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2a Medicine > Liver > Flashcards

Liver Flashcards

1
Q

What is chronic liver failure?

A

Loss of the liver’s ability to regenerate or repair.

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2
Q

What are the types of chronic liver failure?

A
  • Fulminant hepatic failure: within 8 weeks of onset of underlying illness
  • Late-onset hepatic failure: 8-26 weeks since onset
  • Chronic decompensated hepatic failure: latent period >6months.
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3
Q

What are the causes of chronic liver failure?

A 
Toxins:
•	Alcohol
•	Paracetamol poisoning (most common acute cause)
Infections:
•	Viral hepatitis
•	EBV
•	CMV.
Neoplastic:
•	Hepatocellular carcinoma.
Metabolic:
•	Wilson’s
•	A1At deficiency
•	Haemochromatosis.
Others:
•	Acute fatty liver of pregnancy
•	Ischaemia
•	Autoimmune liver disease.
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4
Q

What is the pathophysiology of chronic liver disease?

A

Generally destruction of the hepatocytes, the development of fibrosis in response to chronic inflammation. The destruction of the architecture of the nodules of the liver removes the ability of the liver to adequately perform functions, repair and regenerate.

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5
Q

What are the symptoms of chronic liver disease?

A
  • Jaundice
  • Ascites
  • Variceal haemorrhage secondary to portal hypertension
  • Hepatic encephalopathy
  • Mental state shows drowsiness and confusion due to cerebral oedema.
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6
Q

What do the investigations in chronic liver disease show?

A
  • Raised bilirubin

* Glucose low as no glucogenesis.

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7
Q

How do you treat chronic liver failure?

A
  • Treat symptoms e.g. mannitol for hepatic encephalopathy

* Liver transplant.

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8
Q

What are the complications of chronic kidney failure?

A

Infection and haemorrhage.

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9
Q

What is cirrhosis?

A

Not a specific disease. Is an end stage of all progressive chronic liver diseases, which once fully developed is irreversible and may be associated clinically with symptoms and signs of portal hypertension and liver failure. Characterised by loss of normal hepatic architecture, nodular regeneration and bridging fibrosis.

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10
Q

What are the causes of cirrhosis?

A 
Common:
•	Chronic alcohol abuse
•	Non-alcoholic fatty liver disease
•	Hepatitis B±D
•	Hepatitis C.

Others:
• Primary biliary cirrhosis
• Autoimmune hepatitis (presents as high ALT)
• Hereditary haemochromatosis (iron overload)
• Wilson’s disease
• Alpha-Antitrypsin deficiency
• Drugs e.g. amiodarone and methotrexate.

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11
Q

What is the pathophysiology of cirrhosis?

A
  1. Chronic liver injury results in inflammation, matrix deposition, necrosis and angiogenesis which all cause fibrosis.
  2. Liver injury causes necrosis and apoptosis, releasing cell contents and reactive oxygen species (ROS)
  3. This activates hepatic stellate cells and tissue macrophages (Kupffer cells)
  4. Stellate cells release cytokines that attract neutrophils and macrophages to the liver and so there is further inflammation and necrosis which causes fibrosis
  5. Results in severe reduction in liver function as fibrosis in non-functioning.
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12
Q

What are the two types of cirrhosis?

A
  • Micronodular cirrhosis: regenerating nodules usually <3mm in size with uniform involvement of the liver. Often caused by alcohol or biliary tract disease
  • Macronodular cirrhosis: nodules of varying size and normal acini (functioning unit of liver) may be seen within larger nodules. Often caused by chronic viral hepatitis.
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13
Q

What is decompensated cirrhosis?

A

When the liver is damaged to the point that it cannot function adequately and overt clinical complications (such as jaundice, ascites, variceal haemorrhage and hepatic encephalopathy) are present. Events causing decompensation include infection, portal vein thrombosis and surgery.

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14
Q

What are the symptoms of compensated cirrhosis?

A
  • Asymptomatic

* Non-specific e.g. weight loss, weakness, fatigue.

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15
Q

What are the symptoms of decompensated cirrhosis?

A
  • Jaundice
  • Pruritis
  • Abdominal pain due to ascites.
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16
Q

What are the signs of cirrhosis?

A
  • Bruising
  • Leukonychia: white discolouration on nails due to hypoalbuminaemia
  • Clubbing of the fingers
  • Palmar erythema
  • Spider naevi
  • Dupuytren’s contracture
  • Xanthelasma: yellow fat deposits under skin usually around eyelids
  • Ascites
  • Jaundice
  • Oedema due to decreased albumin in blood.
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17
Q

What are the best indicators for liver function?

A

Serum albumin and prothrombin.

Low albumin and long prothrombin means malfunction.

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18
Q

What are the investigations in cirrhosis?

A
  • Liver biopsy
  • LFTs: serum albumin and prothrombin time best indicators of liver function (raised bilirubin, aspartate amino transferase (AST) and alanine aminotransferase (ALT). Low albumin and long prothrombin means malfunction)
  • Liver biochemistry
  • FBC: low platelets (due to loss of thrombopoteitin)
  • Transient elastography
  • Abdominal ultrasound
  • Abdominal CT
  • Abdominal MRI
  • Upper GI endoscopy for possible oesophageal varices.
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19
Q

What is the treatment for cirrhosis?

A 
Treat underlying cause:
•	Alcohol abstinence
•	Antivirals for hepatitis C
•	Spironolactone for ascites.
Liver transplant.
Good nutrition.
6 month ultrasound screening for hepatocellular carcinoma.
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20
Q

What are the complications of cirrhosis?

A
  • Coagulopathy: fall in clotting factors II, VII, IX and X
  • Encephalopathy: liver flap (flapping tremor with wrist extended) and confusion/coma. This is when toxins e.g. ammonia make it into the brain and cause mental deficits
  • Thrombocytopenia
  • Hepatocellular carcinoma
  • Hypoalbuminaemia
  • Portal hypertension: ascites, oesophageal varices.
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21
Q

What are the causes of portal hypertension?

A

Pre-hepatic: due to blockage of portal vein before liver
• Portal vein thrombosis.
Intra-hepatic: resulting from distortion of liver architecture
• Cirrhosis (most common cause)
• Schistosomiasis
• Sarcoidosis
• Congenital hepatic fibrosis.
Post-hepatic: due to venous blockage outside of the liver
• Right HF
• Constrictive pericarditis
• IVC obstruction.

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22
Q

What is the pathophysiology of portal hypertension?

A

Following liver injury and fibrogenesis (e.g. due to cirrhosis), the contraction of activated myofibroblasts (mediated by endothelin, nitric oxide and prostaglandins) contributes to increased resistance to blood flow.
This leads to portal hypertension which causes splanchnic vasodilation and so a drop in BP. This means increased CO to compensate for BP and salt and water retention to increase blood volume which causes hyperdynamic circulation (increased portal flow). This leads to formation of collaterals between portal and systemic systems e.g. lower oesophagus and gastric cardia.

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23
Q

What are the signs of portal hypertension?

A
  • Ascites
  • Hepatic encephalopathy
  • Splenomegaly
  • Oesophago-gastric varices.
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24
Q

What is a varice?

A

A dilated vein at risk of rupture resulting in haemorrhage and can cause GI bleeding in the GI system.

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25
Q

When are varies likely?

A
  • Around 90% of patients with cirrhosis develop gastro-oesophageal varices over 10 years but only a third will bleed
  • Bleeding likely to occur in large varices or those with red signs at endoscopy and in severe lives disease
  • Tend to develop in lower oesophagus and gastric cardia.
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26
Q

What are the causes of oesophagi-gastric varices?

A 
Pre-hepatic:
•	Portal vein thrombosis.
Intra-hepatic:
•	Cirrhosis (most common cause in UK)
•	Schistosomiasis (most common cause worldwide)
•	Sarcoidosis
•	Congenital hepatic fibrosis.
Post-hepatic: due to venous blockage outside of the liver
•	Budd-Chiari syndrome (hepatic vein obstruction by tumour or thrombosis)
•	Right HF
•	Constrictive pericarditis
•	IVC obstruction.
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27
Q

What is the pathophysiology of varices?

A

At the oesophago-gastric junction, rectum and anterior abdominal wall (via umbilical vein) the portal and systemic capillary beds meet. If portal hypertension is present, the blood takes the path of least resistance which is through the systemic circulation and so bypasses liver and into heart. This causes detoxification and nutrition issues. As portal pressure increases, it can cause a gastric-oesophageal varices to form and rupture which cause massive haemorrhage.

Simply: as these vessels are thin and not meant to transport higher pressure blood, they can rupture. Rupture causes haematemesis and can also mean blood is digested which causes melaena.

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28
Q

What are the symptoms of varices?

A
  • Haematemesis
  • Abdominal pain
  • Rectal bleeding.
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29
Q

What are the signs of varices?

A
  • Hypotension
  • Tachycardia
  • Pallor
  • Signs of chronic liver disease jaundice, easy bruising (liver not produced coagulation factors) and ascites
  • Splenomegaly
  • Ascites.
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30
Q

What is the investigation for varices?

A

Endoscopy.

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31
Q

What is the management for varices?

A

Blood transfusion if anaemic.
Medical:
• Beta blocker to reduce CO and so reduce portal pressure
• Nitrate to cause vasodilation and so reduce portal pressure
• Terlipressin (ADH analogue) to reduce portal pressure
Trans-jugular intrahepatic portoclaval shunt (TIPS).
Correct clotting abnormalities with vitamin K and platelet transfusion.
Variceal banding: band put around varice using endoscopy.

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32
Q

When does alcoholic liver disease typically present?

A

In men aged 40-50s.

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33
Q

What is the simple pathophysiology of alcoholic liver disease?

A
  • Fatty liver to alcoholic hepatitis to alcoholic steatosis to cirrhosis
  • Reduced NAD+ and increased NADH in hepatocytes so less oxidation of fat and more fat synthesis which causes accumulation of fat in hepatocytes
  • Increased reactive oxygen species damages hepatocytes
  • Acetaldehyde reactive oxygen species damages hepatocytes
  • Leads to inflammation and eventual cirrhosis.
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34
Q

What is the pathophysiology of alcoholic liver disease?

A

Fatty liver (steatosis):
• Metabolism of alcohol produces fat in liver
• Cells become swollen with fat (steatosis) with larger amounts
• Fat disappears on alcohol abstinence
• In some cases, collagen is laid down around central hepatic veins which causes cirrhosis without preceding hepatitis
• Alcohol directly affects stellate cells, transforming them into collagen-producing myofibroblast cells
• May progress to fibrosis and cirrhosis if alcohol is not stopped
• Hepatocytes contain macrovesicular droplets of triglycerides on biopsy
• Possibly as a result of mitochondrial damage.

Alcoholic hepatitis:
• In addition to fatty change, there is infiltration by polymorphonuclear leukocytes and hepatocyte necrosis
• If alcohol consumption continues, alcoholic hepatitis can progress to cirrhosis. They usually coexist
• Presence of mallary bodies and giant mitochondria
• Ballooned hepatocytes that contain eosinophilic material called Mallory bodies, surrounded by neutrophils. Fibrosis and foamy degeneration of hepatocytes is possible

Alcoholic cirrhosis:
• Classically of the micronodular type, accompanying fatty change and evidence may be present
• Final stage of alcoholic liver disease
• Destruction of liver architecture and fibrosis
• Regenerating nodules bring micronodular cirrhosis
• Mallory bodies also present.

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35
Q

What are the symptoms of fatty liver?

A

Usually no symptoms. Possible hepatomegaly on examination.

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36
Q

What are the symptoms of alcoholic hepatitis?

A

Rapid onset jaundice. Nausea, anorexia, encephalopathy, fever and ascites.

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37
Q

What are the symptoms of alcoholic cirrhosis?

A

May be asymptomatic. Usually present with complications of cirrhosis. Spider naevei are a classic.

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38
Q

What are the symptoms of alcoholic liver disease?

A
  • RUQ pain
  • Nausea
  • Vomiting
  • Diarrhoea.
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39
Q

What do LFTs show in alcoholic liver disease?

A

GGT and ALP very raised. AST and ALT mildly raised (increased AST>ALT ratio which is usually 2:1).

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40
Q

What does FBC show in alcoholic liver disease?

A

• FBC: thrombocytopenia (low platelets), hypoglycamia (low blood sugar), raised MCV.

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41
Q

What is the management for alcoholic liver disease?

A

Alcohol abstinence because if alcohol intake stops then fat will disappear, and liver goes back to normal.
Diazepam to treat delirium tremens after alcohol withdrawal.
IV thiamine to prevent Wernicke-Korsafodd encephalopathy.
Corticosteroids to control inflammation if there is no renal failure.
Diet high in vitamins and proteins.

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42
Q

What are complications in alcoholic liver disease.

A

Delirium tremens (withdrawal symptoms) commonly seen 12-48 hours after alcohol withdrawal: seizures, insomnia, vomiting, headache, sweating, palpitations and tremulousness. Treated with diazepam.

Wernicke-Korsakoff encephalopathy. Triad of:
•	Confusion
•	Ataxia
•	Nystagmus.
Give IV thiamine to prevent.
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43
Q

What is non-alcoholic fatty liver disease likely caused by?

A

Insulin resistance.

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44
Q

Who does non-alcoholic fatty liver disease affect?

A 
Affects individuals with metabolic syndromes:
•	Obesity
•	Hypertension
•	Diabetes
•	Hyperlipidaemia
•	Hypertriglyceridaemia.
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45
Q

What are the risk factors for non-alcoholic fatty liver disease?

A
  • Obesity (70%)
  • Diabetes (35-75%)
  • Hyperlipidaemia (20-80%).
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46
Q

What is the pathophysiology of non-alcoholic fatty liver?

A

Results from fat deposition in the liver.
Healthy -> steatosis -> steatohepatitis -> fibrosis and cirrhosis.

Non-alcoholic steatohepatitis (NASH) is fat sometimes with inflammation and fibrosis. Is an important cause of “cryptogenic” cirrhosis.

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47
Q

What are the symptoms of non-alcoholic fatty liver?

A 
Usually no symptoms, liver ache in 10%.
•	Fatigue and malaise
•	RUQ pain
•	Jaundice
•	Hepatomegaly.
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48
Q

What do LFTs show in non-alcoholic fatty liver?

A

Commonest cause of mildly elevated LFTs, raised ALT and sometimes AST.

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49
Q

What investigation distinguishes between NASH and NAFL?

A

Liver biopsy.

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50
Q

What is the management for non-alcoholic fatty liver?

A

Still no effective drug treatments. Weight loss works, the more the better.

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51
Q

What is acute pancreatitis?

A

Sudden inflammation and haemorrhaging of the pancreas due to its own digestive enzymes (autodigestion). Usually reversible.

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52
Q

What are the causes of pancreatitis?

A 
Remember I GET SMASHED:
I diopathic
G all stones
E thanol (alcohol)
T rauma (kinfe wound injury)
S teroids
M umps/malignancy
A utoimmune e.g. SLE
S corpion stings
H hyperlipidaemia and hypercalcaemia
E ndoscopic retrograde cholangiopancreatography
D rugs e.g. azathioprine, metronidazole, tetracycline, furosemide.
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53
Q

What is the pathophysiology of acute pancreatitis?

A

The pancreases releases exocrine enzymes that cause autodigestion of the organ. Final common pathway is increased intracellular calcium which causes the activation of intra-cellular proteases and the release of pancreatic enzymes. This can lead to acinar cell injury and necrosis which causes inflammatory cells and the release of mediators and cytokines to produce local inflammatory response. Can progress to multiple organ failure.

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54
Q

What is the pathophysiology of alcoholic induced acute pancreatitis?

A
  • Increases zymogen secretion from acinar cells while decreasing fluid and bicarbonate in the ducts so thick and viscous pancreatic juice which can obstruct the pancreatic duct
  • Blocked duct causes pancreatic juices to become backed up which increases pressure and may distend the ducts
  • Zymogen granules may fuse with lysosomes which brings trypsinogen into contact with lysosomal enzymes converting it to trypsin and so digestive enzyme cascade activation and autodigestion of pancreas (acute pancreatitis)
  • Alcohol also stimulates cytokine release so immune response and neutrophils release superoxides and proteases.
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55
Q

What is the pathophysiology of gallstone induced pancreatitis?

A
  • Become lodged in the sphincter of Odi which blocks release of pancreatic juices
  • Block the bile duct causing back pressure in the pancreatic duct
  • Similar to alcohol.
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56
Q

What are the symptoms of acute pancreatitis?

A
  • Epigastric pain radiating to the back, relieved by sitting forwards
  • Nausea and vomiting
  • Coma and multiple organ failure are possible and may delay diagnosis.
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57
Q

What are the signs of acute pancreatitis?

A
  • Cullen’s sign (bruising around periumbilical region), this ecchymoses suggests necrotising
  • Grey Turner’s sign (bruising on flanks), this ecchymoses suggests necrotising
  • Tachycardia
  • Abdominal guarding and tenderness
  • Distension.
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58
Q

What enzyme is massively raised in acute pancreatitis?

A

Amylase.

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59
Q

What do the LFTs show in acute pancreatitis?

A
  • Raised serum amylase (3x more than normal)
  • Raised serum lipase (more sensitive than amylase)
  • Lipase to amylase >2 suggests alcoholic
  • Raised ALT and AST
  • Elevated ALT >150 suggests gallstones.
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60
Q

What would show on an abdominal X-ray in acute pancreatitis?

A

Abdominal X-ray shows no psoas shadow (raised retroperitoneal fluid).

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61
Q

What is the management for acute pancreatitis?

A
  • NG tube
  • IV fluid and maintain electrolyte balance
  • Pain relief
  • May need bowel rest
  • Treat complications.
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62
Q

What are the complications of acute pancreatitis?

A
  • Acute respiratory distress syndrome is the leading cause of death
  • Sepsis
  • Pancreatic pseudocyst
  • Hypovolaemic shock from ruptured vessels
  • DIC
  • Pancreatic necrosis
  • Pancreatic ascites
  • Pancreatic abscess.
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63
Q

What is chronic pancreatitis?

A

Persistent inflammation due to structure changes such as fibrosis, atrophy and calcification. Generally irreversible.

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64
Q

What are the 2 types of chronic pancreatitis?

A
  • Large duct pancreatitis

* Small duct pancreatitis: tends not to be associated with calcification.

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65
Q

What care the causes of chronic pancreatitis?

A
  • Repeated bouts of acute pancreatitis
  • Alcohol abuse
  • Cystic fibrosis (main cause in children)
  • Tumours
  • Pancreatic trauma (knife wound).
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66
Q

What is the pathophysiology of chronic pancreatitis?

A

Inappropriate activation (possibly prompted by alcohol) of enzymes within the pancreas leads to precipitation of protein plugs within the duct lumen, forming a nidus for calcification. This leads to ductal hypertension, and therefore pancreatic damage. In addition to cytokine activation, this causes pancreatic inflammation, morphological change and possible permanent loss of function. End result is pancreatic fibrosis.

With each bout of acute pancreatitis there is the potential for ductal dilatation and damage to pancreatic tissue.

Stellate cells lay down fibrotic tissue which causes narrowing of ducts and acinar cell atrophy.

In conditions like alcoholic acute pancreatitis, calcium deposits of various sizes can accumulate on plugs that form the ducts.

Healthy tissue is replaced by misshapen ducts, fibrosis and calcium deposits is chronic pancreatitis.

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67
Q

What are the symptoms of chronic pancreatitis?

A
  • Epigastric pain that radiations to back, may be linked to eating meals
  • Nausea and vomiting.
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68
Q

What are the signs of chronic pancreatitis?

A

Jaundice possible due to obstruction of the common bile duct.

Malabsorption due to endocrine dysfunction:
• Weight loss
• Steatorrhea
• Vitamin deficiency.
Exocrine dysfunction:
• Diabetes mellitus.
These are due to insulin and lipase deficiency.

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69
Q

What are the investigations in chronic pancreatitis?

A
  • CT abdomen
  • Abdominal ultrasound
  • Abdominal X-ray to show calcifications
  • ERCP/MRCP
  • Bloods: may show low lipase and amylase as there may not be enough healthy tissue to make the enzymes. Faeceal elastase.
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70
Q

What is the management for chronic pancreatitis?

A

Lifestyle modification: less alcohol, healthier diet, more exercise.
Pain control.
Replace digestive enzymes (aids functionality and pain by down regulating the release of pancreatic enzymes) and nutritional supplements.
Insulin for diabetes.
Local resection to alleviate duct dilatation/duct stones.

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71
Q

What is the complication of chronic pancreatitis?

A

Diabetes.

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72
Q

What is biliary colic?

A

The term used for pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder.

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73
Q

What are the symptoms of biliary colic?

A

The pain of stone-induced ductular obstruction is of sudden onset, severe but constant and has a crescendo characteristic.

Pain is temporary and stops when gallstone dislodges.

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74
Q

What is cholecystitis?

A

Inflammation of the gallbladder.

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75
Q

What causes cholecystitis?

A

Gallstone impaction into the cystic duct or gallbladder neck.

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76
Q

What is the pathophysiology of cholecystitis?

A

Large fatty meals stimulate CCK which signals bile release from the gall bladder. When the GB has a gallstone in it, the squeezing of the GB can get it lodged in the cystic duct. Bile stasis becomes a chemical irritant and stimulates mucosa in wall to release mucus and inflammatory enzymes which causes inflammation, distension and pressure build up. Bacteria can start to grow e.g. E. coli and invade into gallbladder wall to cause peritonitis.

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77
Q

What are the symptoms of cholecystitis?

A
  • Midepigastric to RUQ pain
  • Fever
  • Nausea and vomiting.
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78
Q

What are the signs of cholecystitis?

A
  • Murphy’s sign: tenderness that is worse on inspiration

* Muscle guarding.

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79
Q

What investigations are performed in cholecystitis?

A
  • Ultrasound of abdomen
  • FBC: high WBC count (leucocytosis)
  • LFTs: to exclude liver/bile duct pathology.
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80
Q

What is the management of cholecystitis?

A
  • Laparoscopic cholecystectomy

* Analgesia and fluids if needed.

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81
Q

What is the complication of cholecystitis?

A

Peritonitis.

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82
Q

What generally causes ascending cholangitis?

A

Gallstones.

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83
Q

What are the causes of ascending cholangitis?

A

Generally caused by gallstones.

Infection of the biliary tree e.g. E.Coli, Klebsiella, enterococcus (group D strep). Most often secondary to common bile duct obstruction by gallstones (choledocholithiasis).

Benign biliary strictures, often following surgery, malignancy or associated chronic pancreatitis.

Primary sclerosing cholangitis.

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84
Q

What are the risk factors for ascending cholangitis?

A
  • Fair (Northern European and Hispanic)
  • Female
  • Fat (obese)
  • Fertile (pregnancy, under 40).
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85
Q

What is the pathophysiology of ascending cholangitis?

A

Normally bacteria can’t go up the common bile duct as bile and pancreatic juices travel down and flush bacteria out. Obstruction of the common bile duct causes stasis of bile and invasion of bacteria from duodenum. This increases susceptibility to infection. High pressure on the common bile duct due to obstruction can causes spaces between the cells which allows the bacteria and the bile access to the blood stream which can cause bacteraemia and jaundice.

Can be obstructed by stone, cancer, stricture, parasite (ascaris). Also, infection can be introduced through intervention e.g. ERCP.

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86
Q

What are the symptoms of ascending cholangitis?

A

Charcot’s triad:
• Jaundice: dark urine and pale stools
• RUQ pain
• Fever.

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87
Q

What are the signs of ascending cholangitis?

A 
Reynold’s pentad:
•	Jaundice
•	RUQ pain
•	Fever
•	Shock: hypotension and tachycardia
•	Confusion (bacteraemia causes septic shock so leaky vessels and hypotension so less blood to organs such as the brain and confusion).

Also rigors.

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88
Q

What is the definitive investigation for ascending cholangitis?

A

Endoscopic Retrograde Cholangiopancreatography (ECRP).

Can remove blockage.

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89
Q

What is very high if there is a bile duct obstruction?

A

Bilirubin.

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90
Q

What are the investigations in ascending cholangitis?

A
  • Ultrasound abdomen to detect stone/stent/stricture
  • FBC: raised WBCs, ESR and CRP, raised serum bilirubin (very high if bile duct obstruction) and serum alkaline phosphatase, ALP, AST, ALT
  • ERCP is definitive. Can remove blockage
  • Magnetic resonance cholangiopancreatography (MRCP) to locate stone
  • LFTs
  • CT
  • Blood culture if septic.
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91
Q

What are the differentials for ascending cholangitis?

A

Biliary colic: RUQ pain only

Cholecystitis: RUQ pain and maybe fever.

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92
Q

What is the management for ascending cholangitis?

A
  • IV antibiotics e.g. co-amoxiclav
  • Fluids
  • ERCP (endoscopic retrograde cholangiopancreatography to image/stent/remove stone
  • Shockwave lithotripsy
  • If this fails then laparoscopic/open cholecystectomy.
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93
Q

What is the complication of ascending cholangitis?

A

Sepsis.

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94
Q

What does bile contain?

A

Bile contains cholesterol, bile pigments (broken down from Hb) and phospholipids.

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95
Q

When do gallstones typically present?

A

<30. More common in Females.

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96
Q

What are the 2 types of gallstone?

A

Cholesterol gallstones (more common):
• Cholesterol supersaturation
• Nucleation factors
• Reduced gallbladder motility.

Pigmen gallstones:
• Chronic haemolysis (sphereocytosis and sickle cell) in which bilirubin production is increased
• Cirrhosis
• Possible as a complication of cholecystectomy and with duct strictures.

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97
Q

What are the risk factors for gallstones?

A
  • Female
  • Fat
  • Fertile (pregnancy)
  • Family history
  • Forty (age)
  • Obesity
  • Smoking.
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98
Q

What is the pathophysiology of cholesterol gallstones?

A
  • Cholesterol is held in solution by detergent action of bile salts and phospholipids which forms micelles and vesicles
  • Only form in bile which has an excess of cholesterol (lithogenic bile) where there is a relative lack of bile salts and phospholipids
  • The formation of cholesterol crystals and gallstones in lithogenic bile is promoted by factors that favour nucleation such as mucus and calcium
  • Gallstone formation further promoted by reduced gallbladder motility and stasis.
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99
Q

What is the pathophysiology of pigment gallstones?

A
  • Consist of bilirubin polymers and calcium bilirubinate
  • Caused by excess of bilirubin
  • Seen in patients with chronic haemolysis (e.g. hereditary spherocytosis and sickle cell disease) in which bilirubin production is increased and cirrhosis
  • Pigment stones may also form in bile ducts after.
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100
Q

What are the symptoms of gallstones?

A

Majority of gallstones are asymptomatic.

Biliary or gallstone colic: sudden, severe but constant epigastric pain (may have a RUQ component and may radiate over right shoulder and scapular region). Pain usually increases for around 15 minutes, stays constant for a few hours then decreases once the stone has dislodged. Starts several hours after a meal. May be worse at night. Caused by a gallstone impacting on the cystic duct or the ampulla of vater.

Second most common is acute cholecystitis where distension of the gallbladder causes necrosis and ischaemia.

Nausea and vomiting and sweating.

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101
Q

Where is the pain in biliary/gallstone colic?

A

Sudden, severe but constant epigastric pain (may have a RUQ component and may radiate over right shoulder and scapular region).

102
Q

When does biliary colic pain begin?

A

Several hours after a meal.

103
Q

What is the management for gallstones?

A

Ursodeoxycholic acid decreases cholesterol

Gallbladder stones: laparoscopic cholecystectomy and bile acid dissolution therapy (<1/3 success).

Bile duct stones: ERCP with sphincterotomy and removal (basket or balloon), crushing (mechanical or laser) and stent replacement.

IV antibiotics if necessary.

Surgery for large stones.

104
Q

What are the complications of gallstones?

A
  • Jaundice if biliary obstruction
  • Acute cholecystitis is cystic duct impaction
  • Pancreatitis if blocks pancreatic duct
  • Gallstone ileus if occludes intestinal lumen
  • Empyema is obstructed gallbladder fills with pus
  • Cholangitis if inflammation of the gallbladder as a result of bile duct blockage.
105
Q

What is viral hepatitis?

A

Inflammation of the liver. Acute is onset to 6 months. Chronic is over 6 months.

106
Q

What causes acute hepatitis?

A 
Viral infection:
•	Hep A, B +/- D, C and E
•	Herpes virus e.g. HSV, VZV, EBV, CMV
•	Other viruses.
Non-viral infection:
•	Spirochaetes e.g. leptospirosis
•	Mycobacteria e.g. TB
•	Parasite e.g. toxoplasma
•	Bacteria e.g. Coxiella (Q fever).
Non-infection:
•	Alcohol
•	Non-alcohol fatty liver disease
•	Drugs
•	Toxins/poisoning
•	Pregnancy
•	Autoimmune 
•	Hereditary metabolic.
107
Q

What causes chronic hepatitis?

A 
Infection:
•	Hep B+/- D
•	Hep C
•	Hep E especially if a patient is immunocompromised
Non-infection: 
•	Alcohol
•	Non-alcohol fatty liver
•	Drugs
•	Toxins
•	Autoimmune
•	Hereditary metabolic.
108
Q

What are the symptoms of acute hepatitis?

A
  • Can be asymptomatic
  • General malaise
  • Myalgia
  • GI upset
  • Abdominal pain.
109
Q

What are the signs of acute hepatitis?

A
  • +/- jaundice (pale stools, dark urine)
  • Tender hepatomegaly
  • Raised AST, ALT +/- bilirubin.
110
Q

What are the signs of chronic hepatitis?

A
  • +/- signs of chronic liver disease: clubbing, palmar erythema, Dupuytren’s contracture, spider naevi
  • LFTs can be normal even in context of cirrhosis
  • Initially in cirrhotic patient, liver disease is compensated so liver function is maintain with normal albumin and clotting
  • Decompensated is with jaundice, ascites, low albumin, coagulopathy, encephalopathy.
111
Q

What are the complications of hepatitis?

A
  • Hepatocellular carcinoma
  • Portal hypertension
  • Varices
  • Bleeding.
112
Q

What vaccinations are available for hepatitis?

A

A for travellers and B in immunisation.

113
Q

What is Hepatitis A?

A

RNA virus. Acute only. Notifiable disease.

114
Q

What is the most common acute viral hepatitis in the world?

A

Hepatitis A.

115
Q

What are the risk factors for Hepatitis A?

A
  • Shellfish
  • Travellers
  • Food handlers.
116
Q

What is the pathophysiology of Hepatitis A?

A

Hep A is a picornavirus. It replicates in the liver, is excreted in bile and then excreted in faeces for around 2 weeks before the onset of clinical illness and up to 7 days after.

Disease is maximally infectious just before the onset of jaundice. Short incubation period of 2-6 weeks.

Causes acute hepatitis only.

Transmitted by faeco-oral route by ingestion of contaminated food or water.

117
Q

What are the symptoms of hepatitis A?

A 
Pre-icteric phase: constitutional (non-specific) symptoms + abdominal pain.
Icteric phase (few days to 1 week later): jaundice and hepatosplenomegaly.
118
Q

What is immunity like after Hepatitis A?

A

100%.

119
Q

What antibodies are tested for in Hepatitis A?

A

Antibody tests for HAV antibodies. Initial antibody produced is anti-HAV IgM (non-specific) then replaced by longer lasting HAV-IgG.

120
Q

What do the bloods show in Hepatitis A?

A
  • FBC shows reduced WBC count

* Raised ESR.

121
Q

What does the liver biochemistry show in Hepatitis A?

A
  • Prodromal stage: normal serum bilirubin, raised serum AST or ALT
  • Icteric stage: once jaundice has presented, serum bilirubin reflects level of jaundice.
122
Q

What is the management for Hepatitis A?

A
  • Supportive
  • Monitor liver function (INR, albumin, bilirubin, etc.)
  • Fulminant hepatic failure/acute liver failure (0.35%)
  • Management of close contacts (human normal immunoglobulin (HNIG), vaccine).
123
Q

What is the primary prevention for Hepatitis A?

A

Hep A vaccination, 6-12 months after first (e.g. travellers, MSMs, IDUs).

124
Q

What is Hepatitis E?

A

RNA virus and acute only (can be chronic in immunosuppressed).

125
Q

Who is Hepatitis E more common in?

A

Older men.

More common than Hepatitis A in the UK.

126
Q

What is the genotype in Hepatitis E?

A

GT.

127
Q

What are the symptoms for Hepatitis E?

A
  • > 95% cases asymptomatic
  • Usually self-limiting acute hepatitis (fulminant hepatitis rare but increased risk in pregnancy with GT1/2) and occasional acute-on-chronic liver failure (high mortality)
  • Extra hepatic manifestations e.g. neurological
  • Risk of chronic infection (Genotype 3/4 only) in immunosuppressed patients e.g. transplant recipients, HIV patients. Rapid progression to cirrhosis and fibrosis.
128
Q

What antibodies are involved in Hepatitis E?

A

HEV.

129
Q

What is the transmission for Hepatitis E?

A

Faeco-oral route which is water or food-borne. Found in undercooked pork.

130
Q

What is the investigation for Hepatitis E?

A

Nucleic acid amplification test.

131
Q

What is the treatment for Hepatitis E?

A

Acute infection:
• Supportive
• If someone develops fulminant hepatitis/acute-on-chronic liver failure then liaise with hepatology/liver transplant centre and consider ribavirin which is anti-viral medication.
Chronic infection (in the immunosuppressed):
• Reverse immunosuppression if possible
• If HEV RNA persists then treat with ribavirin.

132
Q

What is Hepatitis B?

A

DNA virus and acute + chronic hepatitis.

133
Q

Where is Hepatitis found?

A

Semen and saliva.

134
Q

What are the risk factors for Hepatitis B?

A
  • Healthcare personnel
  • Emergency and rescue teams
  • CKD/dialysis patients
  • Travellers
  • Homosexual men
  • IV drug users.
135
Q

What is the pathophysiology of Hepatitis B?

A
  • The complete virus comprises of an inner core or nucleocapsid surrounded by an outer envelope of surface protein (Hep B surface antigen HBsAg)
  • HBsAg produced in excess by infected hepatocytes and can exist separately from whole vision in serum and body fluid
  • After penetration into hepatocytes, the virus loses its coat and the virus core is transported to the nucleus without processing
  • Both cirrhosis and chronic infection can lead to hepatocellular carcinoma which is very bad and the main cause of death in Hep B patients
  • This chronic Hep B will result in continuing hepatocellular damage.
136
Q

What is the transmission for Hepatitis B?

A 
Blood-borne transmission:
•	Needle stick
•	Tattoos
•	Sexual 
•	Blood products
•	IV drug abusers
•	Vertical transmission from mother to child in utero or soon after birth.
137
Q

When is antibody produced in Hepatitis B?

A

Majority will clear surface antigen (HBsAg) within 6 months and will produce surface antibody to show they’ve been exposed to infection.
1-5% of immunocompetent will get chronic infection.

138
Q

What are the symptoms of Hepatitis B?

A 
Pre-icteric phase: constitutional (non-specific) symptoms + abdominal pain
Icteric phase (few days to 1 week later): jaundice and hepatosplenomegaly.
139
Q

What are the antibody tests in Hepatitis B?

A

Antibody tests (Hepatitis B surface antigen):
• HBsAg present 1-6 months after exposure
• HBsAg present for more than 6 months implies carrier status
• Anti-HBs are antibodies to Hepatitis B.

140
Q

What is the management for Hepatitis B?

A

Acute:
• Supportive
• Monitor liver function
• Fulminant hepatic failure (0.1%-0.5%): consider oral nucleoside analogue e.g. tenofovir, entecavir and liaise with hepatology/liver transplant centre
• Management of contacts (HV vaccine +/-HBIG).

Chronic:
• Pegylated interferon-alpha 2a: immunomodulatory stimulates the immune response. Weekly subcutaneous injection and 48 week long treatment course. Offers best chance of treatment-free control. Side effects: myalgia flu like symptoms, low WBC and platelets, mental health disturbance, autoimmune disease (thyroid, diabetes)
• Nucleoside analogues e.g. tenofovir, entecavir : inhibit viral replication. One tablet once a day. High barrier to resistance, minimal side effects, renal monitoring (TDF), may be required lifelong. Not a cure.

141
Q

What is Hepatitis D?

A

Incomplete RNA virus and acute + chronic hepatitis.

142
Q

What does Hepatitis D require?

A

HBV for assembly.

143
Q

What are the risk factors for Hepatitis D?

A
  • Healthcare personnel
  • Emergency and rescue teams
  • CKD/dialysis patients
  • Travellers
  • Homosexual men
  • IV drug users.
144
Q

What are the symptoms of Hepatitis D?

A 
Pre-icteric phase: constitutional (non-specific) symptoms + abdominal pain
Icteric phase (few days to 1 week later): jaundice and hepatosplenomegaly.
145
Q

What is the transmission of Hepatitis D?

A

Blood-borne.

146
Q

What is the pathophysiology of Hepatitis D?

A

Hepatitis D virus is an incomplete RNA particle enclosed in a shell of HBsAg.
Virus is unable to replicate on its own but is activated by the presence of HBV. If acquired simultaneously with HBV (co-infection) causes increased severity of acute infection.
Co-infection:
• Infection of HBV + HBD
• Clinically indistinguishable from acute icteric (jaundice) HBV infection
• Serum IgM anti-HDV in the presence of IgM anti-HBV confirms co-infection
Superinfection:
• When someone with chronic HBV gets HDV this causes secondary acute hepatitis with increased rate of liver fibrosis progression.

147
Q

What are the investigations in Hepatitis D?

A

Antibody tests.

Hepatitis D antibody and if positive, test HDV RNA.

148
Q

What is the management in Hepatitis D?

A
  • Pegylated interferon-α (future: Myrcludex B) only affected in 30% of patients
  • Can be acquired simultaneously with HBV (increased risk of fulminant hepatitis in acute infection)
  • Alternatively acquired after HBV: acute on chronic hepatitis and accelerated progression to liver fibrosis.
149
Q

What is Hepatitis C?

A

RNA flavivirus and acute + chronic hepatitis.

150
Q

What are the risk factors for Hepatitis C?

A

IV drug users and receiving blood products.

151
Q

What are the complications of Hepatitis C?

A

Can result in chronic hepatitis and therefore high risk of hepatocellular carcinoma.

152
Q

What is the route of transmission for Hepatitis C?

A

Blood borne.

153
Q

What are the investigations for Hepatitis C?

A

Hepatitis C testing (HCV ab):
• If not detected, no recent HCV exposure
• Can be negative in acute infection and in immunocompromised patients
• If detected, HCV exposure.

HCV RNA:
• Not detected means no current HCV
• Detected means current HCV.

154
Q

What is the management for Hepatitis C?

A 
Directly acting anti-virals (DAAs):
Combination of DAAs from two or more of three drug classes, usually combined with ribavirin (RBV): NS5A (-asvir), NS5B (-buvir) and NS3/4A protease (-previr) inhibitors.
High SVR12 (cure) rates, >95% in non-cirrhotic patients.
155
Q

What is immunity like in Hepatitis C?

A

Previous infection does not confer immunity and can be re-infected.

156
Q

Is autoimmune hepatitis acute or chronic?

A

Can be both.

157
Q

Who is autoimmune hepatitis more common in?

A

Females.

158
Q

What are the investigations in autoimmune hepatitis?

A

Type 1: anti-nuclear antibody (ANA), anti-smooth muscle antibody (ASMA).
Type 2: anti-LKM-1 or anti-liver cystolic-1 (anti-LC-1) antibodies
Liver biopsy.

159
Q

What is the management for autoimmune hepatitis?

A

Immunosuppression: prednisolone +/- azathioprine.

160
Q

What is raised in hepatocellular carcinoma?

A

AFP.

161
Q

What is the treatment for hepatocellular carcinoma?

A
  • Surgical resection
  • Radiofrequency ablation
  • TACE, chemotherapy.
162
Q

Where do most pancreatic cancers occur?

A

Exocrine component of the pancreas.

163
Q

What is the majority of pancreatic cancers?

A

Majority are adenocarcinoma and are of ductal origin.

164
Q

What are the risk factors for pancreatic cancer?

A
  • Smoking
  • Excessive alcohol or coffee intake
  • Excessive use of aspirin
  • Diabetes
  • Chronic pancreatitis
  • Family history
  • Genetic mutations: presence of PRSS-1 mutation.
165
Q

Where do pancreatic cancers arise?

A
  • Originates in ductal epithelium and evolves from pre-malignant lesions to full-invasive cancer
  • 60% arise in pancreatic head
  • 25% arise in body
  • 15% arise in tail.
166
Q

What are the symptoms of pancreatic cancer?

A 
•	Anorexia
•	Weight loss
•	Acute pancreatitis.
Body and tail of pancreas:
•	Epigastric pain that radiates to bac that is relieved by sitting forward
Head of pancreas:
•	Painless jaundice
•	Weight loss.
167
Q

What are the investigations for pancreatic cancer?

A
  • Abdominal ultrasound or CT

* Biopsy.

168
Q

What is the management for pancreatic cancer?

A
  • Surgery

* Palliative therapy.

169
Q

What is haemochromatosis?

A

Deficiency of the iron regulatory hormone hepcidin which leads to iron overload.

170
Q

What is the cause of haemochromatosis?

A

Genetic disorder. 90% have mutations in HFE gene: C282Y, H63D. Autosomal recessive, incomplete penetrance.

171
Q

What is the pathophysiology of haemochromatosis?

A

Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas. Leads to fibrosis and functional organ failure.

172
Q

What are the symptoms of haemachromatosis?

A 
Often asymptomatic until later.
•	Fatigue
•	Weakness
•	Arthropathy
•	Heart problems.
Advanced disease:
•	Bronzing of the skin
•	Diabetes
•	Hepatomegaly
•	Athropathy.
173
Q

What suggests a diagnosis of haemachromatosis?

A

Diagnosis suggested by raised ferritin and transferrin saturation, confirmed by HFE genotyping and liver biopsy. Total iron binding capacity reduced and serum iron raised. LFTs can be normal.

174
Q

What is the prognosis for haemachromatosis?

A

If cirrhosis:
• Present, risk of hepatocellular carcinoma
• Not present and treated, normal life expectancy.

175
Q

What is the management for haemachromatosis?

A

Management Iron removal may lead to regression of fibrosis.

Phlebotomy (removal of blood ever 2 weeks. Tends to require insulin.

176
Q

What is Wilson’s disease?

A

Disorder of copper metabolism causes copper build up in the liver.

Story: 
Wilson liked to count his coppers. Until one day he got acute hepatitis. His friend Kay was a flasher in the lights (Slit lamps and Kayser-Fleischer rings). She had loads of energy and was from class 7B (ATP7B). She gave Jason Derulo (Caeruloplasmin) a sunflower (sunflower cataracts) but he wasn’t impressed. He still zinged (zinc) her phone through until he found a replacement (transplant). Wilson was mad (neurological symptoms) and had a statue made (bronze skin).
177
Q

When is the onset of Wilson’s disease?

A

Onset usually in 20-30s.

178
Q

What is the cause of Wilson’s disease?

A

Mutation in ATP7B. Autosomal recessive.

179
Q

What are the symptoms of Wilson’s disease?

A

Hepatic:
• Acute liver failure
• Chronic hepatitis.
Psychological:
• Behavioural problems common, might lead to diagnosis.
Eyes:
• Kayser-Fleischer ring (bronze ring on the cornea), usually seen on examination with a slit lamp
• Sunflower cataracts also seen with a slit lamp.

180
Q

What is the pathophysiology of Wilson’s disease.

A

ATP7B codes for a P type ATPase which acts in hepatocytes to move copper across intracellular membranes. Copper transporting action directly supports production of ferroxidase caeruloplasmin, as well as secretion of copper into bile. Serum levels of copper are low. Hepatic retention of copper develops which causes liver injury (cirrhosis, failure).

181
Q

What are the investigations for Wilson’s disease?

A

Slit lamp analysis of eyes to detect Kayser-Fleischer rings.

Low serum caeruloplasmin.

182
Q

What is the management for Wilson’s disease?

A

Avoid alcohol.
Prevent intestinal copper absorption: chelation agents such as zinc.
Hepatic: around 5% of those who present with liver failure will need a transplant.
Neurology: deep brain stimulation.

183
Q

What is alpha-1-antitrypsin deficiency?

A

Disease of serine protease inhibitor alpha-1-antitrypsin.

184
Q

What are the symptoms of alpha-1-antitrypsin deficiency?

A

Lungs: presents between 30-50 (younger in smokers)
• COPD like symptoms
• Early onset emphysema.
Liver:
• Not always present
• Neonates may present jaundice and hepatitis
• Possible cirrhosis and liver failure.

185
Q

What is the cause of alpha-1-antitrypsin deficiency?

A

Mutation in SERPINA1 gene. Autosomal recessive, low penetrance.

186
Q

What is the pathophysiology of alpha-1-antitrypsin deficiency?

A

A1AT inhibits the action of neutrophil-protease enzymes in the lung, produced in the presence of inflammation, infection or smoking. In deficiency, elastase can break elastin without inhibition, so destroys alveolar walls and causes emphysematous change.

187
Q

What is the investigation in alpha-1-antitrypsin deficiency?

A

Serum levels of A1AT.

188
Q

What is the management for alpha-1-antitrypsin deficiency?

A

Lung: as COPD, cessate smoking, corticosteroids, bronchodilators, treat infection.
Liver: cessate drinking. In liver failure, possibly transplant.

189
Q

What is peritonitis?

A

Inflammation of the peritoneum.
Generalised inflammation of abdominal cavity.
Peritonism is the tensing of muscles to prevent movement of the peritoneum.

190
Q

What are the 2 types of peritoneum?

A

Parietal peritoneum:
• Covers the abdominal wall
• Somatic innervation
• Sensation is well localised.

Visceral peritoneum:
• On organs e.g. stomach, liver and colon
• Autonomic innervation
• Sensation is not well localised.

191
Q

What are the causes of peritonitis?

A
  • A ppendicitis: umbilicus to RIF pain
  • E ctopic pregnancy: low abdominal pain, sudden onset, tachycardia, low BP
  • I nfection with TB (Bacterial is most common. Gram-negative e.g. E. Coli and Klebsiella. Gram-positive staphylococcus e.g. S. Aureus)
  • O bstruction: colicky pain, history of abdominal surgery
  • U lcer: epigastric pain radiating to shoulder
  • Peritoneal dialysis.
192
Q

What are the causes of inflammation in peritonitis?

A
  • Inflamed organ
  • Air: ulcers, stabbings
  • Pus
  • Faces
  • Luminal contents: not faeces until it reaches colon
  • Blood: usually spleen.
193
Q

What are the common causes of abdominal pain?

A
  • Gastritis: epigastric pain
  • Cholecystitis: right hypochondrium, mid-clavicular line
  • Pancreatitis: midway between epigastric and umbilicus
  • Appendicitis: right iliac fossa
  • Diverticulitis: left iliac fossa.
194
Q

What are the risk factors?

A

Appendicitis.

195
Q

What are the symptoms of peritonitis?

A
  • Dull pain that becomes sharp

* Systemic symptoms and generally unwell.

196
Q

What are the signs of peritonitis?

A
  • Pain relieved by resting hands on abdomen, stops movement of peritoneum and therefore pain
  • Guarding/rebound tenderness
  • Absence of bowel sounds
  • Rigid abdomen
  • Pain worse on coughing or moving
  • Patient wants to lie still
  • Sepsis/septic shock: hypotension, tachycardia, oliguria, fever.
197
Q

What are the investigations for peritonitis?

A
  • CT Scan
  • Clinical examination: rigid and guarding, laying still
  • Abdominal XR: dilated bowel, flat fluid level, gas under diaphragm
  • Bloods: FBCs, U&Es, LFTs, clotting factors
  • Ascitic tap: high neutrophil count.
198
Q

What is the treatment for peritonitis?

A
  • Broad spectrum antibiotics: metronidazole
  • Fluid resuscitation: IV fluids and electrolytes
  • Urinary catheter
  • Surgery: laparotomy i.e. big cut, laparoscopy i.e. key-hole surgery. Treat problem: patch hole, remove organ/cause. Wash-out infection.
199
Q

What are the complications of peritonitis?

A

Sepsis: peritoneum is thin, has a large SA and is well drained by lymphatics. Suspect sepsis if BP is low.

200
Q

What are ascites?

A

Abnormal accumulation of fluid within the abdominal cavity.

201
Q

What are the causes of ascites?

A

Impaired blood outflow:
• Fluid cannot move forward through system e.g. due to a clot
• Raised pressure and vessels causing fluid to leak out of vessels
• Seen in: cirrhosis i.e. portal hypertension, Budd-Chiari syndrome (occlusion of hepatic veins that drain liver), cardiac failure, constrictive pericarditis.
Decreased oncotic pressure, low protein:
• With less protein e.g. albumin, there is an inability to pull fluid back into intravascular space
• This fluid then accumulates in peritoneum
• Seen in: hypoalbuminaemia, nephrotic syndrome and malnutrition
Local inflammation e.g. peritonitis.

202
Q

What are the risk factors for ascites?

A
  • High sodium diet
  • Hepatocellular carcinoma
  • Splanchnic vein thrombosis resulting in portal hypertension.
203
Q

What is the pathophysiology of ascites?

A

High protein fluid (exudate, extremely bad):
• Cloudy fluid
• Low serum to ascites albumin gradient
• Causes: peritoneal cause e.g. cancer, sepsis, TB and nephrotic syndrome.

Low protein fluid (transudate):
• Clear fluid
• High serum to ascites albumin gradient (>11g/L)
• Outflow problem (i.e. portal hypertension)
• Decreased oncotic pressure
• No issues with cell membrane
• Caused by cirrhosis
• Management is to treat underlying cause, diet, diuretic and drainage.

204
Q

What are the symptoms of ascites?

A
  • Severe pain, suspect bacterial peritonitis

* Abdominal swelling.

205
Q

What are the signs of ascites?

A
  • Shifting dullness: patient lies on back and percuss left flank (will sound dull), get them to lie on side and percuss again (will sound resonant as fluid moved)
  • Abdominal distension
  • Protruding ascites
  • Presence of raised veins
  • Flank dullness
  • Fluid thrill
  • Bulging flanks.
206
Q

What are the investigations for ascites?

A
  • Ascitic tap: culture, gram stain, cytology, protein
  • Ultrasound
  • Presence of fluid confirmed by demonstrating shifting dullness.
207
Q

What is the management for ascites?

A
  • Treat underlying cause
  • Reduce sodium to help liver and reduce fluid
  • Diuretic: oral spironolactone (spares K+) ± Furosemide
  • Paracentesis (drain fluid).
208
Q

What are the complications of ascites?

A

Spontaneous Bacterial Peritonitis: suspect in any ascitic patient that deteriorates
• Bugs: E. Coli, Klebsiella, Enterococcus
• Investigations: Ascitic tap shows raised neutrophils
• Management: cefotaxime
• Prophylaxis: ciprofloxacin.

209
Q

What are the types of liver abscess?

A

Bacterial: faecal flora e.g. E. coli, Klebsiella spp etc.

Ameobic: entamoeba histolytica
• RUQ pain, fever, pyrexia of unknown origin
• Seen on ultrasound or CT
• Antibiotics and drainage.

Hydatid: echinococcus granulosa (Dog tapeworm)
• Insidious RUQ pain, eosinophilia
• Rupture which causes anaphylactic shock
• Albendazole and PAIR.

210
Q

What is a hernia?

A

Protrusion of organ or tissue out of the body cavity it normally lies in.

211
Q

What are the types of hernia?

A
  • Reducible hernia: can be pushed back into abdominal cavity with manual manoeuvring
  • Irreducible: cannot be pushed back in. Obstructed is where the intestine is obstructed within hernia due to pressure from edges of hernia but blood flow is maintained. Incarcerated is where the contents of hernial sac are stuck inside by adhesions e.g. adhesions between the intestines and hernial sac
  • Strangulated: blood supply of the sac is cut off resulting in ischaemia. ± gangrene/perforation of hernial contents.
212
Q

What are the causes of hernias?

A
  • Muscle weakness: age trauma.

* Body strain: constipation, heavy lifting, pregnancy, chronic cough.

213
Q

What is an inguinal hernia?

A

Protrusion of abdominal cavity contents through the inguinal canal.

214
Q

What is the commonest type of hernia?

A

Inguinal hernia.

215
Q

Who are inguinal hernias most common in?

A

Males over 40.

216
Q

What are the risk factors fo an inguinal hernia?

A
  • Male
  • Chronic cough
  • Constipation
  • Heavy weight lifting
  • Ascites.
217
Q

What are the 2 types of inguinal hernia?

A 
Direct: less common (20%)
•	Protrudes directly into the inguinal canal
•	Medial to inferior epigastric vessels
•	Rarely strangulates.
Indirect: more common (80%)
•	Protrudes through the deep inguinal ring
•	Lateral to inferior epigastric vessels
•	Can strangulate.
218
Q

Where is a common site of herniation?

A

The inguinal canal:
• Short passage that extends medially and inferiorly through inferior part of abdominal wall
• Extends from deep inguinal ring to superficial ring
• Acts as a pathway by which structures can pass from abdominal wall to external genitalia
• It is a potential weakness in abdominal wall and therefore common site of herniation.

219
Q

What are the symptoms of an inguinal herniation?

A

Usually asymptomatic: if painful then indicates strangulation.

220
Q

What are the signs of inguinal herniation?

A
  • Bulging: associated with coughing or straining (bowel movements, heavy lifting)
  • Appearance of lump.
221
Q

What is the management of an inguinal hernia?

A
  • Medically: use of truss to contain and prevent further progression of hernia
  • Surgery.
222
Q

What is a femoral hernia?

A

Bowel comes through the femoral canal below the inguinal ligament.

223
Q

What is the pathophysiology of a femoral hernia?

A

Bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin. Likely to be irreducible and to strangulate due to the rigidity of the canal’s borders. The neck of the hernia is felt inferior and lateral to the pubic tubercle. Inguinal hernias are superior and medial to this point.

224
Q

What is the management of a femoral hernia?

A
  • Surgical repair

* Herniotomy (ligation and excision of sac).

225
Q

What is a hiatus hernia?

A

Part of the stomach herniated through the oesophageal hiatus of diaphragm.

226
Q

What are the differential diagnoses for a hiatus hernia?

A
  • Inguinal hernia
  • Lipoma
  • Femoral aneurysm
  • Psoas abscess
  • Saphena varix: dilation of saphenous vein at junction of femoral vein in groin.
227
Q

What are the types of hiatus hernia?

A

Sliding:
• Oesophageal-gastric junction slides through the hiatus and lies above the diaphragm
• No symptoms other than reflux symptoms.
Rolling/Para-oesophageal:
• Uncommon: gastric fundus rolls up through hiatus alongside the oesophagus. Therefore, the gastro-oesophageal junction remains below the level of the diaphragm
• Treated via surgery.

228
Q

What is the risk factor for hiatus hernia?

A

Obesity.

229
Q

What are the symptoms of hiatus hernia?

A

Symptomatic GORD.

230
Q

What are the investigations for a hiatus hernia?

A
  • Barium swallow: confirms diagnosis

* Upper GI endoscopy.

231
Q

What is the management for a hiatus hernia?

A
  • Lose weight
  • Treat reflux symptoms
  • Surgery: to prevent strangulation.
232
Q

What are the functions of the liver?

A
  • Glucose and fat metabolism
  • Detoxification and excretion: bilirubin, ammonia and drugs/hormones/pollutants
  • Protein synthesis: albumin and clotting factors e.g. vitamin K
  • Defence against infection (Reticuloendothelial system).
233
Q

What are the 2 types of liver injury?

A

Acute:
• Recovery
• Liver failure.
Chronic:
• Cirrhosis: disorganisation and fibrous scarring
• Liver failure: varices due to portal hypertension and hepatoma.

234
Q

What is the presentation of acute liver injury?

A
  • Malaise
  • Nausea
  • Anorexia
  • Jaundice
  • Confusion (rarer)
  • Bleeding (rarer)
  • Liver pain (rarer): consider obstruction or malignancy.
235
Q

What is the presentation of chronic liver injury?

A
  • Ascites
  • Oedema
  • Haematemesis (varices) vomiting blood
  • Malaise
  • Anorexia
  • Wasting
  • Easy bruising
  • Itching
  • Erythema nodosum
  • Spider naevi
  • Hepatomegaly
  • Abnormal LFTs
  • Jaundice (rarer)
  • Confusion rarer).
236
Q

How does jaundice present in liver biochemistry?

A

Raised serum bilirubin.

237
Q

What is the pathophysiology of jaundice?

A
  1. Damaged or old erythrocytes are engulfed by a macrophage (mainly in spleen and liver)
  2. Haemoglobin is broken down into haem and globin
  3. Globin is broken down into amino acids and then recycled for generation of new erythrocytes in bone marrow
  4. Haem broken down using haemoxygenase enzymes which removes the iron (which is recycled back to the bone marrow for new RBCs via transferrin) leaving a porphyrin ring
  5. Ring is opened up to form biliverdin via haem oxygenase (which is toxic)
  6. Biliverdin (green colour) is then converted to unconjugated bilirubin (yellow colour) by the enzyme biliverdin reductase
  7. Unconjugated bilirubin travels into the blood bound to albumin travels to the liver. This ensures no unconjugated bilirubin is excreted in the urine because at high concentrations, unconjugated bilirubin can slowly diffuse into peripheral tissues where it is toxic.
  8. Bilirubin is then removed from circulation in the sinusoids by hepatocytes. This is a passive process, which occurs down a concentration gradient
  9. Once inside the hepatocyte, UDP glucuronyl transferase (UDP-GT) attaches glucuronic acid to become conjugated bilirubin (now water soluble and less toxic) which is ready for excretion
  10. Now the bilirubin is conjugated, it travels in the biliary canaliculi (thin tube that collects bile from hepatocytes) to the right or left hepatic duct. These then join to form the common hepatic duct which then drain into the gallbladder via the cystic duct.
  11. When a fatty meal has been eaten, CCK causes the release of bile (with conjugated bilirubin) from the gallbladder into the duodenum via the ampulla of Vater. CCK also causes relaxation of the sphincter of Oddi allowing this to happen
  12. In the ileum, bilirubin is broken down into urobilinogen by intestinal bacteria
  13. 90% of the urobilinogen continues into the large intestine where it reduced to stercobilinogen which is then acted upon by different colonic bacteria to form stercobilin (colours the faeces) and excreted through the rectum
  14. The remaining 10% of the urobilinogen is reabsorbed into the blood, binds to albumin and travels back to the liver and then 5% goes to the kidneys where it is oxidised to urobilin to colour urine, the other 5% goes back to the duodenum by the bile duct (enterohepatic circulation).
238
Q

What are the 3 types of jaundice?

A 
1. Pre-hepatic: excess breakdown of Hb which increases total unconjugated bilirubin 
•	Increased unconjugated bilirubin
•	Normal stool and urine
•	Causes:  more haemolysis
•	Malaria
•	Sickle cell anaemia
•	Foetal Hb in newborns.
2. Hepatic: failure of hepatocytes to take up, metabolise or excrete bilirubin
•	Increased unconjugated and conjugated bilirubin
•	Dark urine and normal/pale stools
•	Causes
•	Viral hepatitis
•	Drugs
•	Alcohol
•	Cirrhosis
3. Post-hepatic: obstruction in biliary system e.g. gallstone
•	Increased conjugated bilirubin
•	Dark urine and pale stools
•	Causes
•	Gallstones
•	Pancreatitis: head of pancreas blocks common bile duct.
239
Q

What is urine like in jaundice?

A

Pre-hepatic: normal.

Hepatic/post hepatic: dark.

240
Q

What are stools like in jaundice?

A

Pre-hepatic: normal.

Post-hepatic: pale.

241
Q

What are liver tests like in jaundice?

A

Pre-hepatic: normal.

Post-hepatic: abnormal.

242
Q

Is there itching in jaundice?

A

Pre-hepatic: no.

Post-hepatic: maybe.

243
Q

What does a liver history entail?

A
  1. Dark urine, pale stools, itching?
  2. Symptoms
    a. Biliary pain
    b. Rigors (shivering)
    c. Abdomen swelling
    d. Weight loss
  3. Past history
    . Biliary disease/intervention
    a. Malignancy
    b. HF
    c. Blood products
    d. Autoimmune disease
  4. Drug history: drugs/herbs started recently
  5. Social history
    . Alcohol
    a. Potential hepatitis contact
    i. Irregular sex
    ii. IVDU
    iii. Exotic travel
    iv. Certain foods
    b. Family history/system review (rarely helpful)
    • Liver enzymes, very high AST/ALT suggests liver disease (some exceptions)
    • Biliary obstruction, 90% have dilated intrahepatic bile ducts on ultrasound
    • Further imaging
    • CT
    • Magnetic resonance cholangiogram (MRCP)
    • Endoscopic retrograde cholangiogram (ERCP).
244
Q

What is the advanced form of NAFLD?

A

NASH.

245
Q

What is primary biliary cirrhosis/cholangitis?

A

Autoimmune destruction of the bile ducts which causes cirrhosis.

246
Q

Who is primary biliary cirrhosis/cholangitis more common in?

A

Women aged 40-50 constitute 90% of patients

247
Q

What is the cause of primary biliary cirrhosis/cholangitis?

A

Autoimmune.

248
Q

What is the pathophysiology of primary biliary cirrhosis/cholangitis?

A
  • Interlobar bile ducts are damaged by chronic autoimmune granulomatous inflammation resulting in bile leaking out into blood and other liver cells which causes inflammation and bile stasis (similar symptoms to cholestasis and obstructive jaundice)
  • Advanced stage can lead to cirrhosis due to autoimmune attack and infiltration of bile.
249
Q

What are the symptoms of primary biliary cirrhosis/cholangitis?

A
  • Asymptomatic: discovered on routine examination or screening
  • Lethargy and fatigue
  • Hepatomegaly
  • Leakage of: Bile (pruritis, itchy skin and jaundice) and cholesterol (pigmented Xanthelasma: yellow fat deposits under skin around eyelids), Xeropthalmia (dryness of conjunctiva and cornea amd corneal arcus.
  • Joint pain and arthropathy
  • Variceal bleeding.
250
Q

What do the antibody tests show in primary biliary cirrhosis/cholangitis?

A
  • Presence of Anti-Mitochondrial Antibodies (AMA)

* Raised serum IgM.

251
Q

What do LFTs show in primary biliary cirrhosis/cholangitis?

A
  • Raised ALP and GGT

* Raised cholesterol.

252
Q

What is the management for primary biliary cirrhosis/cholangitis?

A
  • Ursodeoxycholic acid: reduces cholesterol absorption and improves bilirubin and aminotransferase levels
  • Cholestyramine: reduces cholesterol absorption
  • Bisphosphonates: for osteoporosis
  • Vitamin ADEK supplementation
  • Liver transplant.

2a Medicine (11 decks)

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