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Kyla's Phase 2a Flashcards > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

Define cholecystitis

A

Inflammation of the gallbladder

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2
Q

Main cause of cholecystitis

A

Gallstone impaction into the cystic duct or neck of gallbladder

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3
Q

First line investigations for cholecystitis

A
  • Abdominal ultrasound scan
  • FBC (high WBC count)
  • LFTs (exclude liver/bile duct pathology)
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4
Q

Results of imaging in a patient with cholecystitis

A
  • Thickened gallbladder
  • Stones or sludge in gallbladder
  • Fluid around the gallbladder
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5
Q

Patient presents with RUQ that radiates to the right shoulder, positive Murphy’s sign, tachycardic and fever. Diagnosis?

A

Cholecystitis

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6
Q

Gold standard imaging for cholecystitis diagnosis

A

Mangnetic resonance cholangiopancreatography (MRCP)

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7
Q

Differential diagnoses for cholecystitis

A
  • Acute cholangitis
  • Chronic cholangitis
  • Appendicitis
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8
Q

First line management for cholecystitis

A
  • IV fluids
  • Analgesia
  • Antibiotics
  • Endoscopic retrograde cholangio-pancreatography (ERCP)
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9
Q

Complications of cholecystitis

A
  • Sepsis
  • Gangrenous bladder
  • Perforation -> peritonits
  • Gallbladder empyema
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10
Q

What positive clinical examination sign is suggestive of cholecystitis?

A

Murphy’s sign
(acute pain + sudden stopping of inspiration)

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11
Q

Define biliary colic

A
  • Term to describe pain associated with temporary obstruction of the cystic or common bile duct by a stone migrating from the gallbladder
  • Sudden onset, serve but constant, has a crescendo characteristic
  • Pain is temporary -> stops when gallstone dislodges
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12
Q

What is ascending/acute cholangitis?

A

Life-threatening condition - caused by an ascending bacterial infection of the biliary tree
(High mortality - sepsis + septicaemia)

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13
Q

Causes of acute/ascending cholangitis

A
  • Gallstones in common bile duct (stops bile flow -> jaundice)
  • Infection introduced during ERCP procedure
  • Benign + malignant strictures
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14
Q

Most common organisms to cause ascending/acute cholangitis

A
  • Escherichia coli
  • Klebsiella species
  • Enterococcus species
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15
Q

Risk factors for ascending/acute cholangitis

A

4Fs:
* Female
* Fat
* Fertile = pregnancy, under 40
* Fair = Northern European and Hispanic

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16
Q

Pathophysiology of ascending/acute cholangitis

A
  • Obstruction of common bile duct → stasis of bile → invasion of bacteria from duodenum
  • High pressure on the CBD (due to the obstruction) can cause spaces between the cells to widen which allows the bacteria and the bile access to the blood stream → bacteraemia + jaundice
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17
Q

Key signs of ascending/acute cholangitis
(name of triad)

A

Charcot’s triad
* RUQ pain
* Fever
* Jaundice (dark urine + pale stools) (raised bilirubin)

(Theres also shock - hypotension + tachycaridia)

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18
Q

Symptoms of ascending cholangitis

A
  • Reynold’s pentad: bacteria → septic shock → leaky vessels → hypotension → less blood flow to organs e.g. brain → confusion
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19
Q

First line investigations for ascending cholangitis

A
  • Transabdominal ultrasound (dilated bile duct, common bile duct stones)
  • FBC (raised WBCs)
  • ESR + CRP (raised)
  • Serum bilirubin (raised)
  • Blood cultures (usually gram-negative)
  • Serum LFTs (raised transaminases + alkaline phosphatase)
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20
Q

Management for ascending cholangitis

A
  • Endoscopic reterograde cholangiopancreatography (ERCP) - to remove stones from bile duct
  • IV fluids
  • IV antibiotics (co-amoxiclav)
  • If this fails → laparoscopic/open cholecystectomy
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21
Q

Complications of ascending cholangitis

A
  • Aute pancreatitis
  • Sepsis
  • Septicaemia
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22
Q

What is the condition that involves intrahepatic + extrahepatic ducts become strictured + fibrotic?

A

Primary sclerosing cholangitis
* (Sclerosing → stiffening, hardening)
* (Cholangitis → inflammation of bile ducts)

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23
Q

Who is the typical patient that presents with primary sclerosing cholangitis and primary biliary cholangitis/cirrhosis?

A
  • Primary sclerosing cholangitis → young and middle aged men (often with IBD)
  • Primary biliary cirrhosis → middle-aged women (other autoimmune, rheumatoid conditions)
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24
Q

What condition are 70% of primary sclerosing cholangitis cases associated with?

A

Ulcerative colitis
(So if a patient has UC and has liver symptoms → think about primary sclerosing cholangitis)

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25
Q

Risk factors for primary sclerosing cholangitis

A
  • Male
  • Aged 30-40
  • Ulcerative colitis (IBD)
  • Family history - genetic predisposition
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26
Q

A 32 y/o male patient presents with jaundice, chronic RUQ pain, and is feeling itchy (pruritus). You examine him and find that he has hepatomegaly. DIagnosis?

A

Primary sclerosing cholangitis

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27
Q

What does a ‘cholestatic picture’ on LFTs indicate?

A

Decreased or slowed release of bile
(Liver cells = are not being directly injured - but are instead responding to bile stasis)
* ↑ALP, ↑GGT, ↑Bilirubin
* Mild ↑/ normal ALT, AST

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28
Q

What does a ‘obstructive picture’ on LFTs indicate?

A

Obstruction of the bile ducts
(Bile builds up in the liver, leading to inflammation + injury)
* ↑ALP, ↑GGT
* Mild ↑/ normal ALT, AST

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29
Q

First line investigations for primary sclerosing cholangitis

A

LFTs
* ↑ALP (most deranged)
* ↑GCT
* ↑Bilirubin
* ↑/N ALT + AST

Abdominal ultrasound

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30
Q

Gold standard investigation for primary sclerosing cholangitis

A

Magnetic resonance cholangiopancreatography (MRCP)
(May show bile duct lesions or strictures

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31
Q

Antibodies for primary sclerosing cholangitis

A

No specific antibodies for PSC!
* Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%
* Antinuclear antibodies (ANA) in up to 77%

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32
Q

First line management for primary sclerosising cholangitis

A
  • ERCP = dilate + stent strictures
  • Ursodeoxycholic acid = slow progression
  • Cholestyramine = a bile sequestrate (reduce pruritus)

Curative: Liver transplant

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33
Q

Complications of primary sclerosing cholangitis

A
  • Cirrhosis -> end-stage liver disease
  • Ascites
  • Oesophageal varcies
  • Acute bacterial cholangitis
  • Cholangiocarcinoma
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34
Q

What is primary biliary cholangitis/cirrhosis?

A

Autoimmune destruction of the bile ducts → cirrhosis

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35
Q

What is the typical patient to present with primary biliary cholangitis/cirrhosis?

A

Middle aged woman with other immune or rheumatoid conditions

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36
Q

A middle aged woman with rheumatoid arthritis presents with pruritus, abdominal pain (RUQ), jaundice, pale stools, fatty yellow deposits on her eyelids (Xanthelasma) and signs of cirrhosis (ascites and splenomegaly). Diagnosis?

A

Primary biliary cirrhosis/cholangitis

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37
Q

What is the most specifc antibody test for primary biliary cholangitis/cirrhosis?

A

Anti-mitochondria antibodies (AMA)

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38
Q

Investigations for primary biliary cholangitis/cirrhosis

A

Antibody tests
* Anti-mitochondrial antibodies
* Anti-nuclear antibodies

LFTs
* ↑ALP (first to be raised - obstructive pathology)
* ↑GCT
* ↑Bilirubin (later)

Abdominal ultrasound
Liver biopsy - diagnosing + staging
ESR (raised)
IgM (raised)

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39
Q

First line management for primary biliary cholangitis/cirrhosis

A
  • Ursodeoxycholic acid
  • Cholestyramine
  • ADEK supplementation
  • Biphosphonates (for osteoporosis)
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40
Q

Complications for primary biliary cholangitis/cirrhosis

A
  • Advanced liver cirrhosis
  • Portal hypertension
  • Osteoporosis
  • Hyperlipidaemia
  • Fat soluble vitamin deficiencies
  • Steatorrhoea (greasy stools due to lack of bile salts to digest fats)
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41
Q

What is the mnemonic for the causes of pancreatitis?

A

I GET SMASHED
- I–Idiopathic
- G–Gallstones
- E–Ethanol (alcohol consumption)
- T–Trauma
- S–Steroids
- M–Mumps
- A–Autoimmune
- S–Scorpion sting
- H–Hyperlipidaemia
- E–ERCP
- D–Drugs (furosemide, thiazide diuretics and azathioprine)

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42
Q

What people are likely to present with acute pancreatitis?
(Men and women)

A
  • Gallstones → women + older
  • Alcohol → men + younger
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43
Q

Define acute pancreatitis

A

Sudden inflammation + haemorrhaging of the pancreas - due to its autodigestion

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44
Q

Where do gallstones get lodged to cause acute pancreatitis?

A

The spincter of Odi
(Blocks the release of pancreatitis juices)

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45
Q

A patient presents with acute onset of severe epigastric pain that radiates to the back. They have a low grade fever, N+V and slightly tachcardic. On examination the abdomen is distended and they have bruising around the periumbilical region and on flanks. Diagnosis?

A

Acute pancreatitis

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46
Q

What are the two clinical signs associated with acute pancreatitis?

A
  • Cullen’s sign (bruising around periumbilical region)
  • Grey Turner’s sign (bruising on flanks)
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47
Q

What is the key lab test for pancreatitis?

A

Lipase (more specific + sensitive than amylase)
X3 upper limit

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48
Q

What are the factors that cause alcoholic liver disease?

A
  • Alcohol comsumption (prolonged and heavy)
  • Genetic predisposition
  • Immunological immune response
  • (Rx - Hepatitis C)
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49
Q

In 3 threes what is the pathophysiology of alcoholic liver disease?

A

Fatty liver → hepatitis → cirhhosis
Fatty liver → Alcoholic hepatitis → alcoholic steatosis (cells become swollen with fat) → cirrhosis

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50
Q

Metabolism of alcohol produces what in the liver?

A

Fat

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51
Q

What is the cellular pathway in which alcohol causes cirrhosis?

A
  • Alcohol = transforms stellate cells into collagen-producing myofibroblast cells
  • Some cases: Collagen = laid down around the central hepatic veins → cirrhosis without preceding hepatitis
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52
Q

What are the signs and symptoms of alcoholic liver disease?

A

Signs:
* Hepatomegaly
* Ascites
* Jaundice
* Weight loss/ gain

Symptoms:
* RUQ pain
* N + V
* Diarrhoea
* Fatigue

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53
Q

Name some complications (/conditions) from alcohol

A
  • Alcoholic liver disease
  • Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
  • Alcohol Dependence and Withdrawal
  • Wernicke-Korsakoff Syndrome (WKS)
  • Pancreatitis
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54
Q

Name the signs of liver disease

A
  • Jaundice
  • Hepatomegaly
  • Spider Naevi
  • Bruising (due to abnormal clotting)
  • Ascites
  • Gynaecomastia
  • Palmar Erythema
  • Caput Medusae – engorged superficial epigastric veins
  • Asterixis – “flapping tremor” in decompensated liver disease
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55
Q

What blood tests what indicate alcoholic liver disease?

A
  • FBC (raised MCV)
  • LFTs
    • Transaminases (ALT + AST) (elevated): AST>ALT ratio (usually 2:1)
    • Gamma-GT (very elevated)
    • ALP (raised in later disease)
  • Bilirubin (elevated - in cirrhosis)
  • Serum albumin (low - impaired function of liver)

U+Es = deranged in hepatorenal syndrome

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56
Q

What imaging Ix can be used in alcoholic liver disease?

A
  • Ultrasound (see fatty changes)
    • ‘FibroScan (check stiffness of liver → gives indication of fibrosis)
  • CT and MRI scans (look for fatty infiltration of liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes, ascites)
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57
Q

What is the gold standard Ix for alcoholic liver disease?

A

Liver biopsy

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58
Q

What Ix is used to confirm a diagnosis of alcohol-related hepatitis or cirrhosis?

A

Liver biopsy

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59
Q

DDx for alcoholic liver disease

A
  • Cholecystitis
  • Hepatits B virus
  • Hepatitis C
  • Hepatitis A
  • Acute liver failure
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60
Q

What are the stages of alcohol withdrawal?

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”

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61
Q

How does delirium tremens present?

A
  • Acute confusion
  • Severe agitation
  • Delusions + hallucination
  • Tremor
  • Tachycardia
  • Hypertension
  • Hyperthermia
  • Ataxia (difficulties with coordinated movements)
  • Arrhythmias
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62
Q

Managment of alcoholic liver disease

A
  • Acohol abstinence (delirium tremens risk → treat with diazepam)
  • IV thiamine → prevent Wernicke-Korsakoff encephalopathy
  • Diet high in vitamins + protein
  • Liver transplant
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63
Q

What is the triad of Wernecke-Korsakoff encephalopathy?

A
  • Confusion
  • Ataxia (poor muscle control)
  • Nystagmus (rhythmica, repetitive and involuntary movement of the eyes)
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64
Q

Complications of alcoholic liver disease

A
  • Cirrhosis
  • Liver failure
  • Hepatic encephalopathy
  • GI bleeding
  • Portal hypertension
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65
Q

What is NAFLD?

A

Non-alcoholic fatty liver disease = NAFLD
* Disease due to accumulation in liver → associated with inflammation → interfere with functioning of liver cells

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66
Q

What can NAFLD progress to?

A
  • Hepatitis
  • Cirrhosis
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67
Q

What are the stages of NAFLD?

A

Non-alcoholic steatohepatitis (NASH) → fibrosis → cirrhosis
* NAFLD = steatosis without inflammation
* NASH = steatosis + hepatic inflammation - indistinguishable from alcoholic steatohepatitis

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68
Q

What are the Rx of NAFLD?

A

Same as cardiovascular disease:
* Obesity
* Type 2 diabetes
* Hyperlipidaemia
* High cholesterol

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69
Q

What are the signs and symptoms of NAFLD?

A

Signs:
* Hepatomegaly
* RUQ pain
* Jaundice

Symptoms:
* Fatigue + malaise

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70
Q

What do the LFTs look like in NAFLD?

A

All a little elevated
Serum ALT>AST level = NAFLD

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71
Q

What are the proportions/ratio for the LFTs (transaminases) in alcoholic liver disease and NAFLD?

A
  • Alcoholic liver disease (AST>ALT → 2:1)
  • NAFLD (ALT>AST)
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72
Q

How do you distinuish between NAFLD and NASH on a liver biopsy?

A

> 5% fat content → NAFLD

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73
Q

What imaging Ix can you perform for NAFLD?

A

Ultrasound liver
(Confirm hepatic steatosis (fatty liver))

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74
Q

What is the fiest line Ix to measure fibrosis in the liver?

A

Enhanced Liver Fibrosis (ELF) blood test
(ELF - santa is not an alcoholic)

NAFLD fibrosis scoreis the2nd line assessment for liver fibrosis

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75
Q

How do you differentiate between alcoholic liver disease and NAFLD?

A

Quantification of alcohol intake

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76
Q

What are the pharmacological treatment for NAFLD?

A

No licensed drug treatment
(Just lifestyle changes and maybe statins for hyperlipidaemia)

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77
Q

What is the treatment of liver fibrosis?

A
  • Vitamin E
  • Pioglotazone
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78
Q

What is liver cirrhosis characterised by?

A
  • Loss of normal hepatic architecture
  • Nodular regneration
  • Bridging fibrosis
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79
Q

Brief pathology of liver cirrhosis and portal hypertension

A
  • Liver cirrhosis = result of chronic inflammation + damage to liver cells
  • Damaged liver cells = replaced with scar tissue (fibrosis)
  • Nodules of scar tissue = form within the liver
  • Fibrosis = affects the structure + blood flow through the liver → causing increased resistance in the vessels leading to the liver
    • = Portal hypertension
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80
Q

What are tissue macrophages in the liver called?

A

Kupffer cells

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81
Q

What is the pathology of cirhosis caused by chronic liver injury and liver injury?

A
  • Chronic liver injury results in inflammation + matrix deposition + necrosis + angiogenesis → fibrosis
  • Liver injury = causes necrosis + apoptosis → releasing cell contents + reactive oxygen species (ROS)
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82
Q

What causes micronodular and macronodular cirrhosis?

A
  • Micronodular = alcohol + biliary tract disease
  • Macronodular = chronic viral hepatitis
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83
Q

What does ‘compensated’ mean in terms of liver function?

A

When the liver can still function effectively + there are no (or few) noticeable clinical symptoms

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84
Q

What does ‘decompensated’ mean regarding liver function?

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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85
Q

What are the signs of liver cirrhosis? Mneumonic?

A

BASH OJ
- Bruising – due to abnormal clotting
- Ascites
- Splenomegaly – due to portal hypertension
- Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
- **Oedema** - decreased albumin in blood
- Jaundice – caused by raised bilirubin

Symptoms:
* Compensated → asymptomatic; non-specific (weight loss, fatigue)
* Decompensated → Pruritis, abdominal pain (due to ascites)

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86
Q

What vassopressin analogue is used to causes vasoconstriction in oesophageal varices?

A

Terlipressin

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87
Q

What is the gold standard Ix to confirm liver cirrhosis?

A

Liver biopsy….Obvs!

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88
Q

Patient has liver cirrhosis and the blood tests come back. What what they look like?

A
  • Serum albumin + prothrombin time = best indicators of liver function
    • Albumin (low)
    • Prothrombin (elevated)
  • Bilirubin (raised)
  • AST (raised)
  • ALT (raised)
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89
Q

Why might you have hyponatraemia in severe liver disease?

A

Hyponatraemia = indicates fluid retention in severe liver disease.

(Also, Urea and creatinine become deranged in hepatorenal syndrome)

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90
Q

What scan do NICE recommned for patients that are risk of liver cirrhosis every two years?

A

FibroScan (‘Transient elastography’)

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91
Q

Why might you perform an upper GI endoscopy on someone with liver cirrhosis?

A

When portal hypertension is suspected → for oesophageal varices

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92
Q

What scoring system is used to classify the severity of liver cirrhosis?

A

Child-Pugh Score

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93
Q

What scoring system gives you the estimated 3 month mortality for someone with liver cirrhosis?

A

MELD Score
(Helps guide referral for liver transplant)

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94
Q

What is the management for liver cirrhosis?

A
  • Treat underlying cause
    • Alcohol abstinence
    • Antivirals for Hep C
    • Spironolactone for ascites
  • Good nutrition - high protein + low sodium diet
  • Liver transplant

Every 6 months:

  • Ultrasound screening for hepatocellular carcinoma
  • MELD score
  • Endoscopy every 3 years in patients without known varices
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95
Q

What are the complications of liver cirrhosis?

A
  • Coagulopathy - fall in clotting factors clotting factors II, VII, IX, and X
  • Thrombocytopenia
  • Hypoalbuminaemia
  • Portal hypertension
    • Ascites
    • Oesophageal varices
    • Variceal bleeding
  • Hepatocellular carcinoma
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96
Q

What is jaundice a result of?

A

Raised/excess bilirubin

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97
Q

What is bilirubin a component of?

A

Bile

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98
Q

What is pre-hepatic jaundice? Causes?

A

Excess of Hb → increases total unconjugated bilirubin
* Malaria
* Sickle cell anaemia

99
Q

What is hepatic jaundice? Causes?

A

Failure of hepatocytes to take up, metabolise or excrete bilirubin
* Viral hepatitis
* Drugs, alcohol
* Cirrhosis

Increased unconjugated + conjugated bilirubin

100
Q

How does hepatic jaundice present?

A
  • Dark urine
  • Normal/pale stools
101
Q

What is post-hepatic jaundice? Causes?

A

Obstruction in the biliary tree
* Gallstones
* Pancreatitis (head pf pancreas blocks common bile duct)

Increased conjugated bilirubin

102
Q

What does dark urine, pale stool and itching indicate?

A

Hepatic or post-hepatic jaundice

103
Q

A patients test results come back:
* Cholestatic pattern of serum LFTs (elevated ALP, GGT)
* Anti-mitochondrial antibody

Diagnosis?

A

Primary biliary cholangitis

104
Q

What is Cullen’s sign and which condition does it present in?

A

Bruising around the preumbilical region
(Acute pancreas)

105
Q

What is Grey Turner’s sign and which condition does it present in?

A

Bruising on flanks
(Acute pancreatitis)

106
Q

First line tests for acute pancreatitis?

A

LFTs:
* Raised serum lipase (lipase to amylase > 2 suggests alcoholic)
* Raised ALT and AST (elevated ALT>150 suggests gallstones)

CRP
Transabdominal ultrasound (initial assessment of gallstones)

107
Q

What scoring system is used to assess the severity of pancreatitis?

A

Glasgow score
* (0-1: mild pancreatitis)
* (2: Moderate pancreatitis)
* (3 or more: severe pancreatitis)

108
Q

Management for acute pancreatitis?

A
  • Initial resuscitation (ABCDE approach)
  • IV fluids
  • Analgesia
  • Treatment of gallstones in gallstone pancreatitis (ERCP/cholecystectomy)
  • Antibiotics (evidence of infection)
  • Treatment of complications (endoscopic or percutaneous drainage of large collections)
109
Q

What is chronic pancreatitis?

A
  • Chronic inflammation due to structural changes (fibrosis, atrophy, calcification)
  • Results in fibrosis + reduced function in pancreatic tissue
  • Generally irreversible
110
Q

Difference between acute and chronic pancreatitis?

A
  • Acute pancreatitis = a self-limiting and reversible pancreatic injury associated with mid-epigastric abdominal pain and elevated serum pancreatic enzymes
  • Chronic pancreatitis = characterised by recurrent or persistent abdominal pain and progressive injury to the pancreas and surrounding structures, resulting in scarring and loss of function.
111
Q

Causes of chronic pancreatitis?

A
  • Alcohol use (most common)
  • Repeated bouts of acute pancreatitis
  • Cystic fibrosis - main cause in children
  • Tumours
  • Pancreatic trauma
112
Q

Rx for chronic pancreatitis?

A
  • Alcohol
  • Smoking
  • Family history
  • Coeliac disease
113
Q

What are the signs and symptoms of chronic pancreatitis?

A

Similar to acute pancreatitis - but less intense + longer lasting
* Epigastric pain that radiates to the back (may be linked to eating meals)
* N + V

  • Endocrine dysfunction: Malabsorption (weight loss, steatorrhoea, vitamin deficiency)
  • Exocrine dysfunction: Diabetes Mellitus
114
Q

Ix for chronic pancreatitis

A
  • Lab tests
    • May have low lipase + amylase (as there may not be enough healthy tissue to make enzymes)
    • Faecal elastase
  • Transabdominal ultrasound
  • Abdominal X-ray (calcifications)
  • CT abdomen
  • ERCP/MRCP
115
Q

What is the management of chronic pancreatitis?

A
  • Lifestyle modification → stopping smoking + alcohol
  • Analgesia - pain management
  • Replace digestive enzymes + nutritional supplements (i.e. lipase)
    • Otherwise lack of enzymes = leads to malabsorption of fat, greasy stools (steatorrhea) + deficiency in fat-soluble vitamins
  • ERCP with stenting (treat strictures + obstruction to the biliary system + pancreatic)
  • Surgery (pseudocysts, abscesses, severe chronic pain)
116
Q

What are the complications of chronic pancreatitis?

A
  • Chronic epigastric pain
  • Loss of exocrine function, resulting in a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract
  • Loss of endocrine function, resulting in a lack of insulin, leading to diabetes
  • Damageandstricturesto the duct system, resulting in obstruction in the excretion of pancreatic juice and bile
  • Formation ofpseudocystsorabscesses
117
Q

What is ascites?

A

Abnormal accumulation of fluid within the peritoneal cavity

118
Q

What conditions can impair blood flow and result in ascites?

A
  • Cirrhosis i.e. portal hypertension
  • Cardiac failure
  • Constrictive pericarditis
119
Q

What conditions can decrease the oncotic pressure (low protein), leading to ascites?

A
  • Hypoalbuminaemia
  • Malnutrition
  • Nephrotic syndrome
120
Q

What serious condition that causes local inflammation causes ascites?

A

Peritonitis

121
Q

What is exudate ascites?

A
  • High protein
  • Extremely bad
  • Causes: Cancer, sepsis, TB, nephrotic syndrome
122
Q

What is transudate ascites?

A
  • Low protein fluid
  • Causes: Cirrhosis
123
Q

How do you manage ascites? Briefly

A
  • Treat underlying cause
  • Diet
  • Diuretic
  • Drainage
124
Q

What are the signs of ascites?

A
  • **Abdominal swelling **
  • Shifting dullness
    • Flank dullness
    • Bulging flanks
  • Jaundice
  • Oedema

(Abdominal swelling with shifting dullness)

125
Q

What should you suspect if a patient with ascites complains of severe pain?

A

Bacterial peritonitis

126
Q

What are Ix for ascites?

A
  • Presence of fluid = confirmed by demonstrating shifting dullness
  • Ultrasound
  • Ascitic aspiration → culture, gram stain, cytology, protein, amylase
  • Serum Ascites Albumin Gradient (SAAG)
127
Q

What SAAG tell you?

A

Serum Ascitic Albumin Gradient (SAAG)
* Defines the presence of portal hypertension in patients with ascites

128
Q

A patient presents with ascites, they have a history of liver disease, what Ix do you perform to establish whether portal hypertension is also present?

A

SAAG
(Serum Ascites Albumin Gradient)

129
Q

What are the management options to treat ascites?

A

Treat underlying cause, diet, diuretic, drainage
* Treat underlying cause
* /Low sodium diet
* Aldosterone antagonist diuretics (spironolactone)
* Paracentesis (ascitic tap or ascitic drain)
* Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin)

130
Q

What is spontaneous bacterial peritonitis (SBP)?

A

Infection develops in the ascitic fluid + peritoneal lining without a clear cause
(not secondary to ascitic drain or bowel perforation)

131
Q

An ascitic patient starts to deteroriate, what should you suspect?
(They develop hypotension)

A

Spontaneous bacterial peritonitis (SBP)

132
Q

What are the common organisms that can cause spontaneous bacterial peritonitis?

A

Escherichia coli
Klebsiella pneumoniae
Gram positive cocci (staphylococcus + enterococcus)

133
Q

What is the prophylaxis and management of SBP?

A

Prophylaxis: Ciprofloxacin
Management: IV cephalosporin (cefataxime)

134
Q

What infection is commonly seen in patients with end-stage liver disease?

A

Spontanous Bacterial Peritonitis?

135
Q

Rx for SBP?

A
  • Decompensated hepatic state (usually cirrhosis)
  • GI bleeding
  • Endoscopic sclerotherapy for oesophageal varices
  • Low ascitic protein/complement
136
Q

What are the signs and symptoms for SBP?

A

Signs:
* Ascites
* Deranged bloods - raised: WBC, CRP, Creatinine, metabolic acidosis
* Altered mental status
* GI bleeding
* Hypotension
* Ileus

Symptoms:
* Fever
* Abdominal pain
* Vomiting

137
Q

Read: Ix results for SBP

A
  • FBC
    • Leukocytosis (maybe)
    • Anaemia (potential GI bleeding)
  • Blood cultures
    • Growth of causative organism
  • LFTs
    • Liver enzymes (elevated)
    • Bilirubin (elevated)
    • Albumin (decreased)
138
Q

What are two major complications of SBP?

A
  • Sepsis
  • Renal failure
139
Q

What is portal hypertension?

A

Increased back pressure into the portal system
- Liver cirrhosis = ↑resistance of blood flow in the liver
- As a result, ↑back-pressure into the portal system

140
Q

What are the 3 categories for portal hypertension? Give an example of each

A

Pre-hepatic: due to bloackage of portal vein before liver
* Portal vein thrombosis

Intrahepatic: resulting from distrortion of liver architecture
* Cirrhosis (most common)
* Sarcoidosis

Post-hepatic: due to venous blockage outside of the liver
* Right HF
* IVC obstruction

141
Q

What are the key presentations of portal hypertension?

Mnemonic

A

ABCDE
- A - Ascites
- B - Bleeding (haematemesis, piles)
- C - Caput medusae
- D - Diminished liver
- E - Enlarged spleen

142
Q

What are the signs and symptoms of portal hypertension?

A

Signs:
* **Ascites **
* Hepatic encephalopathy
* Splenomegaly
* Oesophago-gastric varices
* Jaundice
* Signs + symptoms of encephalopathy

Symptoms:
* Bleeding from * Oesophago-gastric varices

143
Q

Ix for portal hypertension

A
  • Paracentesis (SAAG) - determine if portal hypertension is cause of ascites
  • Upper endoscopy - diagnose/treat varices
  • CT/MRI scan
    • Ascites
    • Cirrhosis
    • Splenomegaly
  • FBC
  • LFTs
144
Q

How do you treat portal hypertension?

A
  • Beta-blockers (decrease portal venous pressure)
  • Non-selective beta-blockers (prophylaxis)
  • Antibiotics (prophylaxis for SBP)
  • Diuretics + sodium restriction (for ascites)
145
Q

What complications can portal hypertension lead to?

A
  • Oesophageal varices
  • Caput medusae (distension of abdominal wall veins)
  • Ascites (increased hydrostatic pressure + hypoalbuminaemia)
  • Spontaneous bacterial peritonitis
  • Anaemia, thrombocytopenia, leukopenia
146
Q

What are oesophageal varices?

A

Oesophageal varices are dilated collateral blood vessels that develop as a complication of portal hypertension, usually in the setting of cirrhosis.
(Cirrhosis → Portal hypertension → oesophago-gastric varices)

147
Q

Where do oesphago-gastric varices tend to develop?

A

In the lower oesophagus + gastric cardia

148
Q

What is the cause of oesphago-gastric varices?

A

Portal hypertension
(Rx: cirrhosis, alcoholism)

149
Q

Read: Pathology of oesophago-gastric varices

A
  • As these vessels are thin and not meant to transport higher pressure blood, they can rupture
  • Rupture → haematemesis
  • Rupture → blood digested → melaena
150
Q

Signs and symptoms of oesophago-varices

A
  • Haematemesis
  • Melaena
  • Abdominal pain
  • Rectal bleeding
  • Hypotension
  • Tachycardia
  • Ascites
  • Splenomegaly
  • Pallor
  • Signs of chronic liver damage (jaundice, easy bruising, ascites)
151
Q

A patient presents with haematemesis, abdominal pain. O/E find ascites, hypotension, and splenomegaly. You suspect oesphago-gastric varices. What Ix do you perform to confirm the diagnosis?

A

GI endoscopy

152
Q

How might someone with oesophago-gastric varices blood results look like?

A
  • FBC
    • Microcytic anaemia
    • And/or thrombocytopenia
  • U&Es
    • Hyponatraemia
      • Due to fluid overload or use of diuretics may be present in patients with cirrhosis with ascites
  • LFTs
    • Elevated transaminases (with aspartate aminotransferase/alanine aminotransferase ratio ≥1)
    • Elevated alkaline phosphatase
    • Elevated bilirubin
  • Urea and creatinine
    • Elevated
153
Q

What are some DDx for oesophago-gastric varices?

A
  • Peptic ulcer disease
  • Mallory-Weiss tear
  • Hiatal hernia
154
Q

What would someone’s serum urea levels look like if they have a GI bleed?

A

Elevated urea (elevated without creatinine)
(Result of breakdown of blood in the stomach in cases of acute bleeding)

155
Q

What is haemochromatosis?

A
  • Iron storage disorder
  • Excessive total body iron
  • Deposition of iron in tissues

Excess iron deposition due to high levels of hepcidin

156
Q

Haemochromatosis is caused by high levels of what?

A

Hepcidin

157
Q

What is the genetic mutation that causes haemochromatosis?

A
  • Human Haemochromatosis protein (HFE) gene - on chromsome 6
  • Autosomal recessive
158
Q

Why does haemochromatosis present later in women?

A

Menstruation regulates iron elimination from the body

159
Q

A white male patient presents with skin pigmentation complaining joint pain and chronic tiredness. O/E you detect hepatomegaly. Possible diagnosis?

A

Haemochromatosis

160
Q

What are the signs and symptoms of haemochromatosis?

A

Signs:
* Skin pigmentation (bronze/grey discolouration)
* Hair loss
* Erectile dysfunctiom
* Hepatomegaly

Symptoms:
* Chronic tiredness
* Arthralgias (joint pain)
* Amenorrhoea
* Cognitive symptoms (memory + mood disturbance)

161
Q

What investigations should you request for someone with haemochromatosis?

A
  • Transferrin saturation (Iron overload → high transferrin saturation)
  • Serum ferritin level
  • Genetic testing (confirm diagnosis)

Liver biopsy (Perl’s stain used to establish iron conc in parenchymal cells)
MRI (iron deposits in liver + heart)

162
Q

DDx for haemochromatosis

A
  • Hepatitis B
  • Hepatitis C
  • Non-alcoholic fatty liver disease (NAFLD)
163
Q

Management for haemochromatosis

A
  • Venesection - weekly
  • Monitoring serum ferritin
  • Avoid alcohol
  • Genetic counselling
164
Q

Complications of haemochromatosis?

A
  • Type I diabetes (iron deposits in pancreas)
  • Liver damage/cirrhosis
  • Endocrine (iron deposits in pituitary glands)
  • Cardiomyopathy (iron deposits in the heart
  • Hypothyroidism (iron deposits in the thyroid)
165
Q

What is Wilson’s disease?

A

Autosomal recessive disorder of copper accumulation + toxicity
(ATP7B gene mutation)

166
Q

What happens in Wilson’s disease (pathology)?

A

When hepatic storage is exceeded → copper is released into the circulation → deposited into other organs

167
Q

What are the key presentations (groups of Sx) for Wilson’s disease?

A
  • Kayser-Fleischer ring in cornea (brownish circles in eyes)
  • Hepatic problems
  • Neurological problems
  • Psychiatric problems
168
Q

A patient presents with brown circles around their pupils. What are these and what condition are they associated with?

A
  • Kayser-Fleischer rings
  • Indication of Wilson’s disease
169
Q

What are the signs of Wilson’s disease?

A
  • Kayser-Fleischer rings in cornea
  • Osteopenia
  • Haemolytic anaemia (RBCs being broken down too fast)
  • Renal tubular damage (leading to renal tubular acidosis)
170
Q

What are the neurological symptoms found in Wilson’s disease?

A
  • Concentration + coordination
  • Dysarthria (speech difficulties)
  • Dystonia (abnormal muscle tone)
  • Parkinsonism (copper deposition in the basal ganglia)
    • Asymmetrical in Wilson’s disease (differentiates from Parkinson’s)
171
Q

A patient presents with Parkinsonism Sx with Kayser-Fleischer rings in their eyes. Possible diagnosis?

A

Wilson’s disease

172
Q

What is the first-line and gold standard Ix for Wilson’s disease

A

First line:
* Low serum caeruloplasmin (carries copper in the blood)

Gold standard:
* Liver biopsy (diagnostic)
* 24-hr urine copper assay (elevated)

173
Q

What is the management for Wilson’s disease

A

COPPER CHELATION
* Penicillamine
* Trientene

174
Q

Major complication of Wilson’s disease?

A

Liver failure

175
Q

What genetic mutation causes Alpha-1 Antitrypsin Deficiency?

A

Autosomal recessive mutation in Alpha-1 antitrypsin
Chromosme 14

176
Q

What is the alpha-1 antitrypsin enzyme responsible for?

A

Neutralising neutrophil elastase

177
Q

Who does Alpha-1 antitrypsin deficiency typically affect?

A

Men aged 32-41

178
Q

Pathology of alpha-1 antitrypsin deficiency

A
  • Elastase = digests connective tissues (secreted by neutrophils)
  • Alpha-1-antitrypsin (A1AT) = mainly produced by the liver (travels around the body)
  • A1AT = inhibits neutrophil eastase enzyme → offering protection
179
Q

What are the 2 major organs affected by alpha-1-antitrypsin deficiency?

A
  • Liver: Liver cirrhosis (after 50 years)
  • Lungs: Bronchiectasis + emphysema (after 30 years)
180
Q

A patient presents which jaundice, wheezing, productive cough and exertional dyspnoea. What condition(s) do they have?

A
  • Liver cirrhosis
  • Bronchiectasis + emphysema
    ALPHA-1-ANTITRYPSIN DEFICIENCY
181
Q

What are the first line and gold standard testing for A1AT deficiency?

A

First line:
* Serum alpha-1-antitrypsin (low)
* Liver biopsy (cirrhosis, Acid-Schiff positive staining globules)
* High resolution CT thorax (diagnoses bronchiectasis + emphysema)

Gold-standard:
* Genetic testing for A1AT gene

182
Q

DDx for Alpha-1-Antitrypsin deficiency

A
  • Viral hepatitis
  • Alcoholic liver disease
  • Asthma
  • COPD
  • Bronchiectasis
183
Q

Mx for Alpha-1-antitrypsin deficiency

A
  • Stop smoking (emphysema)
  • Symptomatic management
  • Organ transplant (for end-stage liver or lung disease)
  • Monitor for complications
184
Q

What is a complication of A1AT deficiency?

A

Granulomatosis with polyangiitis (Wegener’s granulomatosis)

185
Q

What is Wernicke’s encephalopathy?

A

Neurological emergency resulting from thiamine (vitamin B1) deficiency
(Result from excessive alcohol)

186
Q

Which presents first; Wernicke’s encephalopathy or Korsakoff’s syndrome?

A

Wernicke’s encephalopathy

187
Q

What can result in a thiamine deficiency?

A
  • Decreased intake (oral or parenteral)
  • Relative deficiency - due to increased demands
  • Malabsorption in the GI tract
188
Q

How does Wernicke’s encephalopathy present?

A
  • Confusion
  • Occulomotor disturbances (disturbances in eye movements)
  • Ataxia (difficulties iin coordinated movement)
189
Q

Ix for Wernicke’s encephalopathy

A
  • Therapeutic trial of parenteral thiamine
  • FBC (infection, raised WBC count)
  • LFTs (elevated)
  • Blood alcohol level
190
Q

DDx for Wernicke’s encephalopathy

A
  • Alcohol intoxication
  • Alcohol withdrawal
  • Viral encephalitis
191
Q

Prevention + treatment of Wernicke’s pathology?

A

Thiamine supplementation + abstaining from alcohol

192
Q

Name 2 complicatiosn of Wernicke’s encephalopathy

A
  • Korsakoff’s psychosis
  • Hearing loss
  • Seizures
193
Q

Difference between Wernicke’s encephalopathy and Korsakoff’s syndrome?

A

Features of Wernicke’s encephalopathy
- Confusion
- Oculomotor disturbances (disturbances of eye movements)
- Ataxia (difficulties with coordinated movements)

Features of Korsakoffs syndrome
- Memory impairment (retrograde and anterograde)
- Behavioural changes

(Memory + behaviour = difference)

194
Q

Difference between acute and chronic hepatits?

A
  • Acute = liver inflammation 6 months or less
  • Chronic = more than 6 months
  • All cases are acute in the first instance → some go on to cause chronic hepatitis
195
Q

Which types of hepatitis are transmitted by the faecal-oral route and are linked to contaminated food + water?

A

HepA and HepE

196
Q

What is the treatment for HepA and HepE?

A

Supportive treatment as they are self-limiting

197
Q

Which forms of hepatitis are preventable by vaccine?

A

HepA and HepB

198
Q

Which forms of Hepatitis are blood-borne?

A

Hep B,C,D

199
Q

Which two forms of hepatitis can only be acute?

A

HepA and HepE

200
Q

Which is teh only form of hepatitis that is made of dsDNA?

A

Hepatitis B

201
Q

Which form of hepatitis does HepD need?

A

Hep D
(Best BuDs)

202
Q

How is HepB transmitted?

A

3Bs:
* Bodily fluids
* Blood
* Birth

203
Q

Is HepA a notifiable disease?

A

Yeah

204
Q

What are the causes of HepA in high-income countries?

A
  • Travel
  • Sex (MSM)
  • Iv drug users
205
Q

What are some Rx for HepA?

A
  • Shellfish
  • Travellers
  • Food handlers
  • Poor access to clean drinking water
206
Q

What are the phases of presentation hepatitis A?

A
  • Incubation period (28 days)
  • Pre-icteric phase (non-specific symptoms + abdo pain)
  • Icteric phase (jaundice + hepatosplenomegaly)
    • Icteric = jaundice
  • 100% immunity after infection
207
Q

Ix for Hepatitis A

A
  • Antibody tests (HAV antibodies)
  • LFTs (raised AST + ALT + bilirubin)
  • FBC (reduced WBC count)
  • Raised ESR
208
Q

What are the antibodies in the acute and chronic phase of HepA?

A

Acute: Anti-HAV IgM (non-specific)
Chronic: Anti-HAV IgG (longer lasting)

209
Q

DDx causes of HepA

A
  • Other causes of jaundice
  • Other types of viral + drug-induced hepatitis
210
Q

Mx for HepA

A
  • SUPPORTIVE
  • Monitor liver function (INR, albumin, bilirubin, etc.)
  • Acute liver failure (’fulminant hepatitis’) in <1%
    • Liaise with hepatology/liver transplant centre
  • Management of close contacts (HNIG (human normal immunoglobulin), vaccine)
  • Primary prevention: Hep A vaccination
    • e.g. travellers, MSMs, IDUs
211
Q

Mx for HepA

A
  • SUPPORTIVE
  • Monitor liver function (INR, albumin, bilirubin, etc.)
  • Acute liver failure (’fulminant hepatitis’) in <1%
    • Liaise with hepatology/liver transplant centre
  • Management of close contacts (HNIG (human normal immunoglobulin), vaccine)
  • Primary prevention: Hep A vaccination
    • e.g. travellers, MSMs, IDUs
212
Q

Complications for HepA

A
  • Pancreatitis
  • Acalculous cholecytitis
213
Q

When can HepE become chronic?

A

In immunocompromised patients

214
Q

Which genotype of HepE is linked to undercooked meat?

A

G3&4

215
Q

Which type of hepatitis is linked to undercooked pork?

A

HepE
(pork-EEEE)

216
Q

A patient presents with an acute neurological problem and abnormal LFTs. What is a possible viral diagnosis?

A

HepE

217
Q

What are the anitbodies found in the acute and chronic phases of HepE?

A
  • Acute: Anti-HEV IgM
  • Chronic: Anti-HEV IgG
218
Q

Serology for HepE in immunocompromised patients is unreliable. What do you have to measure and monitor?

A

HEV RNA in serum +/- stool

219
Q

What anti-viral do you give in HepE cases?

A

Ribavirin

220
Q

Someone can have HepB and be co-infected with which other type of hepatitis?

A

HepD

221
Q

Rx or HepB

A
  • Healthcare personnel
  • Emergency + rescue teams
  • KD/dialysis patients
  • Travellers
  • MSM
  • IV drug users
222
Q

What serology do you perform for HepB?

A

Acute: Anti-HB core IgM
Chronic: Anti-HB core IgG

  • If they have e-antigen (eAg) → high levels of infections
  • Presence of e-antibody (eAb) → lower levels of infection
223
Q

What is the management for acute and chronic hepatitis B?

A
  • Acute: Supportive treatment
  • Chronic: Pegylated interferon-alpha 2
    • Neucloside analogues (tenofovir, entecavir)
224
Q

What do you check to check the vaccine response to HepB?

A

Anti-HB surface antibody (sAb)

225
Q

Preventation of HepB

A
  • Check vaccine response with anti-HB surface antibody (sAb)
  • Antenatal screening (HBsAg testing) of pregnant mothers
    • HBV vaccination administered to baby at birth at 1,2,3,4,12 moths
  • Screening + immunisation
    • Sexual + household contacts
    • Blood products
  • Sterile equipment + universal precautions in healthcare
  • Immunisation of healthcare workers + higher risk groups (MSMs, IV drug users)
226
Q

Which hepatitis is common in Eastern Europe?

A

Hep D

227
Q

Ix for HepD

A
  • Same as HepB - antibody test
  • Hep D antibody → if positive, test HDV RNA
228
Q

Management for HepD?

A

Pegylated interferon-alpha 2a

229
Q

Can you be re-infected with HepC?

A

Yes

230
Q

What is the serology process for HepC testing?

A

HCV antibody (can be negative in acute infections/immunocompromised patients) → HCV RNA (detected = current HCV) → HCV genotype (1a, 1b, 3)

231
Q

What medications do you use when treating HepC?

A

Direct acting ant-virals (DAAs)
* Ribavirin + 2 DAAs
(Glecaprevir/Pibrentasvir, Elbasvir/Grazoprevir) - ends in -vir

232
Q

Genetic risk factor for autoimmune hepatitis

A

HLA-DR3.DR4
(Young female)

233
Q

Signs and symptoms of autoimmune hepatitis?

A
  • Fever
  • Jaundice
  • Hepatosplenomegaly
    (Wide spectrum: asymptomatic to cirrhosis + liver failure)
234
Q

Lab results for autoimmune hepatitis

A

↑↑ALT
↑AST
↓Albumin
↑Prothrombin time

235
Q

Antibodies present in type one autoimmune hepatitis?

A

Antinuclear antibodies (ANA)

236
Q

Do you perform a liver biopsy for autoimmune hepatitis?

A

Yes

237
Q

Mx for autoimmune hepatitis?

A

Immunosuppression: Prednisolone +/- azathoprine
Liver transplant (if resistant to drug therapies)

238
Q

Complications of hepatitis?

A
  • Acute liver failure
  • Chronic liver failure
  • Hepatocellualr carcinoma
  • Long-term suppression that can lead to malignancies
239
Q

What is the underlying pathology of hepatic encephalopathy?

A

As liver fails, nitrogenous waste e.g. ammonia builds up in circulation and passes to brain → permanent brain damage (ammonia is neurotoxic)

  • Ammonia = produced by intestinal bacteria - when they they break down proteins + absorbed in the gut
  • Ammonia builds up due to:
    • Functional impairment of liver cells = prevents the metabolising the ammonia - into harmless waste products
    • Collateral vessels between the portal + systemic circulation = mean that ammonia bypasses liver altogether → enters the systemic system directly
240
Q

Risk factors hepatic encephalopathy

A
  • Hypovolaemia
  • Constipation
  • Diuretic overdose
  • Exces protein intake
  • Hypokalaemia + hyponatraemia
241
Q

How does hepatic encephalopathy present?

A
  • Acute → reduced consciousness + confusion
  • Chronic → changes to personality, memory, mood

Signs:
- Hepatomegaly
- Ascites
- Jaundice
- Peripheral oedema

Symptoms:
- Mood disturbances
- Sleep disturbances
- Motor disturbances
- Advanced neurological deficits

242
Q

How is a diagnosis of hepatic encephalopathy diagnosed?

A

Based on:
* Reported neurological deficits
* Laboratory abnormalities showing severe liver dysfunction
* LFTs (abnormal)
- Coagulation profile (elevated prothrombin time)

243
Q

Mx for a patient with hepatic encephalopathy

A
  • Laxative (lactulose) = help clear ammonia from the gut before it is absorbed
  • Antibiotics (rifaximin) = reduces the number of bacteria in the gut producing the ammonia
  • Nutritional support: Nasogastric feeding

Kyla's Phase 2a Flashcards (10 decks)

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