progresses, or if there is worrying gas in the gall bladder, or if perforation/GI obstruction become an issue.
78
Define Murphy's sign
Murphy’s sign is elicited during abdominal examination. The patient is instructed to fully expire. The examiner’s hand is placed under the costal margin in the mid-clavicular line. The patient is instructed to take a deep breath. Tenderness when the gall bladder comes into contact with the palpating hand will cause the patient to suddenly stop breathing in.
79
What is Courvoisier's sign/law
Courvoisier's law states that in the presence of a palpably enlarged gallbladder which is nontender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones.
80
When would a T-tube be used?
A T-Tube may be inserted through the skin into the common bile duct in order to put contrast medium into the biliary tree, or to drain bile
81
What are the most common bacterial infections found in acute cholecystitis?
* The most common infections include
* E.Coli
* C. Perfinigens
* Klebsiella.
These are gas producing organisms and may lead to emphysematous cholecystitis.
82
In a patient with acute cholecystitis, what are the right upper quadrant physical signs that support this diagnosis
Tenderness and muscle guarding/rigidity will be present; Murphy’s sign will be present
CP1
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