Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CP1 > HPB > Flashcards

HPB Flashcards

1
Q

What is jaundice?

A

= yellow discoloration of the sclera, skin and mucous membranes secondary to hyperbilirubinaemia.

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

What is the normal range of bilirubin and at what value is jaundice typically clinically visible?

A

normal varies, but is typically from 3 – 21 mmol/L.

Generally the bilirubin needs to be around twice the upper limit (~40-50+) to be clinically visible.

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

what is the cause of pruritus in jaundice?

A

generally due to excess bile salts in the skin rather than the bilirubin itself

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

Physiology of bilirubin in the body

A
  1. Bilirubin is a product of haemoglobin breakdown. When a red cell is broken down (typically in the spleen), this releases unconjugated bilirubin (UCB).
  2. UCB is fat soluble and binds to albumin before being transported to the hepatocytes of the liver.
  3. In the liver it is conjugated by a hepatic enzyme. This conjugated bilirubin (CB) is then stored in the gallbladder as part of bile.
  4. Bile is released during digestion, where the CB is then broken down in the small intestine into Urobilinogen.
  5. Urobilinogen then takes 1 of 3 paths:
    => Converted to stercobilin in the gut and excreted in the stool
    => Absorbed into blood before being excreted by the kidney in the urine.
    => Recycled back to the liver to be re-excreted in bile.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 categories of causes of jaundice?

A
  1. Pre-hepatic
  2. Hepatic
  3. Post-hepatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What occurs in pre-hepatic jaundice?

A

Increased breakdown of RBCs leads to increased UCB – this overwhelms the capacity of the hepatocytes to conjugate it
=> There will be leftover UCB in the bloodstream and results in jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of pre-hepatic jaundice

A

Severe Malaria

Pernicious anaemia

Sickle cell disease (these may die faster than normal RBCs)

Thalassaemia

Transfusion reactions

Autoimmune haemolytic anaemias

Gilbert’s Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Gilbert’s Syndrome

A

= an autosomal recessive inherited condition – defective gene encoding for the hepatic conjugation enzyme.

Intermittent jaundice in the absence of haemolysis or underlying liver disease.

Will see isolated elevated UCB on investigation

Benign and self-limiting condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What occurs in hepatic/hepatocellular Jaundice?

A

Can be either:

  1. UCB not conjugated at a sufficient rate, leading to increased circulating UCB.
  2. A degree of obstruction means that CB not being transported into biliary ducts, CB builds up in the hepatocytes and ends up in the bloodstream (increased circulating CB).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of hepatic jaundice?

A

Viral hepatitis

Alcoholic hepatitis/cirrhosis

Drug-induced liver injury

  • Paracetamol overdose
  • Iatrogenic – e.g. flucloxacillin, co-amoxiclav, anti-epileptics

Autoimmune hepatitis

Wilson’s disease

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

Wilson’s disease

A

very rare autosomal recessive disorder of copper metabolism.

Can result in excess deposition of copper in tissues.

Clinical sign – Kayser Fleischer rings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What occurs in post-hepatic/Obstructive jaundice?

A

Blockage of the biliary tree obstructs drainage and causes bile (containing CB) to back up into the liver.

Pressure backs up bile between hepatocytes back to vasculature and CB is pushed back into the bloodstream (conjugated hyperbilirubinaemia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of post-hepatic/Obstructive jaundice

A

Gallstones in common bile duct.

Cholangiocarcinoma

Strictures

Pancreatic cancer

Primary sclerosing cholangitis

Primary biliary sclerosis

Abdominal masses

Drug-induced cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pre-hepatic jaundice - urine and stool colour

A

Urine will be normal

Stools will be normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hepatic jaundice - urine and stool colour

A

Urine will be dark

Stool may be slightly pale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Post-hepatic jaundice - urine and stool colour

A

Urine will be dark

Stool will be pale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes dark urine in jaundice?

A

Excess of conjugated bilirubin, which can be excreted in the urine

(Unconjugated cannot be excreted in the urine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes pale stools in jaundice?

A

Pale stools occur if conjugated bilirubin cannot be converted to stercobilin in the gut (i.e. if there is an obstruction preventing bile from reaching the intestine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Charcot’s Triad?

What typically causes this?

A

= jaundice, fever (usually with rigors), and RUQ pain

Indicates an ascending cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

DDx for jaundice with abdominal pain?

A

Pancreatitis, gallstones, ascending cholangitis

Sickle cell, drug-induced hepatitis, alcoholic hepatitis, viral hepatitis, cholangiocarcinoma, pancreatic cancer.

Haemolytic jaundices are classically painless, apart from sickle cell crisis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

DDx for jaundice with fever?

A 
Malaria (periodic fever; every third day)
Viral hepatitis
Cholangiocarcinoma
Pancreatitis
Ascending cholangitis

(Gallstones (only if infected))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

DDx for jaundice with weight loss?

A

Severe malaria, pernicious anaemia – loss of appetite.

Cholangiocarcinoma, pancreatic cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

DDx for jaundice and ETOH excess?

A

Alcoholic hepatitis – generally misuse over a long period of time, but also sometimes binge-drinking.

Pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

DDx for jaundice and exotic travel?

A

Severe malaria

Viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

DDx for jaundice and steatorrhoea?

A

Typically obstructive/post-hepatic cause – lack of bile in the intestines leads to less fat absorption

Can be intra-hepatic if there is cholestasis, but less common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are signs of chronic liver disease on examination?

A

Spider naevi (>5, above the nipple line)
Palmar erythema
Clubbing
Bruising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are caput medusae a sign of?

A

Portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is carotenaemia?

A

= increased beta-carotene levels in the blood.

This can occur following excessive consumption of carotene-rich foods, such as carrots, squash, and sweet potatoes.

Causes yellowing of skin but the sclera are spared - important to differentiate it from jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Courvoisier’s Law

A

jaundice with a palpable (enlarged) but painless gallbladder suggests malignant obstruction of the biliary tree until proven otherwise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

OE - nodular/decreased size of liver suggests…

A

cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

OE - Hepatomegaly sugests

A

malignancy or acute hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

OE - enlarged spleen

A

malignancy or extravascular haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What investigations should be done in a jaundiced patient?

A

Observations
Full abdo exam

Urinalysis
FBC, CRP, LFTs, U&Es
Coagulation (liver synthetic function)
Lipase/Amylase

USS Liver/biliary tree?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what does raised ALP/GGT typically indicate?

A

biliary obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does raised ALT/AST typically indicate ?

A

hepatocellular damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What would normal ALP/GGT and ALT/AST in a jaundiced patient suggest?

A

pre-hepatic cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the two components of the spleen?

What do they do?

A
  • White Pulp: B + T cells within “screen” blood coming through for bacteria/viruses and attack or form antibodies against any they detect.
  • Red Pulp: Filters out old/damaged red blood cells. Also a store for ~1/3 of your platelets.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Splenomegaly

A

= enlarged spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Hypersplenism

A

= overactive spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the causes of splenomegaly?

A
  1. Increased Demand
  2. Infiltration
  3. Abnormal blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What might cause increased demand of the spleen?

A
  • Removal of defective RBCs – sickle cell, thalassaemia, spherocytosis
  • Extramedullary haematopoiesis
  • Infection – sepsis, EBV infection, AIDs, viral hepatitis, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What might cause infiltration of the spleen?

A
  • Malignant – most typically lymphomas, but also leukaemias and metastases
  • Benign – cysts, haematomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What might cause abnormal blood flow to the spleen?

A
  • Vascular – portal/hepatic/splenic vein obstruction

- Infection – hepatic schistosomiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Acute Pancreatitis

A

= acute inflammatory process involving pancreas.

can range from mild, self-limiting disease to complete necrosis of pancreas

occurs on a background of a normal pancreas and can return to normal (whereas chronic pancreatitis has irreversible changes).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Chronic Pancreatitis

A

= caused by progressive inflammation and irreversible damage to structure and function.

Alcohol abuse is most common cause for this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the two functions of the pancreas?

A
  1. Endocrine - Alpha and beta cells
    => Secretes hormones like insulin and glucagon into the bloodstream for glucose homeostasis.
  2. Exocrine - Acinar cells
    => Secrete amylases, lipases and proteases into the duodenum to aid digestion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How does the pancreas protect itself from digestive enzymes?

A
  1. Keeping the enzymes away from sensitive tissues in vesicles (zymogen granules).
  2. Storing the enzymes as proenzymes (Zymogens) which first need to be activated by the protease trypsin.

=> Trypsinogen is needed to activate trypsin, which in turn activates zymogens
=> there are several trypsin inhibitors, which can bind to trypsin and inactivate it if it becomes prematurely active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Pathophysiology of acute pancreatitis

A

If trypsinogen is activated too early, this can lead to acute pancreatitis.

This might happen due to :

  1. injury to acinar cells
  2. due to impaired secretion of proenzymes into the duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the 2 most common causes of acute pancreatitis?

A
  1. GALLSTONES

2. ALCOHOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Mnemonic for the causes of acute pancreatitis

A

“I GET SMASHED”

  • I – idiopathic
  • G – gallstones
  • E – ethanol
  • T – trauma (particularly puncture/stab wounds)
  • S – steroids
  • M – mumps
  • A – autoimmune (e.g. SLE, Sjogrens)
  • S – scorpion stings
  • H – hyperglycaemia/hypertriglyceridaemia
  • E – ERCP
  • D – drugs (e.g. azathioprine, furosemide, immunosuppresants)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How does alcohol abuse cause acute pancreatitis?

A

With alcohol abuse, there is increased zymogen release from acinar cells. Alcohol also causes a decrease in fluids and bicarbonates in ducts.

This means pancreatic juices are thick and sludge-like (with many enzymes, but not much fluid) which can form a plug and block ducts.

=> Increase in pressure can cause distension of the ducts.

=> Distension can bring zymogen granules in contact with lysosomes which may contain digestive enzymes – can cause a cascade of pancreatic autodigestion.

=> In response to this, there is a release of cytokines, leading to an immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do gallstones cause acute pancreatitis?

A

With gallstones, they usually travel down the bile duct and get lodged at the Sphincter of Oddi, thereby blocking it.

This then becomes a similar situation to alcohol-induced acute pancreatitis where there is backing up to pancreatic juices.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Pancreatitis - clinical presentation

A

Nausea and Vomiting

Epigastric pain (with radiation to the back)
=> Sometimes relieved by sitting forward.

Cullen’s sign

Grey-Turner’s sign

Signs of sepsis – tachycardia, fever, rigid abdomen, shock.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Grey-Turner’s sign

A

Bruising around flanks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Cullen’s sign

A

Bruising around periumbilical region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Pancreatitis - investigations

A
  1. Bloods:
    - Amylase – usually elevated
    - Lipase – these are elevated as well and are specific for pancreatitis
    - Bone profile – to look at calcium levels (for hypercalcaemia)
    - Triglycerides – to check for elevated triglyceride levels

(and do normal bloods such as FBC, U+Es, LFTs, CRP)

  1. ABG – used for checking lactate and PaO2.
  2. AXR – may show ileus
  3. Abdo USS – used to confirm/exclude gallstones.
  4. CT Abdo – not routine but can confirm diagnosis when uncertainty present.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Severity scoring in acute pancreatitis

A

Glasgow scoring system - a score above 3 is severe disease

P – PaO2 <8 kPa
A – Age >55
N – Neutrophils, WCC > 15x109/L
C – Calcium <2mmol/L
R – Renal, urea >16 mmol/L
E – Enzymes, LDH >600 IU/L or AST >200 IU/L
A – Albumin <32 g/L
S – Sugar, glucose >10 mmol/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

management of acute pancreatitis

A

Fluids – aggressive fluid resuscitation

Analgesia and antiemetics
NG tube
Adequate oxygenation
Antibiotics – if evidence of infection/necrosis

ERCP – if gallstone pancreatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Why is fluid resuscitation important in pancreatitis?

A

Important to compensate for 3rd space losses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Complications of pancreatitis

A

Pancreas Pseudocyst/Abscess
Necrosis of pancreas

Hypovolaemic shock
Disseminated Intravascular Coagulation
Acute Respiratory Distress syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Necrosis of the pancreas

A

The inflammatory process causes blood vessels to become leaky and then rupture, leading to pancreatic tissue swelling.

This causes premature activation of lipases which then starts to destroy peripancreatic fat.

The fat and tissues liquefy and can start necrosing (process called Liquefactive Haemorrhagic Necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

how are pancreas pseudocyst and abscess formed?

what may the clinical presentation be?

A

When fibrous tissue surrounds necrotic tissues and fills with pancreatic juices.

The pseudocyst can also become infected to become an abscess and presents as sepsis.

This may cause abdominal pain, loss of appetite and a palpable tender mass.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what is the best way to assess for a pseudocyst/abscess of the pancreas?

A

Abdominal CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Why can ARDS occur in pancreatitis?

A

massive inflammation => leaky blood vessels, which allows fluid to build up in the lungs and causes difficulty breathing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the functions of the liver?

A

Storage of iron, copper, and vitamins

Metabolism of drugs and alcohol

Metabolism of key nutrients

Synthesis of proteins (albumin, clotting factors, complement, transferrin)

Excretion (bile and bilirubin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How does the liver metabolise key nutrients?

A

Carbohydrates – storage as glycogen when fed, release of glucose when fasting.

Fat – produces and processes circulating lipoproteins

Protein – processes digested amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is acute liver failure?

A

= sudden impairment of a previously healthy liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is acute on chronic liver failure?

A

= decompensation of chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is fulminant liver failure?

A

= sudden massive necrosis of liver cells with severe impairment of liver function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Clinical features of liver failure

A

Abdominal pain
Fatigue
Nausea
Symptoms related to complications

Jaundice
Ascites
Liver flap
Signs of pre-existing liver disease (in acute on chronic failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Complications of liver failure

A

Bleeding
Spontaneous Bacterial Peritonitis
Hypoglycaemia
Hepatic encephalopathy

72
Q

Why can there be increased bleeding in liver failure?

A

Reduced production of clotting factors by the liver, combined with the presence of oesophageal varices in chronic disease, creates a risk of massive oesophageal haemorrhage.

73
Q

Spontaneous Bacterial Peritonitis

A

In ascites, presence of static fluid in the peritoneum promotes bacterial growth and leads to sepsis.

74
Q

Why can there be hypoglycaemia in liver failure?

A

The liver is not effectively performing its usual function of releasing glucose when fasting

75
Q

Hepatic encephalopathy

A

= a collection of neuro-psychiatric symptoms in a patient with decompensated liver disease

In decompensated cirrhosis, the liver is not able to clear ammonia produces by the bowels, so the level in the blood rises

Ammonia crosses the BBB and is processed by astrocytes into glutamine. Accumulation of glutamine creates osmotic imbalance and fluid moves into the cells – this is cerebral oedema, and it impairs normal functioning of the brain

76
Q

Aims of treatment of liver failure

A

Depends on the cause

Prevention of further damage (e.g. stop alcohol)

Symptoms may be managed without curing the disease

Potentially liver transplant, depending on circumstances

77
Q

what are the most common drugs causing liver injury?

A

paracetamol

Abx - flucloxacillin / co-amoxiclav

78
Q

Which patients are more at-risk of a drug-induced liver injury?

A

Those who already have pre-existing liver damage, alcoholism or malnutrition.

79
Q

Predictable vs idiosyncratic drug-induced liver injury

A

Predictable – reaction is dose-depended (e.g. paracetamol overdose)

Idiosyncratic – reaction is due to hypersensitivity in some patients

80
Q

Paracetamol overdose

A

Paracetamol is metabolised in the liver.

In the event of overdose, the metabolic pathways become overwhelmed and there is a build-up of intermediate compounds.

The compounds damage the cells, leading to cell death (acute liver necrosis), and potential liver failure

81
Q

Acute vs long-term paracetamol overdose

A

deliberate massive overdose
=> after 24hrs there is a noticeable rise in AST and ALT, => after 48hrs there may be symptoms of jaundice and confusion.

This process is gradual in patients with a long term, low level overdose (e.g. accidentally taking too many paracetamol tablets daily for several weeks), but can be just as harmful.

82
Q

What is hepatitis?

A

= inflammation within the liver

can be acute or chronic (inflammation persists for >6 months).

83
Q

Acute causes of hepatitis

A 
Hepatitis A-E
Other viruses – EBV, CMV, Yellow fever
Parasitic – malaria
Autoimmune
Drug reactions
Alcohol
84
Q

Chronic causes of hepatitis

A 
Hepatitis B +/- Hepatitis D virus
Hepatitis C virus
Autoimmune hepatitis
Alcohol
Hyperlipidaemia (NAFLD)
Drugs (methyldopa, nitrofurantoin)

Metabolic disorders (Wilson’s disease, alpha1-antitrypsin deficiency, haemochromatosis)

85
Q

Pre-icteric phase of hepatitis

A

malaise, arthralgia, headache, anorexia, aversion to cigarette smoke, vague RUQ pain

86
Q

Icteric phase of hepatitis

A

jaundice, dark urine, pale stools, pruritis, skin rash

87
Q

What is the long-term outcome of chronic hepatitis?

A

will gradually progress to cirrhosis

an increased risk of hepatocellular carcinoma

88
Q

Hepatitis A

A

Endemic in Africa and South America

Transmission is via the faecal-oral route and via shellfish.

Acute, often asymptomatic and naturally cleared (self-limiting)

Unlikely to progress to chronic infection.

On blood tests, the most notable feature is increased AST

Usually, no specific treatment needed

There is a vaccine available for travellers or those at high risk

89
Q

Hepatitis B

A

Spread through bodily fluids – via blood or sex
Endemic in the Mediterranean, Far East, and Africa

Hepatitis B vaccine is now given to all UK babies, also to unvaccinated adults who are at a high risk.

~10% will develop chronic disease, and ~1% develop fulminant liver disease

90
Q

What are risk factors for Hepatitis B infection?

A 
Sharing needles for IV drugs
Sex
Sharing toothbrush or razor
Needlestick injury
Bite injury

Babies of infected mothers (at birth)

Blood transfusion (UK blood is screened for Hep B to reduce this risk)

Dialysis patients (less common now)

Use of unsterilized equipment for tattoos, piercings, acupuncture, and dentistry

91
Q

Hepatitis C

A

Spread via blood and sex – risk factors are the same as for Hepatitis B.

Early stages of infection are usually mild or asymptomatic
=> 85% of those infected will develop a chronic silent infection.

Chronic hepatitis C infection is one of the most common indications for liver transplant in the UK.

There is no vaccine available. As healthcare professionals, please wear PPE and do what you can to avoid needle stick injuries.

92
Q

Hepatitis D

A

Spread via blood and sex

An incomplete RNA virus – on its own it cannot cause an infection.
=> To replicate, it relies on viral proteins from Hepatitis B.

Therefore Hepatitis B vaccination also confers immunity to Hepatitis D.

Hepatitis B+D infection further increases the risk of cirrhosis and acute liver failure

Transplant may be required

93
Q

Hepatitis E

A

Spread via the faecal-oral route, shellfish, and undercooked pork

Endemic in Asia
Becoming more common: in the UK, Hepatitis E is now the most common cause of acute hepatitis

Usually causes a self-limiting acute infection

Unlikely to progress to chronic infection

There is no vaccine

94
Q

Autoimmune Hepatitis

A

Most likely to affect those with other autoimmune conditions

May present with either acute or chronic hepatitis (more commonly chronic)

The presence of auto-antibodies will confirm the diagnosis (a blood test)

Treated with immunosuppressant therapy (e.g. prednisolone) long term, but liver transplantation may be required.

95
Q

Presentation of autoimmune hepatitis

A

jaundice, fatigue, deranged LFTs

maybe also:
urticaria, polyarthritis, glomerulonephritis, amenorrhoea

96
Q

Acute Alcoholic Hepatitis

A

Presents after a binge with jaundice, RUQ pain and systemic upset. There may be signs of chronic liver disease if it is acute on chronic presentation.

Bilirubin, prothrombin time and hepatic encephalopathy predict survival.

AST:ALT ratio of 2:1 suggests alcoholic liver disease.

97
Q

Liver cirrhosis

A

= a progressive inflammatory fibrosis of the liver, resulting in loss of the normal hepatocellular architecture and appearance of small nodules of regeneration.

irreversible in later stages and the only potential cure is liver transplant.

Cirrhosis reduces life expectancy.

98
Q

What can precipitate deterioration of liver cirrhosis?

A
  • Alcohol binge
  • Dehydration
  • Infection
  • GI bleed
  • Surgery
99
Q

What are some features of cirrhosis?

A 
Hypoproteinaemia
Clotting problems
Portal hypertension 
Oesophageal varices
Hyperaldosteronism
Hepatorenal syndrome
Ascites
Encephalopathy
100
Q

Causes of cirrhosis

A 
Viral hepatitis (B or C)
Alcoholism
NAFLD
Genetic Disorders
Autoimmune disorders
Drugs - e.g. amiodarone
101
Q

Non-alcoholic fatty liver disease

A

Accumulation of fat within the liver.

Linked to obesity, diabetes, high cholesterol and more common in men

102
Q

Primary Biliary Cirrhosis

A

Usually diagnosed by serology – presence of anti-mitochondrial antibody (~95% of cases)

Pathology – portal inflammation, damage to bile ducts and granulomas

103
Q

Primary Sclerosing Cholangitis:

A

Best diagnosed by imaging (MRI or ERCP)

Pathology is patchy (hit and miss) – typically strictures in the bile ducts;

Strong association with ulcerative colitis;

Can go on to develop cirrhosis due to damage to the bile ducts;

High risk for bile duct cancer

104
Q

Cirrhosis - Hypoalbuminaemia

A

Liver normally produces all serum albumin – it is not produced anywhere else in the body

Albumin is a carrier molecule for many other substances including hormones, drugs, and ions. It also helps to maintain osmotic pressure in the bloodstream.

In cirrhosis, the liver is not able to produce sufficient albumin

Hypoalbuminaemia can result in oedema in the legs, and contributes to development of ascites.

105
Q

Portal Hypertension

A

The portal venous system drains blood from the intestines into the liver. Blood normally drains through the liver, then through the hepatic vein into the IVC.

Cirrhosis creates resistance and inhibits good blood flow through the liver

The blood flow backs up resulting in high blood pressure within the portal venous system and throughout the digestive tract.

Portal hypertension contributes to:

  • Oesophageal varices
  • Haemorrhoids
  • Caput medusae – distension of superficial abdominal wall veins
106
Q

Oesophageal Varices

A

Over time, veins become dilated and bulge into the lumen of the oesophagus

Pre-rupture, they are usually asymptomatic

Rupture of the varices can cause massive upper GI bleed – may be spontaneous or triggered by eating crunchy food

Emergency treatment is with band-ligation, performed by an endoscopist

107
Q

Secondary Hyperaldosteronism in cirrhosis

A

Low serum albumin levels and portal hypertension together result in relative renal hypoperfusion.

Renal hypoperfusion activates the renin-angiotensin-aldosterone system, leading to increased levels of aldosterone. This causes sodium retention in the kidneys and subsequent water retention.

Water retention contributes to lower limb oedema and ascites

108
Q

Hepatorenal Syndrome

A

Hepatorenal syndrome is renal failure in a patient with advanced cirrhosis

There is complex pathophysiology associated with renal hypoperfusion.

A sign of end-stage disease

109
Q

Abnormal clotting in cirrhosis

A

Many coagulation factors are produced in the liver, and production is impaired in cirrhosis.

Portal hypertension changes the blood flow in the spleen and leads to hypersplenism and splenomegaly. The spleen breaks down platelets, and an over-active spleen will break down platelets faster than they are created.

110
Q

Ascites

A

A combination of increased pressure in the portal venous system, hypoproteinaemia, and salt and water retention, cause a build-up of fluid in the peritoneal cavity.

The result is abdominal swelling and shifting dullness on examination.

The fluid is a transudate – i.e. low in protein (<30g/L)

Huge volumes of fluid can accumulate - limiting movement, eating, and causing breathing difficulties.

111
Q

Management of ascites

A
  • Fluid restriction and low salt diet
  • Diuretics (furosemide and spironolactone)
  • Large volume paracentesis
112
Q

Stages of progression of encephalopathy

A
  1. Subtle changes in behaviour, cognition, or sleep pattern
  2. Drowsy, confused, slurred speech, personality change, may have liver flap
  3. Stupor, incoherence, liver flap
  4. Coma
113
Q

How is hepatic encephalopathy managed?

A

Lactulose is given to promote bowel movements and to directly reduce bacterial production of ammonia in the bowel.

114
Q

Signs of cirrhosis on examination

A

Leukonychia – white nails secondary to low albumin
Clubbing
Palmar erythema
Dupuytren’s contracture

Spider naevi
Caput Medusae
Xanthelasma

Gynaecomastia
Atrophic testes
Loss of body hair

Hepatosplenomegaly – then small, shrunken liver in later stages.

115
Q

What imaging is used in cirrhosis??

A

Abdo USS

Sometimes MRI

AXR or CT are not routinely used due to exposure to x rays when they add no further info than USS.

116
Q

What are some more specific tests that can be done in cirrhosis?

A

Fibroscan - info on degree of fibrosis

Ascitic tap - check for SBP or cancerous cells

Liver biopsy - gold standard for definitive diagnosis

117
Q

what can cause the decompensation of cirrhosis?

A

Anything that puts extra strain on the liver has potential to cause decompensation of chronic liver disease, including:
• Dehydration
• Constipation
• Alcohol binge
• Sepsis (patients with ascites are prone to spontaneous bacterial peritonitis but may not always present with obvious symptoms)
• Excessive use of opioids
• GI bleed (leads to extra protein in the bowel, which bacteria turn into ammonia, which the liver metabolises)

118
Q

Prescribing considerations in cirrhosis

A
  • Warfarin – effects are enhanced, and clotting may already be deranged => bigger risk of bleeding
  • Sedatives and opioids may precipitate encephalopathy
  • NSAIDs and steroids can make fluid retention worse
  • Hepatotoxic drugs to avoid include: paracetamol, methotrexate, isoniazid, azathioprine, aspirin etc.
119
Q

What is the hepatopancreatic Duct/Ampulla of Vater ?

A

formed by the joining of the pancreatic duct and common bile duct.

120
Q

What is the sphincter of oddi?

A

prevents the reflux of duodenal contents into the biliary tree and is located between the ampulla of Vater and the wall of the 2nd part of the duodenum

121
Q

What does bile contain?

A

water, cholesterol, bile pigments and phosopholipids

122
Q

Process of release of bile

A
  1. Produced by the liver
  2. Stored and concentrated in the gallbladder
  3. Lipid rich food in the duodenum stimulates CCK release
  4. CCK causes the gallbladder to contract and the sphincter of Oddi to relax.
  5. Bile passes from the GB into the duodenum.
123
Q

Cholelithiasis

A

= stones in the gallbladder.

124
Q

Choledocholithiasis

A

= stones in the bile duct.

125
Q

Cholestasis

A

= reduction/stoppage of bile flow

126
Q

Which 3 factors predispose to gallstone formation?

A
  1. Cholesterol Supersaturation
  2. Stasis of Bile
  3. Increased Hb breakdown - Haemolytic disorders
127
Q

What can cause cholesterol supersaturation?

A

Caused by increased plasma oestrogen (obesity, pregnancy, OCP, female) and depletion of the bile acid pool (terminal ileal resection/disease)

Blood cholesterol levels have very little influence on bile cholesterol

128
Q

What can cause stasis of bile (apart from obstruction)?

A

Lack of stimulus to gallbladder emptying – fasting, TPN

129
Q

Prevalence of gallstones

A

Very common – prevalence of 10%.

Only 1-4% of individuals with gallstones will develop symptoms.

130
Q

Cholesterol gallstones

A

~20% of gallstones

Generally caused by cholesterol supersaturation and bile stasis.

Often solitary, Large (>2.5cm), Smooth

131
Q

Mixed gallstones

A

(predominantly cholesterol)

~75% of gallstones

Multiple stones
“Generations” – a range of colours and shapes

132
Q

Bile pigment gallstones

A

~5% of gallstones

Multiple, Small
Black/brown colour
Irregular and fragile

133
Q

What is the imaging modality of choice for gallstones?

A

USS

only ~10% of gallstones are radiopaque so most won’t show up on AXR.

134
Q

Biliary colic - pathophysiology

A

Stone impacted in neck of GB (Hartmann’s pouch) or cystic duct.

135
Q

What is Hartmann’s pouch?

A

the neck of the gallbladder

136
Q

Biliary colic - pain/symptoms

A

Sudden, sharp, stabbing RUQ-epigastric pain.

Typically radiates to right shoulder
Usually lasts <6 hours.

Pain may be precipitated by eating (especially fatty foods)

May have associated N+V

137
Q

Biliary colic - on examination/investigations

A

Typically unremarkable.
Apyrexial

Presence of stones on USS

138
Q

Biliary colic - management

A 
Analgesia
Outpatient cholecystectomy (within 6 weeks)
139
Q

Why is biliary “colic” not a proper colic?

A

Biliary “colic” involves contraction of smooth muscle, but the pain is more constant than the “on and off” pain of ureteric colic and intestinal colic.

140
Q

What is Cholecystitis ?

A

= inflammation/infection of the gallbladder

141
Q

Cholecystitis - pathophysiology

A

Stone impacted in neck of GB or cystic duct results in super concentrate, irritant bile +/- infection via ascending gut bacteria (Klebsiella, E. coli)

142
Q

Cholecystitis - pain/symptoms

A

Constant RUQ-epigastric pain which persists.
Radiates to right shoulder

May have N+V
Likely to have fever and/or lethargy

143
Q

Why can gallbladder pain radiate to the shoulder?

A

Pain radiating to the shoulder is caused by the inflamed GB irritating the liver capsule, which irritates the diaphragm above which is supplied by C3, C4, C5 (which also supplies sensation to the shoulder)

144
Q

Cholecystitis - on examination

A

Tender RUQ with possible guarding

Murphy’s sign

145
Q

Cholecystitis - investigation findings

A

Raised inflammatory markers
Mildly deranged AST/ALT/ALP/bilirubin

USS showing enlarged gallbladder with stone(s) and thickened walls (inflammation)

146
Q

Murphy’s Sign

A

Whilst applying pressure in the RUQ, ask the patient to inspire deeply.

Murphy’s sign is positive when there is a halt in inspiration due to pain.

A similar manoeuvre in the LUQ should not elicit discomfort.

147
Q

specificity of Murphy’s sign

A

Murphy’s sign is specific (if found, it is likely that the diagnosis is cholecystitis)

BUT it is not sensitive (not everyone with cholecystitis will have a positive Murphy’s sign).

148
Q

what is Cholangitis?

A

= inflammation/infection of the biliary system

149
Q

Cholangitis - pathophysiology

A

Common Bile duct outflow obstruction and ascending infection

150
Q

Cholangitis - pain/symptoms

A

RUQ pain, persistent, may be colicky in nature

Patient is jaundiced, typically unwell and pyrexial with rigors
May also have pruritis, pale stool and dark urine

Often causes sepsis

151
Q

Cholangitis - on examination

A

Tender RUQ with possible guarding

Pyrexial, jaundiced

152
Q

Cholangitis - investigation findings

A

Raised WBCs, blood cultures
Raised bilirubin

Raised ALP/GGT > AST/ALT

USS will show dilated bile ducts +/- GB stones +/- duct stones

153
Q

What investigations should be done in ?gallbladder disease?

A

BEDSIDE:
Observations
Abdominal Exam
Urinalysis +/- pregnancy test

BLOODS:
FBC, U&E, LFT, CRP, amylase
VBG + blood cultures in cholangitis

IMAGING:
Abdominal USS
CT
MRCP/ERCP

154
Q

What are you looking for on abdominal USS in ?gallbladder disease

A

Presence of gallstones or sludge (start of gallstone formation)

Gallbladder wall thickness – thick walls suggest inflammation

Bile duct dilatation >6mm – possible stone/stricture

Pericholecystic fluid – local oedema

155
Q

MRCP

A

= Magnetic Resonance Cholangiopancreatography

Gives detailed information about the biliary tract anatomy of the patient.

Can detect stones.

156
Q

ERCP

A

= Endoscopic retrograde cholangiopancreatography

Gold standard for cholangitis – both diagnostic and therapeutic.

Endoscope is passed via oesophagus into duodenum, fine catheter is passed into the common bile duct.

157
Q

Gallstone Ileus

A

Inflammation of the gallbladder can cause a fistula between the gallbladder wall and the duodenum allowing gallstones to pass into the small bowel directly

If the stone impacts at the terminal ileum this results in small bowel obstruction

158
Q

What is the possible clinical presentation of liver tumours?

A 
Symptoms:
•	RUQ pain, 
•	Weight loss, 
•	Nausea
•	Fever 
•	Late-stage symptoms include jaundice and other symptoms of liver failure.
Signs :
•	hepatomegaly, 
•	irregular liver border,  
•	tender right upper quadrant
•	ascites (late).

Investigations are likely to reveal deranged LFTs, particularly AST and ALT

159
Q

What percentage of liver tumours are primaries/secondaries?

A

90% are metastases

10% are liver primaries – hepatocellular, rare types, cholangiocarcinoma

160
Q

Why is the liver a common site of metastasis?

Where is the primary cancer usually?

A

= 2nd most common site of spread for solid tissue malignancies (after lymph nodes)

due to its rich bloody supply

Primaries are commonly in the lung, GI (pancreas, gastric, colorectal), breast and uterus

161
Q

Primary Hepatocellular Carcinoma

A

= malignant tumour of the hepatocytes

Quite rare in the UK, but common worldwide

can be nodular or infiltrative

162
Q

nodular vs infiltrative hepatocellular carcinoma

A

nodular – one or more discrete masses within the liver

infiltrative – diffuse throughout the liver

163
Q

What are common sites of secondary spread of hepatocellular carcinoma?

A

Bone

Lungs

164
Q

What is the major risk factor for HCC and why?

A

liver cirrrhosis

repeated cycles of damage, inflammation and repair increase the risk of genetic mutations leading to cancer

165
Q

Aside from cirrhosis, what are some other risk factors for HCC?

A

Chronic hepatitis B infection
Hepatitis C

ALD

Haemochromatosis

Primary biliary cirrhosis

NAFLD

166
Q

Prognosis of HCC

A

prognosis is generally poor

At diagnosis, serum alpha-fetoprotein (AFP) level is taken, and this generally correlates with tumour size and grade.
=> High AFP is poor prognostic factor

167
Q

What is a cholangiocarcinoma?

A

cancer in any part of the biliary tree, including inside the liver (intrahepatic)

a type of adenocarcinoma arising from the epithelial cells lining the bile ducts

168
Q

Risk factors for cholangiocarcinoma

A 
Primary sclerosing cholangitis
Anatomical abnormalities of the liver
Diabetes and Obesity
Parasite infection. 
Chronic hepatitis infection
169
Q

Clinical presentation of cholangiocarcinoma

A

Painless Jaundice
Obstructive jaundice
Pruritus
Dark urine and pale stools

Presentation is often late as symptoms occur only after the bile duct is blocked.

170
Q

types of pancreatic cancer

A

normally a ductal adenocarcinoma which arises from the exocrine epithelial cells lining the ducts of the pancreas.

rarer types include - acinar cell carcinoma and cystoadenocarcinoma

171
Q

Risk factors for pancreatic cancer

A

Smoking

Obesity and diabetes (though there is some debate whether diabetes is a contributary cause, or a result of, pancreatic cancer)

Alcohol

Chronic pancreatitis

172
Q

Location of pancreatic cancer

A

2/3rds are in the head of the pancreas

1/3rd are in the body and tail of the pancreas

173
Q

Clinical presentation of pancreatic cancer in head of pancreas

A

Can compress common bile duct - they present late with painless obstructive jaundice

Symptoms include pruritus, pale stools, and dark urine

Stasis of bile can lead to infection (cholangitis) causing abdominal pain and fever

In late stages: ascites, anaemia, fatigue, nausea

174
Q

Clinical presentation of pancreatic cancer in body/tail of pancreas

A

General vague symptoms such as fatigue, weight loss, and nausea.

Ascites is a late feature.

May present with epigastric pain, “boring” and incessant in nature, relieved by sitting forwards. This is caused by local invasion of the coeliac plexus.

Usually very advanced at time of diagnosis

175
Q

Complications of pancreatic cancer

A

New onset diabetes - Type 3c diabetes

Pancreatic exocrine insufficiency
=> Impaired production of pancreatic digestive enzymes causes steatorrhoea and malnutrition.

Venous thrombo-embolism (DVT or PE)
=> Common to most cancers as there is a hypercoagulable state

CP1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions