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Haroon Phase 2A > Liver & Friends > Flashcards

Liver & Friends Flashcards

1
Q

Describe the drug metabolism of aspirin

A

Phase I: - Hydrolysis reaction: Aspirin + H2O —> Salcylic acid + Ethanoic acid Phase II: - Conjugated with glycine or glucuronic acid - Forms a range of ionised products which can be excreted

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2
Q

What is the metabolism reaction of alcohol

A

ADH = alcohol dehydrogenase ALDH = aldehyde dehydrogenase

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3
Q

Treatment for paracetamol overdose

A
  • Activated charcoal within 1 hour of ingestion - Sticks to paracetmol to ensure it’s not absorbed (adsorption), decreases all intestinal absorption - Followed by IV N-Acetyl Cysteine - Increases availability of glutathione to get rid of excess NAPQI
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4
Q

Paracetamol metabolism

A
  • 95%: Phase II conjugation -> excreted - 5%: Phase I conjugation -> NAPQI (hepatotoxic) -> Phase II conjugation -> glutathione (antioxidant) -> excreted
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5
Q

How does paracetamol overdose work?

A
  • Shunting phase 1 pathway as phase 2 is too saturated - Glutathione depleted - Hypertoxicity of NAPQI in liver and inflammation
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6
Q

Functions of the liver (ADMIReS)

A

Albumin Detoxification Metabolism of carbs and billirubin Immunity (Kuppfer cells) Regulation of oestrogen levels e Storage (vitamins ADEK, Fe, Cu, fat)

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7
Q

Liver function tests (LFTs) - markers of liver function

A
  • Bilirubin (mainly unconjugated) - Albumin - Prothrombin time (PT/INR)
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8
Q

Direct markers of liver damage

A

High Bilirubin - Low Albumin - High PT/INR

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9
Q

Enzymes that show liver damage is likely

A
  • AST and ALT - AST:ALT usually around 1
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10
Q

Aetiology of acute liver failure

A
  • Viral: Viral hepatitis, CMV, EBV - Autoimmune hep (more chronic) - Drugs: paracetamol overdose, alcohol, ecstasy - HCC - Metabolic: Wilson’s, haemochromatosis, A1ATD - Budd Chiari syndrome
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11
Q

Aetiology of chronic liver failure

A
  • ALD (Most common) - NAFLD - Viral: Hep B, C, D - Budd Chiari syndrome - Drugs - Autoimmine - PBC + PSC
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12
Q

Risk factors for chronic liver failure

A

alcohol - Obesity - T2DM - Drugs - Inherited Metabolic diseases/existing autoimmunity

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13
Q

Fulminant liver failure

A
  • Rare syndrome of massive multiacinar necrosis - Rapid - Caused by paracetamol overdose in 50% of cases in the UK
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14
Q

Types of fulminant liver failure

A

Hyperacute - Hepatic encephalopathy within 7 days of jaundice Acute - Hepatic encephalopathy within 8-28 days of jaundice Subacute - Hepatic encephalopathy within 5-26 weeks of jaundice

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15
Q

Pathophysiology of acute liver failure

A
  • Declined liver function - Liver loses regeneration/repair ability -> irreversibly damaged - In patient with previously normal liver
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16
Q

West Haven criteria grades 1-4 of hepatic encephalopathy

A
  1. Altered mood, sleep problems 2. Lethargy, mild confusion, asterixis, jaundice 3. Marked confusion, solmonence, ataxia 4. Comatose
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17
Q

Presentation of acute liver failure and their diagnosis

A
  • Jaundice - hyperbilirubinaemia - Coagulopathy - raised PT/INR over 1.5 - Hepatic encephalopathy - EEG - Extent of liver damage: biopsy GOLD STANDARD Top 3 are main characteristics
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18
Q

Diagnosis of acute liver failure

A

Bloods - Imaging - Microbiology

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19
Q

Bloods for acute liver failure

A
  • LFTs show liver damage (High bilirubin, low albumin, high PT/INR) - High serum AST + ALT - High NH3 - Low glucose
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20
Q

Imaging for acute liver failure

A

EEG to grade HE - Abdominal ultrasound to check for Budd Chiari syndrome

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21
Q

Microbiology for acute liver failure

A

to rule out infections - Blood culture, urine cultire, ascitic tap

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22
Q

Treatment of acute liver failure

A

ITU, ABCDE, fluid, analgesia - Treat underlying cause and complications

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23
Q

Treatments for complications of liver failure

A
  • High ICP: IV mannitol - HE: Lactulose (increases NH3 excretion) - Coagulopathy: Vit K - Ascites: Diuretics, esp spironolactone - Sepsis: Sepsis 6 pathway
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24
Q

Assessing prognosis and requierd treatment for chronic liver disease

A

✨Child-Pugh score✨ - Considers bilirubin, ascites presence, serum albumin, PT/INR, hepatic encephalopathy A: 100% 1 year survival B: 80% 1 year survival C: 45% 1 year survival

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25
Q

End stage liver failure

A

Decompensated cirrhosis - A High risk factor for developing hepatocellular carcinoma

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26
Q

Presentation of chronic liver failure

A
  • Same as acute + - Portal hypertension - Oesophageal varices - Caput medusae - Spider naevi (Fig.1) - Palmar erythema - Gynecomastia - Clubbing 🕺 - Fetor hepaticus - Dupuytren contracture
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27
Q

Diagnosis of chronic liver failure

A

liver biopsy to determine extent (fibrosis vs cirrhosis) - LFT, Imaging, ultrasound, ascitic tap culture

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28
Q

Treatment of chronic liver failure

A

Prevent progression (decrease alcohol and BMI, avoid Drugs) - Consider liver transplant if Decompensated liver failure - Manage complications

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29
Q

Bilirubin metabolism

A

img

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30
Q

Alcohol units

A
  • 1 unit = 8g/10ml pure alcohol - Recommended no more than 14 units a week for both men and women Equation: strength (ABV) x volume (ml) ————————————— 1000
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31
Q

Risk factors for alcoholic liver disease

A

chronic alcohol - Obesity - Smoking - Female gender - Genetic

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32
Q

Stages of alcoholic liver disease

A

img

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33
Q

Symptoms of alcoholic liver disease

A
  • Early stages may be asymptomatic Later: - Chronic liver failure symptoms - Alcohol dependency - Hepatomegaly
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34
Q

Assessing alcohol dependency

A
  1. Alcohol use disorder ID test: 10 questions 2. Questionnaire with CAGE questions (>2 = dependent!) - Should you cut down? - Are people annoyed by your drinking? - Do you feel guilty about drinking? - Do you drink in the morning? (eye opening)
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35
Q

Diagnosis of alcoholic liver disease

A

Bloods - LFT shows liver damage - High GGT - AST:ALT > 2 - Macrocytic and megaloblastic anaemia Biopsy to confirm extent: - Mallory cytoplasmic inclusion bodies - Inflammation and necrosis in alcoholic hepatitis

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36
Q

Conservative treatment for alcoholic liver disease

A

Healthy diet, lower BMI - Stop alcohol

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37
Q

Pharmacological treatment for alcoholic liver disease

A
  • Consider steroids short term (Maddrey’s discriminant value of 32) - IV thiamine (Vit B1) so you don’t develop Wernicke Korsakoff syndrome - Could also give folate
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38
Q

Surgical treatment for alcoholic liver disease

A
  • Consider liver transplant for ESLF cases - Must have abstained from alcohol for 3+ months
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39
Q

Complications of alcoholic liver disease

A

Pancreatitis - HE - Ascites - HCC - Mallory-weiss tear - Wernicke Korsakoff syndrome

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40
Q

What is a hernia?

A

Protrusion of an organ through a defect in its containing cavity. Typically bowel

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41
Q

Reducible vs irreducible hernias

A

Reducible - can be pushed back into place Irreducible: - Obstructed - intestinal obstruction - Strangulation - intestinal ischaemia - Incarcerated - contents fixed in sac due to size or adhesions

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42
Q

Rolling hiatal hernias

A

20% - LOS stays in the abdomen - Part of fundis rolls into thorax

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43
Q

Sliding hiatal hernias

A

80% - LOS slides into abdomen

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44
Q

What is a hiatal hernia?

A
  • Stomach herniates through diaphragm aperture - Obese women and 50+ year olds
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45
Q

Symptoms of hiatal hernias

A

GORD - Dysphagia

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46
Q

Diagnosis of hiatal hernias

A

Barium swallow (diagnostic) - Oesophago gastro duodenoscopy - Chest x-ray

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47
Q

Curative treatment for hernias

A

Surgery

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48
Q

What is a femoral hernia?

A

Bowel herniates through femoral cord - Female, mid-old age - Very likely to strangulate due to rigid femoral canal borders

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49
Q

Symptom of femoral hernia

A

Swelling in upper thigh pointing down

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50
Q

Diagnosis of femoral hernia

A

Abdo/pelvic ultrasound if unsure - BUT usually clinical (based on symptoms)

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51
Q

Borders of the femoral TRIANGLE

A

Sartorius laterally Adductor longus medially Inguinal Ligament superiorly ⛵️

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52
Q

Borders of the femoral CANAL (within the femoral triangle

A

Femoral vein laterally Lacunar ligament medially Inguinal ligament anteriorly Pectineal ligament posteriorly

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53
Q

What is an inguinal hernia?

A
  • Spermatic cord herniates through inguinal canal - In males (obviously - History of heavy lifting/abdopressure
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54
Q

Direct inguinal hernias

A
  • 20% - In Hesselbach’s triangle - Medial to inferior epigastrics
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55
Q

Hesselbach’s triangle

A

Rectus abdominis medially Inferior epigastric vessels superiorly/laterally Poupart’s (inguinal) ligament inferiorly 🪦

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56
Q

Indirect inguinal hernias

A
  • 80% - Not in Hesselbach’s triangle - Lateral to inferior epigastrics
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57
Q

Symptoms of inguinal hernias

A

Painful swelling in groin - Points along groin margin

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58
Q

Diagnosis of inguinal hernias

A
  • Usually clinical - Unsure = AUSS (CT/MRI)
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59
Q

Other types of hernias

A
  • Umbilical (in neonates) - Incisional (surgical scars) - Epigastric - Obturator (Howship-Romberg sign) - Diastasis recti - Spigelian
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60
Q

Risk factors for NAFLD

A

Obesity - T2DM - hypertension - Hyperlipidaemia - Middle aged onwards - Family History - Drugs (NSAIDs, amiodarone)

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61
Q

Stages of NFALD

A
  1. Hepatosteatosis (NAFLD) 2. Non-alcoholic steatohapatitis (NASH) 3. Fibrosis 4. Cirrhosis
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62
Q

Symptoms of NAFLD

A

Typically asymptomatic, findings are incidental - if v.severe, present with signs of liver failure

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63
Q

Diagnosis of NAFLD

A
  • first line Deranged LFTs (High PT/INR, low albumin, high bilirubin) high everything else - AST:ALT < 1 - FBC: thrombocytopaenia, hyperglycaemia - Enhanced liver fibrosis blood tests if fibrosis suspected (comes under lft) ELF - Abdominal ultrasound to confirm Fib 4 score (second line) - Assess risk of fibrosis using non-invasive method
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64
Q

Enhanced liver fibrosis blood test for assessing fibrosis

A
  • Measure three markers - HA, PIIINP and TIMP-1 - <7.7 = none-mild fibrosis - ≥7.7 - 9.8 = moderate fibrosis - ≥9.8 = severe fibrosis
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65
Q

FIB-4 score for assessing fibrosis

A

> 2.67 = advanced -> refer to hepatology specialist

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66
Q

Management of NAFLD

A

Weight loss - Exercise - Control diabetes, Blood pressure and cholesterol - Stop Smoking - avoid alcohol - Vitamin E to improve liver function - Pioglitazone to decrease insulin resistance

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67
Q

Complications of NAFLD

A

HE - Ascites - HCC - Portal hypertension - Oesophageal varices

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68
Q

Pathophysiology of viral hepatitis

A

Inflammation of the liver as a result of viral replication within hepatocytes

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69
Q

Virus types of Hepatitis

A

All are single-strand RNA - Apart from hep B, which is double-strand DNA

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70
Q

Which hepatitis needs to be notified to Public Health England?

A

All

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71
Q

Spread of Hep A

A

Faeco-oral spread - Fly vectors - Picornavirus

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72
Q

Which types of hepatitis have 100% immunity after infection?

A

A & E

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73
Q

Risk factors for Hep A

A

Overcrowding - Poor sanitation - Shellfish - Travel - endemic in Africa, Asia, South America, Middle East

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74
Q

Pathophysiology of Hep A

A
  • Incubation for 2 weeks - Replicates in liver, excreted in bile - Self limiting within 6 weeks (having it/vaccine gives 100% immunity) - Acute, mild
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75
Q

Symptoms of Hep A

A

Prodromal phase (1-2 weeks): - Malaise - Nausea and vomiting - Fever Then: - Jaundice - dark urine + pale stools - Hepatosplenomegaly - Skin rash

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76
Q

Diagnosis of Hep A

A

Bloods: High ESR + leukopenia - LFT: Bilirubin High when there is Jaundice - Serology: HAV IgM = acutely infected HAV IgG = chronically infected

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77
Q

Treatment of Hep A

A

Supportive (treatment often Not required) - Travellers vaccine available

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78
Q

Complications of Hep A (Rare)

A

Fulminant liver failure😶‍🌫️

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79
Q

Spread of Hep C

A

Blood-borne and bodily fluids - IVDU - Flavivirus - IVDU more than vertical/sexual transmission - More common in the UK, again common in Africa

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80
Q

Symptoms of Hep C

A

often acutely asymptomatic, allowing it to become chronic Later on - Few patients with flu-like symptoms - chronic causes A sow progressive fibrosis over years + hepatosplenomegaly

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81
Q

Diagnosis of Hep C

A
  • LFTs - Serology: HCVRNA = current infection/diagnoses acute infection HCVAb = presents within 4-6 weeks of infection, if present after 6 months then it’s chronic
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82
Q

Treatment of Hep C

A

Direct acting antivirals, expensive 💸 - NS5A-inhibitor (acivir) - NS5B-inhibitor (buvir) - Previr

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83
Q

Complications of Hep C

A

30% cases progress to chronic liver failure (cirrhosis and HCC risk)

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84
Q

Spread of Hep E

A

Faeco-oral (undercooked pork) - Water - Dogs - Calicivirus

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85
Q

More on Hep E

A
  • Usually self limiting acute hepatitis (95% are asymptomatic) - Commoner than Hep A in the UK (endemic) - Common in Indo-China
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86
Q

Complications of Hep E

A
  • Can cause chronic disease in immunosuppressed - Can cause fulminant liver failure: Normal mortality 1-2%Pregnant ladies 10-20% !!!
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87
Q

Diagnosis of Hep E

A

Serology: HEV IgM = acute infection HEV IgG = recovery, only chronic in immunocompromised patients

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88
Q

Treatment of Hep E

A

Supportive, self limiting - vaccine only in China!🇨🇳

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89
Q

Spread of Hep D

A

Intravenous drug use - Sexually transmitted

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90
Q

Pathophysiology of Hep D

A

acute + chronic (like hep B) - Dependant on surface antigen of hep B to replicate, makes hep B more likely to progress to cirrhosis/HCC - Clinically indistinguishable from acute hep B

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91
Q

Diagnosis of Hep D

A

Manifests as co-infection IgM HDV + IgM HBV

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92
Q

Treatment and complications of Hep D

A

Treat hep B - Can also use inteferons BUT Not that good lol

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93
Q

Spread of Hep B

A
  • Needles (needlestick injury, tattoo, IVDU) - Sexual - Vertical (mother -> child) - Horizontal (between children) Blood borne and found in semen and saliva
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94
Q

Risk factors for Hep B

A

IVDU - MSM - Dialysis patients - Healthcare workers - present worldwide

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95
Q

Symptoms of Hep B

A
  • Similar to Hep A - 1-2 weeks prodrome - Then jaundice (dark urine + pale stools), hepatomegaly, uticaria, arthralgia
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96
Q

Pathophysiology of Hep B

A
  • Acute infection infects hepatocyte, cellular response usually clears it - Incubation 1-6 months
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97
Q

Serology chart for Hep B

A

img

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98
Q

Hepatitis B antigens and antibodies diagram

99
Q

What do all types of hepatitis show?

A

Interface necrosis “Piecemeal necrosis” on histology (don’t ask wjhat it looks like bc idk)

100
Q

Pathophysiology of autoimune hepatitis

A

chronic inflammation of the liver - aka: lupoid hepatitis, Very Rare - T helper cell mediated response vs hepatocytes

101
Q

Risk factors for autoimmune hepatitis

A

Female:male, 1:4 - Nitrofurantoin use - Other Autoimmune diseases - Viral hepatitis - HLA DR3 or DR4

102
Q

Type 1 autoimmune hepatitis

A
  • Adult females - 80% of cases - ANA - antinuclear antibody (found in many other autoimmune diseases but very specific for Type 1 autoimmune hep) - ASMA - antismooth muscle antibody
103
Q

Type 2 autoimmune hepatitis

A
  • Young females - Rarer - ALC-1 (antiliver cystosol) - ALKM-1 (antiliver-kidney microsome)
104
Q

Presentation of autoimmune hepatitis

A
  • 25% asymptomatic - Many = jaundice, fever, hepatosplenomegaly - Anorexia - Lupus-like rash
105
Q

Treatment for autoimmune hepatitis

A

Corticosteroids - prednisolone - Immunosuppressants - azathioprine - hep A+B vaccination (depending on cause) - Last resort - Consider transplant

106
Q

Treatment for Hep B

A
  • Peginterferon alfa-2a - Antiviral therapy - IV Igs for neonates
107
Q

Complications of Hep B

A
  • 5-10% of cases progress to chronic liver failure + HCC risk - HBV-associated decompensation with HCC has the worst prognosis - 90% cases in children become decompested and associated with poor prognosis. TRANSPLANT
108
Q

Progress of chronic liver failure

109
Q

Pathophysiology of liver cirrhosis

A

the result of chronic inflammation and damage to liver cells - when liver cells are damaged, they are replaced with scar tissue, fibrosis, and nodules within the liver - Increased resistance leading to Portal hypertension

110
Q

Aetiology of liver cirrhosis

A
  • Alcoholic liver disease (most common cause in developed world) - Non-alcoholic fatty liver disease - Hepatitis B - Hepatitis C
111
Q

Complications of liver cirrhosis

A
  • Ascites - Portal hypertension - Varices - Jaundice - Spider naevi + caput medusae - Coagulopathy - Hypoalbuminaemia -> oedema - Portosystemic encephalopathy - Hepatorenal and hepatopulmonary syndromes
112
Q

Diagnosis of liver cirrhosis

A

LFTs show liver damage (Most accurate) - FBC: thrombocytopaenia - ALT, AST, ALP are All Deranged - Definitive = liver biopsy

113
Q

Treatment for liver cirrhosis

A

Definitive = liver transplant - Conservative: fluids, analgesia, alcohol abstinence, good nutrition - Treat complications

114
Q

Pathophysiology of ascites

A

Accumulation of fluid in the peritoneal cavity

115
Q

How can liver cirrhosis cause ascites?

A
  • Hypoalbuminaemia (reduced plasma oncotic pressure) - Portal hypertension (increased hydrostatic pressure) - Renal water retention Cirrhosis is the most common cause of ascites (50% of patients develop ascites within 10 years
116
Q

Aetiology of ascites

A
  • Cirrhosis (70%) - Malignancy - Heart failure - TB - Pancreatitis
117
Q

Symptoms of ascites

A
  • Abdominal distension (severe = risk of SBP!) - Pain/discomfort = malignant - Signs of liver disease - May have jaundice and puritis - Shifting dullness
118
Q

Treatment of ascites

A

Treat underlying cause - Diuretic to increase Na+ excretion (spironolactone) + socium restriction - Paracentesis (or indwelling drain for smaller volume) - Peritoneovenkus Shunting

119
Q

Diagnosis of ascites

A
  • Shifting dullness on exam Imaging: x-ray, uss, CT abdomen Ascitic tap: - Cytology (WCC counts) + MC+S - Protein measurement: transudate + exudate
120
Q

Transudate testing for ascites

A
  • <30g/L protein (low) - Serum albumin ascitic gradient is <11g/L - Clear fluid - Fluid due to high hydrostatic pressure - portal htn, budd chiari, constructive pericarditis, CHF, nephrotic syndrome
121
Q

Exudate testing for ascites

A
  • ≥30g/L protein (high) - Serum albumin ascitic gradient is ≥11g/L - Cloudy fluid - Fluid due to inflammation mediated exudation, or low oncotic pressure - malignancy, peritonitis, pancreatitis
122
Q

Prehepatic jaundice

A

unconjugated hyperbilirubinaemia due to Increased RBC breakdown - mainly Caused by haemolytic anaemias - urine Bilirubin negative and urobilinogen High

123
Q

Intrahepatic jaundice

A

Conj/unconj hyperbilirubinaemia, may be mixed - Dark urine - raised Bilirubin in urine and raised bile salts, decrease in urobilinogen - Parenchymal disease: HCC, ALD/NAFLD, hep, hepatotoxic Drugs (eg: rifampicin), Gilbert syndrome, Crigler-Najjar syndrome

124
Q

Post hepatic jaundice

A
  • Conjugated hyperbilirubinaemia due to biliary obstruction - Pale stools + dark urine as bilirubin can’t reach GI tract and builds up in urine - Caused by biliary tree pathologies (eg: choledocholelithiasis, cancers) - High bilirubin and low urobilinogen in urine
125
Q

Biliary tree pathology

A
  • Choledocholithiasis - Pancreatic cancer - Cholangiocarcinoma - Mirizzi syndrome - Drug induced cholestasis - Autoimmune (PBC+PSC) - GALLSTONES
126
Q

What is jaundice?

A

aka: icterus - Yellowing of skin/eyes/mucous membranes due to accumulation of Conjugated or unconjugated Bilirubin - sign of liver dysfunction

127
Q

Four signs to look for when a patient presents with jaundice

A
  • Courvoisier sign - Charcot triad - Reynold’s pentad - Murphy sign
128
Q

Murphy sign

A

RUQ tenderness, ask patient to take A breath in while pressing RUQ - Will wince or Stop inspiring normally in cholecystitis

129
Q

What is pancreatic cancer?

A

Adenocarcinoma (in Most cases) of the exocrine pancreas - of ductal origin - Typically affects the head of the pancreas

130
Q

Risk factors for pancreatic cancer

A
  • Males - 60+ - Smoking - Alcohol - DM - Family history/genetics (PRSS-1 gene mutation) - Chronic pancreatitis
131
Q

What parts of the pancreas does pancreatic cancer usually target?

A

head - 60% - Body - 25% - Tail - 15%

132
Q

Presentation of pancreatic cancer of the head

A

Courvoisier sign - Painless jaundice - Pale stools + dark urine - Palpable gall bladder

133
Q

General presentation of pancreatic cancer

A

Epigastric pain radiating to the back, worse at night (relieved sitting forward) - Trousseau sign - migratory thrombophlebitis - Weight loss and anorexia - Recent diagnosis of DM - Nausea - Vomiting - Constipation

134
Q

Referral for pancreatic cancer

A
  • Over 40 + jaundice - 2 week wait referral for suspected cancer pathway - Over 60 + weight loss + one other symptom - direct access CT scan within 2 weeks
135
Q

Management of pancreatic cancer

A
  • Mainly palliative due to very poor prognosis, 5 year survival rate of 3% - Surgery (Whipple’s procedure) + post-op chemo if no mets
136
Q

Diagnosis of pancreatic cancer

A
  • CT scan and histology from a biopsy - CA19-9 tumour marker (non-specific) - CT TAP scan (thorax, abdomen pelvis) for staging
137
Q

Primary vs secondary liver cancer

A

Primary - Less common - Cancer that originates in the liver - Hepatocellular carcinoma (90%) and cholangiocarcinoma (10%) - There are also benign primary tumours Secondary - More common - Cancer that originates outside of the liver and metastasises to the liver

138
Q

What does hepatocellular carcinoma (HCC) arise from?

A

Liver parenchyma

139
Q

Risk factors of HCC

A
  • Chronic hepatitis virus - C and B - Decompensated liver cirrhosis
140
Q

What does HCC metastasise to?

A
  • Lymph nodes, bones, lungs - Via haematogenous spread (hepatic/portal veins)
141
Q

Symptoms of HCC

A

signs of Decompensated liver failure (Jaundice, Ascites, HE…) - signs of cancer (TATT, unexplained Weight loss, Nausea, vomiting…) - may have irregular hepatomegaly

142
Q

Diagnosis of HCC

A

High serum AFP - Imagine: first line ultrasound, CT for confirmation - biopsy is diagnostic BUT often avoided to Prevent seeding of tumour elsewhere

143
Q

Treatment for HCC

A
  • Surgical resection of tumour - In decompensative cirrhosis -> liver transplant - Prevantative: Hep B vaccine
144
Q

Types of benign primary tumours

A
  • Hepatic adenoma - Focal nodular hyperplasia - Haemangioma - most common, seen in infants as “strawberry mark” on skin within first few weeks of life 🍓
145
Q

What does cholangiocarcinoma arise from

A

the biliary tree - Typically adenocarcinomas

146
Q

Risk factors for cholangiocarcinoma

A

Parasitic flukeworms - biliary cysts - IBD - Primary sclerosing cholangitis

147
Q

Symptoms of cholangiocarcinoma

A

Abdominal pain - Weight loss - Puritis - Fevers - COURVOISER sign (BUT Pancreatic cancer is usually more comon) 🌌late constellation of symptoms as tumour is slow growing🌌

148
Q

Diagnosis of cholangiocarcinoma

A

LFT: High Bilirubin, High ALP - High CEA and CA19-9 - first line = Imaging: Abdominal ultrasound + CT - ERCP (Imaging of biliary tree) - invasive BUT Can be therapeutic and diagnostic

149
Q

Treatment of cholangiocarcinoma

A

Majority of cases inoperable as patients present very late

150
Q

Gilbert’s syndrome

A

Most common in males - T1DM - Autosomal recessive - Most common cause of hereditary Jaundice

151
Q

Pathophysiology of Gilbert’s syndrome and Crigler Najjar syndrome

A

Autosomal recessive - Deficient or abnormal UGT (UDP101), reducing UGT activity - causes an excess in unconjugated hyperbilirubinaemia (in Crigler Najjar, UGT is completely gone)

152
Q

Presentation of Gilbert’s syndrome

A
  • 30% asymptomatic - Typically males around 20 - May present with painless jaundice at a young age
153
Q

Symptoms of Crigler Najjar syndrome

A
  • More severe than Gilbert’s - Jaundice - Nausea and vomiting - Lethargy
154
Q

Treatment of Gilbert’s and Crigler Najjar syndrome

A
  • Gilbert’s: Usually no need - CN: Phototherapy to break down unconjugated bilirubim
155
Q

Complications of Crigler Najjar syndrome

A

more severe progression chances - Can die from kernicterus in childhood - kernicterus is accumulation of Bilirubin in the basal ganglia, causing severe neurological deficits

156
Q

What are gall stones made from?

A
  • Cholestrol (80%) - Pigment - Or mixed
157
Q

Risk factors for biliary tract disease

A
  • Female - Fat (BMI 30+) - Forty (+) - Fertile (pregnant or many children) - Fair also: - Family history - Fatty liver disease (non-alcoholic) - T2DM - Haemolytic conditions
158
Q

Symptoms of gallstones

A

Colicky or sharp pain - Fever - Jaundice - Dietary upset worse after A fatty meal, may come in episodes

159
Q

Diagnosis of gall stones

A

Bloods: - Alanine transaminase - Bilirubin - Amylase Then: First line: Abdominal ultrasound to identify gallstones Or: MRCP (MRI scan) or CT abdomen & pelvis

160
Q

Treatment of gallstones

A

Symptomatic OR asymptomatic and stone blocks CBD: Elective laproscopic cholecystectomy Radiological drain (cholesystostomy) ERCP (endoscopy)

161
Q

Complications of gallstones that may also be signs

A

acute cholecystitis - acute cholangitis - Obstructive Jaundice - Pancreatitis

162
Q

Symptoms of cholecystitis

A

RUQ pain - Fever - Tender gallbladder - Referred pain to tip of right shoulder (phrenic) - Murphy sign positive

163
Q

Diagnosis of cholesystitis

A
  • FBC: leukocytosis + neutrophilia - LFT: normal - Abdo ultrasound shows thickened gallbladder wall 3mm≤ and stones/sludge in and fluid around gallbladder
164
Q

Treatment for cholecystitis

A
  • Surgery within 1 week, typically done within 72 hours - via laproscopic cholecystectomy - Until then: IV fluids, analgesia, antibiotics if necessary, nothing by mouth
165
Q

Complications of cholecystitis

A

Sepsis - gallbladder empyema - Gangrenous gallbladder - Perforation

166
Q

Symptoms of ascending cholangitis

A

Charcot’s triad: - RUQ pain - High fever - Jaundice Reynold’s pentad: - Charcot’s triad + altered mental state + hypotension

167
Q

Diagnosis of ascending cholangitis

A

FBC: leukocytosis - LFT: High Conjugated hyperbilirubinaemia - Abdo ultrasound for CBD dilation and gallstones - MRCP: diagnostic

168
Q

Treatment of ascending cholangitis

A

ERCP (bile duct clearance) - Laproscopic cholecystectomy once stable to Prevent recurrence - Consider risk of Sepsis - Empiricle while waiting Abx - co-amoxiclav

169
Q

MRCP and ERCP

A

MRCP = Magnetic resonance cholangio-pancreatography ERCP = Endoscopic retrogade cholangio-pancreatography

170
Q

Pathophysiology of primary biliary cholangitis

A
  • Intrahepatic autoimmune jaundice affecting intralobular bile ducts - Autoantibodies cause intralobular bile duct damage; chronic autoimmune granulomatous inflammation - Resulting in cholestasis -> Fibrosis, cirrhosis, portal hypertension, infection
171
Q

Risk factors for primary biliary cholangitis

A
  • Female - 40-50 years old - Other autoimmune disease - Smoking
172
Q

Complications of primary biliary cholangitis

A
  • Malabsorption of fats + vit ADEK (=steatorrhoea) - Ostemalacia - Coagulopathy
173
Q

Symptoms of primary biliary cholestasis

A
  • Initially often asymptomatic - Routine test shows high anti-mitochondrial antibodies - Pruritis + fatigue earliest, then jaundice, then hepatosplenomegaly, + xanthelasma
174
Q

Diagnosis of primary biliary cholangitis

A

LFT - rule out acute hepatitis by testing for HepBsAg and HVCAb - Serology - rule out extrahepatic cholestasis Via ultrasound - liver biopsy

175
Q

LFT and serology results for primary biliary cholangitis

A

LFT: - High ALP - High conjugated bilirubin - High albumin Serology: 95% have anti-mitochondrial antibodies (especially M2)

176
Q

Liver biopsy results for primary biliary cholangitis

A
  • Portal tract infiltrate (lymphocyte + plasma cell) - 40% granulamatous - Portal tract fibrosis
177
Q

Treatment for primary biliary cholangitis

A

Ursodeoxycholic acid (reduces intestinal absorption of cholesterol) - Colestyramine to Treat pruritus - Consider Vitamin ADEK supplements - may ultimately need liver transplant

178
Q

Pathophysiology of primary sclerosis cholangitis

A

Autoimmune destruction of intra + extralobular hepatic duct - Blocks the flow of bile out of the liver into the intestines - chronic bile obstruction eventually leads to liver inflammation (hepatitis), fibrosis and cirrhosis

179
Q

Risk factors for primary sclerosing cholangitis

A

male - 40-50 - Strong link to IBD (especially ulcerative cholitis)

180
Q

Presentation of primary sclerosis cholangitis

A
  • 50% asymptomatic until disease advances - Charcot’s sign - Pruritis - Fatigue - Hepatosplenomegaly - IBD
181
Q

Diagnosis of primary sclerosing cholangitis

A
  • Cholestatic LFT - GS imaging: MRCP - Biopsy same as PBC Serology: - HBVsAg/HCVAb -ve - AMA -ve - Coelic screen anti tTG -ve - pANCA +ve in 33-88%
182
Q

Treatment of primary sclerosing cholangitis

A

Conservative: - Colestyramine for pruritis - Fat soluble ADEK - ERCP to dilate and stent structures - Consider liver transplant

183
Q

Causes of acute pancreatitis

A

Idiopathic Gallstones Ethanol🍾🍷🍻 Trauma Steroids Mumps/malignancy Autoimmune Scorpion stings Hypercalcaemia/hyperlipidaemia ERCP Drugs (azathiprine, NSAIDs, ACE inhibitors, tobacco, thiazides)

184
Q

Pathophysiology of acute pancreatitis

A
  • Gall stones obstruct pancreatic secretions - Accumulated digestive enzymes in pancreas - Host defences soon overwhelmed - Causes autodigestion -> inflammation + enzymes leak in blood
185
Q

Symptoms of acute pancreatitis

A

Sudden severe Epigastric pain radiating to the back (DDx: Abdominal aortic aneurysm) - Nausea and Vomiting - Jaundice - Pyrexia - Steatorrhoea - Grey Turner sign and Cullen sign

186
Q

Diagnosis of acute pancreatitis

A
  • Blood test first line: High serum amylase/lipase - Cxr to eclude gastroduodenal perforation - Abdo ultrasound -> diagnostic for gall stones; CT/MRI for extent of damage
187
Q

Glasgow score for severity of acute pancreatitis

A

PaO2 < 8KPa Age > 55 Neutrophils (WBC > 15x109/L) Calcium > 2mmol/L Renal urea > 16mmol/L Enzymes (LDH > 600iu/L or AST > 200iu/L) Albumin < 32g/L Sugar, glucose > 10mmol/L 0-1 - mild pancreatitis 2 - moderate pancreatitis 3+ - severe pancreatitis

188
Q

Treatment for acute pancreatitis

A
  • Rescuscitation if required - IV fluid - IV analgesia - IV antibiotics for infection/associated cholangitis - Nil by mouth - ERCP within 72 hours of pain onset if required
189
Q

Main complication of acute pancreatitis

A

Systemic inflammatory response syndrome (SIRS) 2 ≤ out of: - Tachycardia (90+ bpm) - Tachypnoea (20+ RR) - Pyrexia (38°c <) - High WCC

190
Q

Acute vs chronic pancreatitis

A

Acute - Reversible acute inflammation of the pancreas Chronic - 3+ month history of pancreatic deterioration - Irreversible pancreatic inflammation + fibrosis

191
Q

Causes of chronic pancreatitis

A
  • Alcohol (mc) Also: - CKD - CF - Trauma - Recurrent acute pancreatitis - Cancer - Autoimmune
192
Q

Symptoms of chronic pancreatitis

A

Epigastric pain radiating to back - exacerbated by alcohol - exocrine (eg: Steatorrhoea) and endocrine (eg: T2DM) dysfunction - Pseudocysts or abscesses DDx: Pancreatic cancer, especially of Body and Tail

193
Q

Diagnosis of chronic pancreatitis

A

Faecal elastase Low (indicator of exocrine function) - Abdo ultrasound and CCT to detect Pancreatic calcification and dilated Pancreatic duct (diagnostic)

194
Q

Treatment of chronic pancreatitis

A

alcohol cessation - Dietary modification - analgesia for Abdo pain, first line = NSAIDs - Pancreatic supplements (eg: enzymes, insulin for DM) - ERCP or Surgery if required

195
Q

Pathophysiology of portal hypertension

A
  • Normal pressure in portal vein = 5-8mmHg - Cirrhosis = increased resistance to flow, leads to splanchnic dilation and compensatory increased CO - Fluid overload in portal vein (10+ = bad, 12+ = very bad)
196
Q

Causes of portal hypertension

A

Prehepatic: Portal vein thrombosis Intrahepatic: Cirrhosis (mc in UK), schistomiasis (mc worldwide) Post hepatic: Budd chiari, RHS heart failure, constrictive pericarditis

197
Q

Symptoms of portal hypertension

A
  • Mostly asymptomatic - Present when oesophageal varices rupture - (90% of portal hypertension cases develop oesophageal varices, 1/3 of these rupture)
198
Q

Pathophysiology of oesophageal varices

A

Portal hypertension results in collateral Blood Shunting to gastroesophageal veins - Typically small, become Oesophageal varices at the cardia and lower oesophagus

199
Q

Presentation of haemorrhage of oesophageal varices

A

Haematemesis (vomiting blood) DDx: Mallory-Weiss tear - Tear in oesophageal mucosa - Very acute history - Increased abdominal pressure

200
Q

Diagnosis of oesophageal varices

A

Oesophagogastroduodenoscopy

201
Q

Acute treatment for oesophageal varices

A

Acutely: - Resus until haemodynamically stable - Consider blood trasfusion (Hb < 70g/L or <80g/L w cardiac comorbidity)

202
Q

Stopping bleeding of oesophageal varices

A
  1. IV terupressin (SST is CI) 2. Variceal banding 3. Transjugular intrahepatic portosystemic shunt - decreases portal pressure by diverting blood to other larger veins, SE = hepatoencelopathy
203
Q

Preventing bleeding of oesophageal varices

A

Non-selective beta blocker (eg: propanolol) + nitrates - Repeat variceal banding - Last resort: liver transplant (decompensate cirrhosis)

204
Q

Primary and secondary peritonitis

A

Primary - Ascites - Spontaneus bacterial peritonitis (infection) (mc) Secondary - Underlying cause, eg: bile, malignancy Peritonitis can also be classified as acute or chronic

205
Q

Bacterial causes of SBP

A

Gram -ve = e.coli + klebsiella (colliform rods) - Gram +ve = stap.aureus (cocci)

206
Q

Chemical causes of SBP

A

bile - old clotted Blood - Ruptured ectopic pregnancy - intestinal Perforation (which get ultimately infected)

207
Q

Presentation of SBP

A

Sudden onset severe abdo pain (and shoulder tip pain) then collapse + septic shock, fever - Rigidity helps pain (DDx: renal colic) - Poorly localised -> more localised + ascities usually Symptoms and signs of underlying conditions

208
Q

Diagnosis of SBP

A
  • Ascitic tap shows neutrophilia - Cultures (mc+s) show causative organism - High ESP and CRP - Exclude pregnancy as cause (b-hCG test) and bowel obstruction (abdo xR) - Cxr shows air under diaphragm -> indicates perforated colon
209
Q

Treatment of SBP

A
  • Treat underlying cause; IV fluid + IV antibiotics - Urinary catheterisation + GI decompression - IV Broad spectrum antibiotic therapy - Analgaesia - Surgery = peritoneal lavage
210
Q

Complications of SBP

A

Septicaemia if Not treated Early - Subphrenic/pelvic abscesses - Paralytic ulcers

211
Q

Pathophysiology of haemachromatosis

A
  • Autosomal recessive mutation of HFE gene (chromosome 6) - Excess Fe uptake by transferrin-1 and low hepcidin synthesis (hepcidin regulates Fe homeostasis) - Fe accumulation and fibrosis of liver (+ pancreas, kidney, heart, skin, ant. pituitary)
212
Q

Normal Fe vs Fe in haemochromatosis

A
  • Normal: 3-4g - Haemochromatosis: 20-30g
213
Q

Risk factors for haemochromatosis

A
  • Male - 50s - Genetics - Can be due to excess transfusions (secondary)
214
Q

Symptoms of haemochromatosis

A

fatigue - Joint pain - Hypogonadism (due to anterior pituitary damage) - Slate Grey/bronze skin - liver cirrhosis symptoms - Osteoporosis - Heart failure

215
Q

Gross Fe overload triad

A

bronze statue skin - hepatomegaly - T2DM

216
Q

Diagnosis of haemochromatosis

A
  • Fe studies - Genetic test - Liver biopsy (assess degree of damage with Perl’s Prussian blue stain)
217
Q

Fe studies results in haemochromatosis

A

High serum Fe - High ferritin - High transferrin saturation - Low total iron-binding capacity

218
Q

Treatment of haemochomatosis

A
  • First line: Venesection 3-4 times a year for life - If contraindicated; desfernoxamine (chelation therapy) - Lifestyle, decrease Fe in diet, avoid fruits
219
Q

Pathophysiology of Wilson’s disease

A
  • Autosomal recessive mutation of ATP7B gene on chromosome 13 - Impaired biliary copper excretion and transport bound to caeruloplasmin - Excess Cu accumulation in liver, basal ganglia and cornea
220
Q

The three features of Wilson’s disease

A

Hepatic - Chronic hepatitis - Liver cirrhosis Neurological - Assymetrical parkinsonism - Memory issues - Dysarthria and dystonia - Depression - Full psychosis Opthamological - Kayser-Fleischer rings - Cu deposits in in cornea, greenish brown ringed appearance

221
Q

Diagnosis of Wilson’s disease

A
  • 24 hour urine Cu tests: low serum copper and caeruloplasmin - AST:ALT >4.5 - Liver biopsy - High Cu, hepatitis - MRI brain: cerebellar + basal ganglia degeneration
222
Q

Management of Wilson’s disease

A
  • 1st line - D-Penicillinamine (Cu chelation, lifelong) - Diet change: avoid food high in Cu, shellfish, mushroom - Last resort -> liver transplant
223
Q

Pathophysiology of alpha 1 antitrypsin (A1AT) deficiency

A
  • Autosomal recessive muttion of serdina-1 gene (protease inhibitor) on chromosome 14 causes deficiency of A1AT - A1AT normally inhibits NE, NE degrades elastic tissue Lungs: - Degrades elastic tissue - Alveolar duct collapse - Air trapping - Characteristic panacinar emphysema Liver: - Soon becomes fibrotic; cirrhosis + HCC risk - A1AT is made by the liver so fibrotic will make synthetic liver function even worse - catch 22
224
Q

Presentation of A1AT deficiency

A
  • Young/mid aged man with little to no smoking history but COPD-like symptoms Lung symptoms: - Dyspnoea - Chronic cough - Sputum production - Barrel chest - Pink puffer Liver symptoms: - Jaundice
225
Q

Diagnosis of A1AT deficiency

A
  • Serum A1AT < 20mmol/L - Barrel chest on exam, cxr shows hyperinflated lungs - CT = panacinar emphysema - LFT shows obstruction (FEV1:FVC < 0.7) - Genetic testing
226
Q

Treatment for A1AT deficiency

A

if Smoking, Stop - Manage ephysema, eg: inhalers (SABAs and LABAs) - Consider hepatic decompensation patients for liver transplant

227
Q

What is SAAG?

A
  • Serum albumin ascites gradien - SAAG >1.1g/dL = portal hypertension, suggesting nonperitoneal cause of ascites
228
Q

Acute vs chronic hepatitis

A
  • Acute: First 6 months of liver inflammation - Chronic: Any inflammation beyond 6 months
229
Q

Aetiology of gall stones

A
  • Cholesterol supersaturation (diet, hormones) - Genetic (gallbladder motility) - Haemoglobin turnover (haemolytic anaemia, cirrhosis, sickle cell) 10% of people have gallstones And they acount for 30% of all acute presentations
230
Q

Management of gall stones if not treating directly/straight away

A

NSAIDs for mild pain - IM diclofenac for severe pain - Change lifestyle - decrease Fat in diet

231
Q

Functions of the peritoneum

A

In health: - Visceral lubrication - Fluid and particulate absorption In disease: - Pain perception - Inflammatory and immune response - Fibrinolytic activity

232
Q

What is spontaneous bacterial peritonitis?

A

Peritonitis (infection of the peritoneum), that happens without a hole or a tear. Ascitic fluid is affected

233
Q

Classification of ascites

A

Stage 1: Detectable only after careful examination/uss Stage 2: Easy detectable but relatively small volume Stage 3: Obvious, not tense ascites Stage 4: Tense ascites (large)

234
Q

Cause of failure with lung pathology

A

Alpha 1 antitrypsin deficiency

235
Q

Compensated vs decompensated cirrhosis

A

Compensated - liver is able to override ability to function

236
Q

Ammonia

A

Neurotoxic - causes irreversible brain damage - Because it stops the Krebs cycle

237
Q

Symptoms of liver failure

A

RUQ pain - hepatomegaly - Jaundice - Nausea and Vomiting - Ascites - Bruising or muscle wasting

238
Q

What is it called when a gall stone is trapped in the common bile duct?

A

Choledocholelithiasis

239
Q

Investigations for jaundice

A
  • Bloods - LFTs - First line imaging - ultrasound Normally:- No bilirubin in urine - Urobilinogen in urine
240
Q

Pathophysiology of ALD

A
  • Alcohol dehydrogenase enzymes and cytochromes (2 ways of metabolism) - Risk of forming reactive O2 species, more overload = more O2 species - Eventual scar tissue around central veins, adding to portal hypertension
241
Q

Alcohol withdrawal

A

6-12 hours: tremours, sweating, headaches 12-24 hours: hallucination 24-48 hours: seizures 24-72 hours: delirium tremens (medical emergency)

242
Q

Delirium tremens

A

alcohol stimulates GABA receptors and inhibits glutamate receptors - chronic alcohol leads to upregulation of glutamate receptors and downregulation of GABA receptors - Treat wirh IV Chlordiaepoxide or diazepam

243
Q

What is the name of the cells responsible for fibrosis?

Haroon Phase 2A (14 decks)

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