gastro 3

Question 1

what is biliary colic?

Answer 1

caused by gallstones passing through the biliary tree

Question 2

what can gallstones cause?

Answer 2

gallstones can cause a spectrum of disease, from biliary colic to acute pancreatitis depending on the region of the biliary system involved.

Question 3

what causes gallstones?

Answer 3

Bile is formed from cholesterol, phospholipids, and bile pigments (products of haemoglobin metabolism). It is stored in the gallbladder, before passing into the duodenum upon gallbladder stimulation.

Gallstones form as a result of supersaturation of the bile. There are three main types of gallstones:

Cholesterol stones – composed purely of cholesterol, from excess cholesterol production
There is a well recognised link between poor diet, obesity, and cholesterol stones
Pigment stones – composed purely of bile pigments, from excess bile pigments production
Commonly seen in those with known haemolytic anaemia
Mixed stones – comprised of both cholesterol and bile pigments

the stones lead to biliary stasis

Question 4

what are the risk factors for gallstones?

Answer 4

traditionally the 5F’s
Fat - obesity is thought to be a risk factor due to enhanced cholesterol synthesis and secretion
Female - gallstones are 2-3 more likely in women. Oestrogen causes more cholesterol to be secreted into bile.
Fertile - pregnancy is a risk factor
Forty
Family history

other risk factors including:
diabetes 
crohn's 
rapid weight loss e.g. weight loss reduction surgery 
drugs: fibrates, COCP

Question 5

what are the clinical features of biliary colic ?

Answer 5

biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. There is no inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain
sudden, dull and colicky pain
RUQ pain but may radiate to epigastrium or back
the pain may be precipitated by consumption of fatty foods
nausea and vomiting

Question 6

what is acute cholecystitis?

Answer 6

Acute cholecystitis describes inflammation of the gallbladder

develops secondary to gallstones in 90% of patients - acute calculous cholecystitis
the remaining 10% of cases are referred to as acalculous cholecystiti

Question 7

what are the features of acute cholecystitis?

Answer 7

Right upper quadrant pain
May radiate to the right shoulder
Fever and signs of systemic upset
Murphy’s sign on examination: inspiratory arrest upon palpation of the right upper quadrant
Liver function tests are typically normal
Deranged LFTs may indicate Mirizzi syndrome - a gallstone impacted in the distal cystic duct causing extrinsic compression of the common bile duct

Question 8

what is murphy’s sign?

Answer 8

Whilst applying pressure in the RUQ, ask the patient to inspire. Murphy’s sign is positive when there is a halt in inspiration due to pain, indicating an inflamed gallbladder. This can be achieved more accurately with an ultrasound, namely the sonographic Murphy sign.

Question 9

what investigations would you perform for gallstones?

Answer 9

LFTs
FBC - elevated WBC suggestions inflammation from a complication of the gallstone
serum lipase and amylase - acute pancreatitis
abdominal USS - will show the stones, gallbladder wall will be thickened if there is inflammation, bile duct dilatation indicates possible stones in duct

*if USS inconclusive MRCP - magnetic resonance cholangiopsncreatography

Question 10

what is another word for gallstones?

Answer 10

cholelithiasis

Question 11

how do you manage biliary colic?

Answer 11

pain relief - paracetamol +/- NSAIDs +/- opiates analgesia
elective laparoscopic cholecystectomy within 6 weeks of first presentation
lifestyle factos - low fat diet, weight loss, exercise

Question 12

what investigations would you perform for acute cholecystitis?

Answer 12

CT or MRI of abdomen - if sepsis is suspected request contrast enhanced CT or MRI 
abdominal USS
FBC
CRP
bilirubin 
LFTs
serum lipase or amylase
blood cultures and/or bile cultures

Question 13

how do you manage acute cholecystitis?

Answer 13

analgesia and antiemetics
fluid resus
antibiotic therapy such as co-amoxiclav +/- metronidazole
early laparoscopic cholecystectomy or percutaneous cholecystostomy for those not fit for surgery and not responding to antibiotics

Question 14

what are the complications of gallstones?

Answer 14

Mirizzi Syndrome - A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct. This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts. Diagnosis is confirmed by MRCP and management is usually with laparoscopic cholecystectomy.

Gallbladder Empyema - A gallbladder empyema is when the gallbladder becomes filled with pus. Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis. They are associated with significant morbidity and mortality. The condition is diagnosed by either US scan or CT scan. Treatment is via laparoscopic cholecystectomy (may require intra-operative drainage if tense gallbladder) or percutaneous cholecystostomy (if unsuitable for surgery).

Chronic Cholecystitis- Patients with chronic cholecystitis will typically have a history of recurrent or untreated cholecystitis, which has led to a persistent inflammation of the gallbladder wall. Patients present with ongoing RUQ or epigastric pain with associated nausea and vomiting. It can be diagnosed typically by CT imaging (or often noted on histology post-cholecystectomy). Management in uncomplicated cases is via elective cholecystectomy. Its main complications are gallbladder carcinoma and biliary-enteric fistula.

Bouveret’s Syndrome and Gallstone Ileus
Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel, termed a cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum)

As a consequence, bowel obstruction can occur:

Bouveret’s Syndrome – a stone impacts in the proximal duodenum, causing a gastric outlet obstruction
Gallstone Ileus– a stone impacts at the terminal ileum (the narrowest part of the small bowel), causing a small bowel obstruction

Question 15

what is it called when there are stones in the common bile duct ?

Answer 15

choledocholithiasis

this can result in obstructive jaundice

Question 16

what is ascending cholangitis?

Answer 16

Cholangitis refers to infection of the biliary tract - typically E.coli

It is caused by a combination of biliary outflow obstruction and biliary infection. During an obstruction, stasis of fluid combined with elevated intraluminal pressure allows the bacterial colonisation of the biliary tree to become pathological.

Question 17

what are the causes of ascending cholangitis?

Answer 17

occlusion of biliary tree
gallstones
ERCP
cholangiocarcinoma

other causes: ancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy, and parasitic infections

The most common infective organisms implicated in cholangitis are Escherichia Coli (27%), Klebsiella species (16%), and Enterococcus (15%).

Question 18

what are the clinical features of ascending/acute cholangitis

Answer 18

RUQ/upper abdominal pain and tenderness
jaundice
fever
there may also be pruritus as a result of bile accumulation and pale stools with dark urine

charcot’s triad - jaundice, fever and RUQ pain
Reynold’s pentad - jaundice, fever, RUQ pain, hypotension and confusion.

Question 19

what investigations would you perform for ascending cholangitis?

Answer 19

trans-abdominal USS
ERCP - gold standard

BLOODS
FBC
serum urea - raised in patients with severe disease
serum creatinine - raised in severe disease 
ABG
LFTs
CRP
blood cultures 
U&Es
coagulation panel

Question 20

how do you manage ascending cholangitis?

Answer 20

if acutely ill - patients may present with sepsis
- IV antibiotics - co-amoxiclav +/- metronidazole and fluids

ERCP with or without sphincterotomy and stenting within the first 12-48 hours to remove decompress biliary tree

Question 21

what are the risks of ERCP?

Answer 21

bleeding 0.9%
duodenal perforation 0.4%
cholangitis 1.1%
pancreatitis 1.5%

Question 22

what is liver cirrhosis ?

Answer 22

Liver cirrhosis is the result of chronic inflammation and damage to liver cells. When the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver. This fibrosis affects the structure and blood flow through the liver, which causes increased resistance in the vessels leading in to the liver. This is called portal hypertension.

It is the pathological end stage of any chronic liver disease

Question 23

what are the most common causes of liver cirrhosis?

Answer 23

most common causes:
Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C

rarer causes:
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons Disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (e.g. amiodarone, methotrexate, sodium valproate)

Question 24

what are the signs or liver cirrhosis?

Answer 24

• abdominal distension - secondary to ascites in portal hypertension - symptom of decompensated cirrhosis
• Jaundice and pruritus - secondary to reduced hepatic excretion of conjugated bilirubin into the biliary tree. Pruritus is secondary to impaired bile secretion
• blood in vomit, black stools - secondary to gastrointestinal haemorrhage from gastro-oesophageal varicies in portal hypertension
• hand and nail features - leukonychia, palmer erythema, spider naevi
• facial features - telangiectasia, spider naevi, jaundiced sclera
• abdominal features - collateral circulation, hepatosplenomegaly, distension (however the liver can shrink as it becomes more cirrhotic, splenomegaly is due to portal hypertension)
• gynaecomastia and testicular atrophy in males due to endocrine dysfunction
• bruising due to abnormal clotting
• caput medusae - distended paraumbilical veins due to portal hypertension
• asterixis - flapping tremor - in decompensated liver disease

Question 25

what investigations would you perform for liver cirrhosis

Answer 25

- LFTs - will be deranged - Gamma-glutamyl transferase GGT - elevated - serum albumin - decreased (a marker of hepatic synthetic dysfunction) - serum sodium - reduced - hyponatraemia is a common finding in cirrhotic patients with associated ascites and worsens as liver disease progresses - prothrombin time - prolonged - platelet count - reduced enhanced liver fibrosis blood test - the first line for assessing non-alcoholic fatty liver disease - but currently not readily available USS - may show - Nodularity of the surface of the liver - A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow - Enlarged portal vein with reduced flow - Ascites - Splenomegaly Fibroscan - transient elastography - It helps assess the degree of cirrhosis, should be used to test for cirrhosis. NICE recommend retesting every 2 years in patients at risk of cirrhosis: Hepatitis C Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week) Diagnosed alcoholic liver disease Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test Chronic hepatitis B (although they suggest yearly for hep B) Endoscopy -Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected. CT and MRI scans -CT and MRI can be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites. Liver Biopsy

Question 26

what scores can be used for liver cirrhosis?

Answer 26

Child -pugh score -- it is based on the presence of ascites, hepatic encephalopathy, serum bilirubin, albumin and clotting. Model of end-stage liver disease - MELD - The MELD score is recommended by NICE to be used every 6 months in patients with compensated cirrhosis. It is a formula that takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.

Question 27

how is liver cirrhosis managed?

Answer 27

treatment for underlying chronic liver disease monitor for complications sodium restricition and diuretic therapy for ascites - spironolactone Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma Endoscopy every 3 years in patients without known varices High protein, low sodium diet MELD score every 6 months Consideration of a liver transplant Managing complications liver transplant

Question 28

what are the complications of liver cirrhosis?

Answer 28

Malnutrition Portal Hypertension, Varices and Variceal Bleeding Ascites and Spontaneous Bacterial Peritonitis (SBP) Hepato-renal Syndrome Hepatic Encephalopathy Hepatocellular Carcinoma

Question 29

how do you manage malnutrition in patients with liver cirrhosis?

Answer 29

Cirrhosis leads to malnutrition and muscle wasting to manage this: Regular meals (every 2-3 hours) Low sodium (to minimise fluid retention) High protein and high calorie (particularly if underweight) Avoid alcohol

Question 30

why do patients with liver cirrhosis get portal hypertension and varacies?

Answer 30

The portal vein comes from the superior mesenteric vein and the splenic vein and delivers blood to the liver. Liver cirrhosis increases the resistance of blood flow in the liver. As a result, there is increased back-pressure into the portal system. This is called “portal hypertension”. This back-pressure causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous. These swollen, tortuous vessels are called varices. They occur at the: Gastro oesophageal junction Ileocaecal junction Rectum Anterior abdominal wall via the umbilical vein (caput medusae) Varices do not cause symptoms or problems until they start bleeding. Due to the high blood flow through varices, once they start bleeding patients can exsanguinate (bleed out) very quickly.

Question 31

how do you manage stable varicies?

Answer 31

Propranolol reduces portal hypertension by acting as a non-selective beta blocker Elastic band ligation of varices Injection of sclerosant (less effective than band ligation) Transjugular Intra-hepatic Portosystemic Shunt (TIPS) - allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices. This is used if medical and endoscopic treatment of varices fail or if there are bleeding varices that cannot be controlled in other ways.

Question 32

how do you manage bleeding varacies?

Answer 32

Resuscitation Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors) Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell Urgent endoscopy Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel Elastic band ligation of varices Sengstaken-Blakemore Tube is an inflatable tube inserted into the oesophagus to tamponade the bleeding varices. This is used when endoscopy fails.

Question 33

what investigations would you perform for varicies?

Answer 33

hepatic venous pressure gradient - will assess for clinically significant portal hypertension FBC Coagulation profile oesophago-gastro-duodenoscopy OGD - will show dilated veins in the lower oesophagus

Question 34

why do patients with cirrhosis get ascites?

Answer 34

Ascites is basically fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and in to the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal space causes a reduction in blood pressure entering the kidneys. The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative, meaning low protein content, ascites.

Question 35

how do you manage ascites?

Answer 35

Low sodium diet Anti-aldosterone diuretics (spironolactone) Paracentesis (ascitic tap or ascitic drain) Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid Consider TIPS procedure in refractory ascites Consider transplantation in refractory ascites

Question 36

why do patients with cirrhosis get spontaneous bacterial peritonitis and how does it present?

Answer 36

This occurs in around 10% of patients with ascites secondary to cirrhosis and can have a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation). Presentation Can be asymptomatic so have a low threshold for ascitic fluid culture Fever Abdominal pain Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis) Ileus Hypotension

Question 37

how do you manage spontaneous bacterial peritonitis as a complication of cirrhosis?

Answer 37

Most common organisms Escherichia coli Klebsiella pnuemoniae Gram positive cocci (such as staphylococcus and enterococcus) Management of SBP Take an ascitic culture prior to giving antibiotics Usually treated with an IV cephalosporin such as cefotaxime

Question 38

what is hepato-renal syndrome?

Answer 38

Hepatorenal syndrome occurs in liver cirrhosis. Hypertension in the portal system leads to dilation of the portal blood vessels, stretched by large amounts of blood pooling there. This leads to a loss of blood volume in other areas of the circulation, including the kidneys. This leads hypotension in the kidney and activation of the renin-angiotensin system. This causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney. This leads to rapid deteriorating kidney function. Hepatorenal syndrome is fatal within a week or so unless liver transplant is performed. there will be decreased urine output and increase creatinine

Question 39

why do patients get hepatic encephalopathy?

Answer 39

aka - porto-systemic encephalopathy caused by build up of toxins which affect the brain - mainly ammonia which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut ammonia builds up in those with cirrhosis because the liver can't metabolise ammonia into harmless waste product, and secondary the collateral vessels between the portal and systemic circulation mean that ammonia bypasses the liver all together and enters the system directly.

Question 40

what are the precipitating factors for hepatic encephalopathy?

Answer 40

``` Constipation Electrolyte disturbance Infection GI bleed High protein diet Medications (particularly sedative medications) ```

Question 41

what are the symptoms of hepatic encaphalopathy?

Answer 41

mood disturbance sleep disturbance motor disturbances (ataxia and extrapyramidal symptoms such as muscle rigidity, bradykinesia, hypokinesia, slow monotonous speech, parkinson-like temour) confusion, may be followed by unconsciousness and coma

Question 42

what investigations would you perform for hepatic encephalopathy?

Answer 42

LFTs triphasic slow waves on EEG head CT - absence of other causes and presence of oedema

Question 43

how do you manage hepatic encephalopathy?

Answer 43

Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially. Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract. Nutritional support. They may need nasogastric feeding.

Question 44

what is primary biliary cirrhosis?

Answer 44

aka primary biliary cholangitis the immune system attacks the small bile ducts within the liver - usually seen in middle aged woman The first parts to be affected are the intralobar ducts, also known as the Canals of Hering. This causes obstruction of the outflow of bile, which is called cholestasis. The back-pressure of the bile obstruction and the overall disease process ultimately leads to fibrosis, cirrhosis and liver failure. Bile acids, bilirubin and cholesterol are usually excreted through the bile ducts into the intestines. When there is obstruction to the outflow of these chemicals they build up in the blood as they are not being excreted. Bile acids cause itching, bilirubin causes jaundice and raised cholesterol causes cholesterol deposits in the skin called xanthelasma (xanthoma are larger nodular deposits in the skin or tendons) and blood vessels causing increased risk of cardiovascular disease. Bile acids are normally responsible for helping the gut digest fats. Having a lack bile acids in the stool cause gastrointestinal disturbance, malabsorption of fats and greasy stools. Bilirubin normally causes the dark colour of stools, so a lack of bilirubin can cause pale stools.

Question 45

how does primary biliary cirrhosis present?

Answer 45

``` Fatigue Pruritus GI disturbance and abdominal pain Jaundice Pale stools Xanthoma and xanthelasma Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi) dry eyes dry mouth - symptoms of sjoren's syndrome ```

Question 46

what are the associations with primary biliary cirrhosis?

Answer 46

Middle aged women Other autoimmune diseases (e.g. thyroid, coeliac) Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis) 80% of patients have sjoren's syndrome

Question 47

what investigations would you perform for primary biliary cirrhosis?

Answer 47

Liver Function Tests Alkaline phososphatase is first liver enzyme to be raised (as with most obstructive pathology) Other liver enzymes and bilirubin are raised in later disease Autoantibodies Anti-mitochondrial antibodies is the most specific to PBC and forms part of the diagnostic criteria Anti-nuclear antibodies are present in about 35% of patients Other blood tests: ESR raised IgM raised Liver biopsy is used in diagnosing and staging the disease

Question 48

how do you manage primary biliary cirrhosis?

Answer 48

bile acid analogue - ursodeoxycholic acid - reduces the intestinal absorption of cholesterol if they have cholestatic pruritus - Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids liver transplant in end stage liver disease some patients may be managed with immunosupression with steroid - prednisolone fat soluble vitamin supplementation

Question 49

what are some complications of primary biliary cirrhosis?

Answer 49

cirrhosis osteomalacia and osteoporosis significantly increased risk of hepatocellular carcinoma

Question 50

how can ascites be grouped?

Answer 50

The causes of ascites can be grouped into those with a serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/L as per the table below: SAAG > 11g/L - transudate - indicated portal hypertension, Cirrhosis, Alcoholic hepatitis, Cardiac ascites, Mixed ascites, Massive liver metastases, Fulminant hepatic failure, Budd-Chiari syndrome, Portal vein thrombosis, Veno-occlusive disease, Myxoedema, Fatty liver of pregnancy SAAG <11g/L - exudate - Peritoneal carcinomatosis, Tuberculous, peritonitis, Pancreatic ascites, Bowel obstruction, Biliary ascites, Postoperative lymphatic leak, Serositis in connective tissue diseases

Question 51

how do you manage ascites?

Answer 51

reducing dietary sodium fluid restriction is sometimes recommended if the sodium is < 125 mmol/L aldosterone antagonists: e.g. spironolactone drainage if tense ascites (therapeutic abdominal paracentesis) prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. NICE recommend: 'Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved' a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients

Question 52

why can nephrotic syndrome result in ascites?

Answer 52

kidney damage causes protein to leak into the urine, decreases oncotic pressure and may result in ascites

Question 53

what drug can lead to perforation in bowel obstruction?

Answer 53

metoclopromide as it is a pro-kinetic antiemetic anti emetics which are not pro-kinetic are safe to use in bowel obstruction

Question 54

what surgery can be used for treatment of GORD and what investigations need to be performed before this surgery?

Answer 54

Patients with GORD can be considered for fundoplication surgery they require oesophageal pH and manometry studies, endoscopy, barium swallow and pH monitoring

Question 55

what would bloods show in mesenteric ischaemia?

Answer 55

bloods typically show an elevated white blood cell count associated with a lactic acidosis metabolic acidosis is highly associated with mesenteric ischaemia

Question 56

which vitamin deficiency can lead to easy bruising?

Answer 56

vitamin C deficiency - scurvy Symptoms and signs include: Follicular hyperkeratosis and perifollicular haemorrhage Ecchymosis, easy bruising Poor wound healing Gingivitis with bleeding and receding gums Sjogren's syndrome Arthralgia Oedema Impaired wound healing Generalised symptoms such as weakness, malaise, anorexia and depression

Question 57

how do you manage hepato-renal syndrome?

Answer 57

The ideal treatment is liver transplant vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation volume expansion with 20% albumin transjugular intrahepatic portosystemic shunt

Question 58

what is a useful marker of HCC?

Answer 58

Alpha-fetoprotein

Question 59

what is the stepwise progression of alcoholic liver disease?

Answer 59

1. Alcohol related fatty liver- Drinking leads to a build-up of fat in the liver. If drinking stops this process reverses in around 2 weeks. 2. Alcoholic hepatitis - Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence. 3. Cirrhosis - This is where the liver is made up of scar tissue rather than healthy liver tissue. This is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

Question 60

what are the recommendations for alcohol consumption?

Answer 60

That latest recommendations (Department of Health, 2016) are to not regularly drink more than 14 units per week for both men and women. If drinking 14 units in a week, this should be spread evenly over 3 or more days and not more than 5 units in a day.

Question 61

what is the CAGE questionnaire?

Answer 61

The CAGE question can be used to quickly screen for harmful alcohol use: C – CUT DOWN? Ever thought you should? A – ANNOYED? Do you get annoyed at others commenting on your drinking? G – GUILTY? Ever feel guilty about drinking? E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?

Question 62

what can be used to screen people for harmful alcohol use?

Answer 62

AUDIT - alcohol use disorder identification test It involves 10 questions with multiple choice answers and gives a score. A score of 8 or more gives an indication of harmful use.

Question 63

what are the complications of alcohol?

Answer 63

``` Alcoholic Liver Disease Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma Alcohol Dependence and Withdrawal Wernicke-Korsakoff Syndrome (WKS) Pancreatitis Alcoholic Cardiomyopathy ```

Question 64

what are some signs of liver disease?

Answer 64

``` Jaundice Hepatomegaly Spider Naevi Palmar Erythema Gynaecomastia Bruising – due to abnormal clotting Ascites Caput Medusae – engorged superficial epigastric veins Asterixis – “flapping tremor” in decompensated liver disease ```

Question 65

what investigations would you perform for alcoholic liver diesase?

Answer 65

FBC - raised MCV LFTs - elevated ALT and AST (transaminases) and particularly raised gamma-GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis Clotting - elevated prothrombin time due to reduced synthetic function of the liver U+E may be deranged in hepatorenal syndrome USS - show fatty changes described as increase echogenicity Fibroscan - helps assess degree of cirrhosis Endoscopy - assess for varicies if portal HT suspected CT/MRI liver biopsy

Question 66

how do you manage alcoholic liver disease?

Answer 66

- Stop drinking alcohol permanently - Consider a detoxication regime - Nutritional support with vitamins (particularly thiamine) and a high protein diet - Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis but infection and GI bleeding need to be treated first and do not improve outcomes over the long term - Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy) - Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral

Question 67

what is haemochromatosis?

Answer 67

Haemochromatosis is an AR disorder of iron absorption and metabolism resulting in iron accumulation It is causes by inheritance of mutations in the e human haemochromatosis protein (HFE) gene which is located on chromosome 6 Iron accumulates in multiple organs including liver, heart, anterior pituitary, pancreas and other organs.

Question 68

what are the features of haemochromatosis ?

Answer 68

> early symptoms - fatigue, ED, arthralgia (often in the hands) > bronze skin pigmentation > DM > liver - stigmata of chronic liver disease, hepatomegaly, cirrhosis > cardiac failure - secondary to cardiomyopathy > hypogonadism - 2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)

Question 69

what are the reversible and irreversible complications of haemachromatosis?

Answer 69

reversible - cardiomyopathy and skin pigmentation | irreversible - liver cirrhosis, DM, arthropathy, hypogonadotrophic hypogonadism

Question 70

what investigations would you perform for haemochromatosis?

Answer 70

serum ferritin - ferritin is and acute phase reactant so does go up with inflammation. Performing a serum transferrin saturation (will be greater than 45%) is helpful in distinguishing between a high ferritin caused by iron overload. there will be a low total iron binding capacity Liver biopsy with perl's stain can be used to establish iron concentration in the parenchymal cells MRI can give more detailed picture of the liver and also look for iron deposits in the heart. joint xrays characteristically show chondrocalcinosis

Question 71

what are the complications of haemochromatosis?

Answer 71

- Type 1 Diabetes (iron affects the functioning of the pancreas) - Liver Cirrhosis - Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility) - Cardiomyopathy (iron deposits in the heart) - Hepatocellular Carcinoma - Hypothyroidism (iron deposits in the thyroid) - Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis

Question 72

how do you manage haemochromtosis?

Answer 72

venesection is the first-line treatment - a weekly protocol of removing blood to decrease total iron monitor serum ferritin avoid alcohol 2nd line is iron chelation therapy - desferrioxamine they may need the second line treatment if they have anaemia, severe heart disease or problems with venous access. all patients should receive hep A and hep B vaccination

Question 73

what is Wilsons's disease?

Answer 73

Wilson disease is the excessive accumulation of copper in the body and tissues. It is caused by a mutation in the “Wilson disease protein” - ATP7B gene located on chromosome 13. genetic inheritance is AR

Question 74

what are the features of wilson's disease?

Answer 74

``` Most patients with Wilson disease present with one or more of: Hepatic problems (40%) - hepatitis, cirrhosis Neurological problems (50%) - concentration and coordination difficulties, dysarthria, dystonia, copper in basal ganglia can lead to parkinsonism (tremor, bradykinesia, and ridigity) Psychiatric problems (10%) - depression to psychosis, may have history of behavioural abnormalities (loss of control of emotions, delusions, loss of memory, sexual disinhibition ``` other: - kayser-fleischer rings - renal tubular acidosis - especially Fanconi syndrome - haemolysis - blue nails

Question 75

how is Wilson's disease diagnosed?

Answer 75

- LFTs will be abnormal - 24 hour urine copper excretion will be raised - serum ceruloplasmin will be reduced - low serum copper - MRI brain shows nonspecific changes

Question 76

how do you manage Wilson's disease?

Answer 76

- copper chelation using 1st line - trientine hydrochloride and zinc 2nd line - penicillamine dietary restriction

Question 77

what is Alpha 1 antitrypsin deficiency?

Answer 77

Alpha 1 antitrypsin deficiency is an inherited deficiency of a protease inhibitor called alpha 1 antitrypsin. This leads to an excess of protease enzymes that attack the liver and lung tissue and cause liver cirrhosis and lung disease. Elastase is an enzyme secreted by neutrophils. This enzyme digests connective tissues. Alpha-1-antitrypsin (A1AT) is present in tissues to inhibit the neutrophil elastase and protect tissues. A1AT is coded for on chromosome 14. In A1AT deficiency, there is an autosomal recessive defect in the gene for A1AT. This results in the neutrophil elastase damaging connective tissue

Question 78

what investigations would you perform for alpha 1 antitrypsin deficiency?

Answer 78

plasma AAT level - reduced pulmonary function tests - obstructive picture LFTs Liver biopsy shows cirrhosis and acid-Schiff-positive staining globules (this is a test to stain the breakdown products of the action of the proteases) in hepatocytes

Question 79

how do you manage alpha 1 antitrypsin ?

Answer 79

Stop smoking (smoking dramatically accelerates emphysema) and avoid alcohol Symptomatic management NICE recommend against the use of replacement alpha 1 antitrypsin, however the research and debate is ongoing regarding the possible benefits Organ transplant for end stage liver or lung disease Monitoring for complications (e.g. hepatocellular carcinoma)

Question 80

what are different intra-abdominal infections?

Answer 80

``` Acute diverticulitis Cholecystitis (with secondary infection) Ascending cholangitis Appendicitis Spontaneous bacterial peritonitis Intra-abdominal abscess ```

Question 81

what are common causes of intra-abdominal infections?

Answer 81

``` Anaerobes (e.g. bacteroides and clostridium) E. coli Klebsiella Enterococcus Streptococcus ```

Question 82

causes of acute diarrhoea ?

Answer 82

gastroenteritis (usually accompanied by abdominal pain or nausea/vomiting) Diverticulitis (classically lowe left quadrant pain, diarrhoea and fever) Abx therapy - broad spectrum Abx commonly causes diarrhoea, C.diff is also seen with Abx use Overflow

Question 83

causes of chronic diarrheoa?

Answer 83

``` IBS UC Crohn's colorectal cancer coealiac disease ```

Question 84

what is H.pylori associated with?

Answer 84

peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers) gastric cancer B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients) atrophic gastritis

Question 85

how do you test for H.pylori?

Answer 85

``` urea breath test stool antigen test CLO test serum antibody culture of gastric biopsy ```

Question 86

How do you manage h.pylori?

Answer 86

a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole) if penicillin allergic: a proton pump inhibitor + metronidazole + clarithromycin

Question 87

what causes pyogenic (bacterial) liver abscess?

Answer 87

- often cause is unknown - in the elderly billary sepsis is a common cause - trauma - bacteraemia from portal vein - infection of tumour or cyst - direct extension - e.g. empyema of gall bladder or perinephric abscess - pathogens: (e.coli, streptococcus milleri, klebsiella pneumoniae

Question 88

how does a liver abscess present?

Answer 88

``` fever vomiting weight loss RUQ pain pleuritic/right should pain tender hepatomegaly +/- obstructivejaundice ```

Question 89

how is a liver abscess diagnosed?

Answer 89

blood culture serum alkaline phosphatase, ESR and CRP riased CT abdomen USS

Question 90

how are liver abscess treated?

Answer 90

aspiration of the abscess under USS | Abx - amoxicillin plus ciprofloxacin plus metronidazole

Question 91

what is amoebiasus?

Answer 91

Amoebiasis is caused by Entamoeba histolytica (an amoeboid protozoan) and spread by the faecal-oral route. Infection can be asymptomatic, cause mild diarrhoea or severe amoebic dysentery. Amoebiasis also causes liver and colonic abscesses.

Question 92

what is amoebic dysentery?

Answer 92

profuse, bloody diarrhoea there may be a long incubation period stool microscopy may show trophozoites if examined within 15 minutes or kept warm (known as a 'hot stool') treatment is with metronidazole

Question 93

how does an amoebic liver abscess present?

Answer 93

``` usually gradual onset fever abdo pain anorexia weight loss malaise tender hepatomegaly ```

Question 94

how is amoebiasus managed?

Answer 94

metronidazole for 10 days