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MBBS - Year 3 > The Digestive System - Pancreas and Liver > Flashcards

The Digestive System - Pancreas and Liver Flashcards

1
Q

Imaging modalities of hepatobilliary system

A

Ultrasound (trans-abdominal and endoscopic)
CT
MRI
Nuclear med e.g. PET staging
Angio e.g. tumour embolisation
Radiographs - not v useful

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2
Q

Functions of liver

A

Helps manage body’s metabolism
Bile production
Detoxification

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3
Q

What is the liver covered by

A

Serous membrane (visceral peritoneum) that suspends liver form Abdominal wall and diaphragm
5 peritoneal folds (ligaments)

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4
Q

Ligaments of liver

A

Coronary
L triangular
R triangular
Falciform
Round

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5
Q

Lobes of liver

A

R & L - seen from superior view
Also posterior caudate lobe and anterior quadrate lobe - seen from inferior view

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6
Q

What is the posterior caudate and a anterior quadrate lobes of the liver separated by

A

Porta hepatitis - hepatic artery, hepaxtcic portal vein, common hepatic duct

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7
Q

Role of hepatic artery

A

Carries oxygen-rich blood from heart

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8
Q

Role of hepatic portal vein

A

Carries nutrient-rich blood from GI system incl pancreas

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9
Q

Role of common hepatic duct

A

Drains bile from liver into gallbladder

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10
Q

Functional unit of liver

A

Hepatic lobules

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11
Q

Portal triad of liver

A

Hepatic artery
Portal vein
Common bile duct

Blood vessels drain into sinusoids, before scarring blood to central vein

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12
Q

What do hepatocytes act as a store for

A

Vitamine A, D, E, K, B12
Minerals incl Fe and Cu

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13
Q

Synthesis as a function of heptovytes

A

Proteins incl albumin and coag factors
Lipoporteins inlc VLDL and HDL

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14
Q

Stellate reticuloendothelial cells

A

AKA Kupffer cells
Destroys old RBCs, WBCs, bacteria and foreign substances

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15
Q

Why do we need bile

A

Digestion
Absorption of fat and fat-soluble vitamins in small intestine
Has a role in immunological defence

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16
Q

Bile composition

A

Bile salts (from cholesterol)
Water
IgA
Bilirubin

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17
Q

Where is bile canaliculi found

A

Between adjacent hepatocytes
Drains into bile ductules –> bile ducts

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18
Q

Ducts in gallbladder

A

R and L hepatic duct combine to for common hepatic duct
Common hepatic duct combines with cystic duct to bring bile to gallbladder

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19
Q

How does drug metabolism in the liver typically work

A

Process turns lipophilic molecules into hydrophilic molecules which can be excreted/ eliminated

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20
Q

3 phases of drug metabolism

A

Phase 1 - modification (mainly CYP450)
Phase 2 - conjugation
Phase 3 - further modification and excretion

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21
Q

Common reactions in phase 1 of drug metabolism

A

Oxidation
Sulphodixation
Dealkylation
Deamination

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22
Q

Factors affecting drug metabolising enzymes

A

Pregnancy
Age
Gender
Polymorphisms
Organ transplant
Liver disease
Kidney disease
Drug-drug interaction
Infl mediators
DM

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23
Q

Why are LFTs an over-simplification

A

Poor markers of synthetic function (ability to make things)
Severe liver disease can occur w/out abnormal LFTs

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24
Q

What do LFTs consist of

A

Bilirubin
Albumin
Globulin
ALT
ALP
Gamma GT
NOTE - platelet count, prothrombin time (INR)

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25
Q

What may cause a high bilirubin

A

Over production of bilirubin or failure of excretion

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26
Q

Causes of increased bilirubin production –> hyperbilirubinaemia

A

Haemolysis
Ineffective erythropoiesis
Blood transfusion
Resorption of haemotomas

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27
Q

Causes of decreased hepatic uptake —> hyperbilirubinaemia

A

Gilberts’s syndrome (also decreased conjugation)
Drugs e.g. rifampicin

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28
Q

Where are aminotransferases found

A

Liver, muscle, heart, kidney, brain and pancreas
Intracellular enzymes released injured hepatocytes

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29
Q

What are aminotransferases a measure of

A

Necro-infl

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30
Q

Types of aminotransferases

A

Alanine aminotransferase (ALT) and aspartate aminotrasnbferase (AST)
ALT is more liver spp
ALT: AST ratio can be useful

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31
Q

Causes of raised aminotransferases - pathology

A

Alcohol
NAFLD
C/c hep B and C
CCF

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32
Q

Causes of raised aminotranferases - disorders

A

AI diseases
Haemachromatosis
Wilsons - excess Cu
A1AT deficiency
Coeliac

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33
Q

Meds causing raised transaminases

A

NSAIDs
Abx
HMG-CoA reductase inhibitors
Antiepileptic drugs
Anti-TB drugs
Illicit drugs use

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34
Q

ALP as an LFT

A

Sensitive test for biliary obstruction but not spp

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35
Q

Physiological causes for raised ALP

A

Women in 3rd trimester of pregnancy
Adolescents
Benign, familial

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36
Q

Pathological causes for raised ALP

A

Bile duct obstruction
PBC
PSC
Drug-induced cholestasis
Metastatic liver disease
Bone disease

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37
Q

Where is gGT present

A

In many organs, found particularly high in epithelial cells lining bile ducts

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38
Q

gGT as a maker of biliary obstruction

A

Typically associated w/ ALP

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39
Q

What is gGT inducible by

A

Alcohol
Phenytoin, carbamazepine, barbiturates
Sex hormones

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40
Q

Causes of raised gGT

A

Pancreatic disease
Alcopholism
COPD
Renal failure
DM
MI

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41
Q

Hepatitic vs cholestatic picture of LFTs

A

Hepatitic - Increased ALT and AST (ALT > ALP), increased alb, c/c low albumin
Cholestatic - increased gGT and ALP (ALP > ALT)

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42
Q

Haematological tests as LFTs

A

Prothrombin time is best marker of synthetic function - increased INR
Platelets best marker of portal HTN
Low albumin (typically seen w/ raised CRP)

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43
Q

AST: ALT ratio

A

ALT: AST 2:1 in alcohol related liver disease
ALT: AST in NAFLD and c/c viral hep approaches 1:1 as fibrosis progresses

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44
Q

Gilbert’s syndrome

A

Inability to correctly conjugate bilirubin

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45
Q

Anatomy of pancreas

A

Soft, lobulated retroperitoneal organ
Crosses the trabnspyloric plane
Consists of head, neck, body and tail

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46
Q

Where is uncinate process of pancreas found

A

Behind superior mesenteric vessels

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47
Q

Where is the neck of pancreas found

A

In front of portal veins

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48
Q

Where is the tail of the pancreas found

A

Touches hilum of spleen

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49
Q

Why is the pancreas’ rship to the lesser sac important

A

In pancreatitis, lesser sac can fill with fluid

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50
Q

2 components of pancreas as a gland

A

Exocrine
Endocrine

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51
Q

Which anatomical structures are anterior to the pancreas

A

Stomach
Lesser sac
SMA

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52
Q

Which anatomical structures are posterior to the pancreas

A

Aorta
IVC
R renal artery
R & L renal veins
Superior mesenteric vessels
Splenic veins
Hepatic portal vein
L kidney
L suprarenal gland

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53
Q

Which anatomical structures are superior to the pancreas

A

Splenic artery

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54
Q

Which anatomical structures are lateral to the pancreas

A

Spleen

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55
Q

Which anatomical structures are medial to the pancreas

A

Duodenum (descending and horizontal parts)

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56
Q

Where is the head of pancreas found

A

Lies in loop of D1/D2 as it exits stomach

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57
Q

Types of tissue in pancreas

A

Endocrine (tubular) - 90%
Endocrine (islets) - 2%
Interstitial

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58
Q

Where is exocrine tissue found in the pancreas

A

Surrounding interlobular ducts

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59
Q

Examples of endocrine cells in pancreas

A

Islets store their hormones in distant locations

Beta - insulin
Alpha - glucagon
Delta - SST
PP (pancreatic peptide) - beta cells

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60
Q

PP in disease response

A

Beta cells get replaced with these in 2’ DM

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61
Q

Interstitial tissue of pancreas

A

Specialised pancreatic stellate cells involved in fibrogenesis of pancreatitis and cancer
Ca deposition in c/c pancreatitis

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62
Q

Functional unit of pancreas

A

Lobules

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63
Q

Structure of ducts in pancreas

A

Interlobular ducts come off main duct of pancreas
Interlobular ducts go INTO lobules
Intercalated ducts go into acinus (secretory epithelium)

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64
Q

Effect of autonomic nervous system on pancreas

A

Heavily innervated by ANS

Regulates glandular production
Regulate blood flow

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65
Q

What do pancreatic acinus cells make

A

Enzymes and zymogens
These are then secreted into lumen of duct

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66
Q

What are proteases produced as zymogens

A

Proteases are v powerful
Only activated at small bowel

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67
Q

Examples of zymogens

A

Trypsinogen
Chymotrypsiongen
Proelastase

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68
Q

Examples of active enzyme produced by pancreas

A

Alpha amylase
Lipase
RNAase
DNAase

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69
Q

Control of exocrine secretion of pancreas

A

Response to meal - cephalic, gastric and intestinal phase
Other important driver incl acid in small intestine, fat, proteins and bile acids
Protease levels in gut stimulate/inhibit secretion via -ve feedback

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70
Q

Pancreatic secretions

A

Mixture of fluid, bicarb and digestive enzymes in response to variety of n neurotransmitters and hormones

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71
Q

Activation of zymogens

A

Important in pathophysiology of a/c pancreatitis

Trypsinogen comes out of pancreas and is activated by enterokinase to form trypsin, which then activates all the other zymogens

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72
Q

Common pancreatic procedures

A

Pancreatomies but pancreatic soaring surgery
Whipple’s procedure
Frey’s procedure

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73
Q

Whipple’s procedure

A

Pancreaticoduodenectomy
Complex procedure to remove head of pancreas, duodenum, gallbladder and bile duct

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74
Q

Issues w/ Whipple’s procedure

A

Issues w/ sterility of small bowel - can cause bacteria overgrowth and small bowel should be sterile

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75
Q

When is Frey’s procedure done

A

For benign lesions

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76
Q

Where are pancreatic ductal cells found

A

Just after acinus - cemntroacinar cells (carbonic hydrase)

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77
Q

Proximal vs distal intercalated pancreatic ductal cells

A

Proximal - low cuboidal
Distal - more cuboidal/ columnar and contain more vesicles and granules

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78
Q

Main job of pancreatic ductal cells

A

Make a bicarb rich fluid

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79
Q

What happens as more HCO3- is secreted in pancreatic secretion

A

More Cl- is reabsorbed
Link between CF and c/c pancreatitis

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80
Q

How are biliary canaliculi held together

A

By gap junction between two heoaocytes
Adherens junctions
Tight junctions

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81
Q

How does water enter biliary canaliculi

A

Water can enter via aquaporin 8 (regulated by cAMP) and aquaporin 9
Also paracellular & transcellular

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82
Q

Pathways to make bile slats

A

Classical
Alternative
Neural (extra-hepatic)

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83
Q

What are bile salts produced from

A

Cholesterol

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84
Q

What are the primary bile slats

A

Cholic acid
Chenodeoxycholic acid

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85
Q

Secondary bile acids

A

Primary bile salts that have been conjugated and then chemically modified in the intestine

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86
Q

Examples of 2’ bile acids

A

Deoxycholic acid
Lithocholic acid
UDCA

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87
Q

What is hepatitis

A

A/c or c/c parenchymal liver damage

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88
Q

Dominant sx of hepatitis

A

Jaundice (icterus)
Detectable clinically when the serum bilirubin >50 mmol/L

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89
Q

What is hepatitis associated with in the liver

A

Rise fo ALT in plasma
Los of excretory and synthetic functions

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90
Q

Describe the variability of the extent if damage in hepatitis

A

V variable
From spotty or focal necrosis to massive hepatic necrosis
There is also infiltration of portal tracts and lobules by lymphocytes

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91
Q

Histological features of hepatitis

A

Hepatocytes shows degenerative changes
Hepatocytes undergo necrosis
Necrosis is maximal in zone 3

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92
Q

Degernative changes seee in hepatocytes in hepatitis

A

Swelling
Cytoplasmic granulation
Vacuolation

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93
Q

Necrotic changes seen in hepatocyte sinhepatitis

A

Become shrunken
Eosinophilic Councilman bodies

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94
Q

Causes of hepatitis

A

Viral infections
Drug induced (e.g. paracetomol)
Alcohol
NAFLD
AI hepatitis

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95
Q

Systemic viral infections causing hepatitis

A

EBV and CMV, HSV, VSV
Yellow fever
VHF
Rubella
Mumps
Coxsackie B

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96
Q

Px of hepatitis

A

Abdo pain
Pruritus
Muscle and joint aches
N & V
Jaundice
Fever (viral cause)

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97
Q

Features of Hep C

A

HCV is usually symptomless for decoded while damaging liver
Accounts for 70% cases of c/c liver disease
RNA virus spread by blood and bodily fluids

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98
Q

Signs of hepatitis

A

RUQ pain
Hepatomegaly
Jaundice
Pyrexia

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99
Q

Transmission of HCV

A

Parenteral
Permucosal - sexually
Vertical

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100
Q

Which condns are HCV associated w/

A

Liver disease
DM
B-cell proliferative disorders
Depression
Cognitive

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101
Q

Risk factors associated w// HCV

A

Tranfusion/ transplant w/ unsterilised equipment
IVDU
Haemodialysis (duration of treatment)
Multiple sex partners

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102
Q

Natural hx of HCV

A

Most pts (80%) fail go clear virus and develop c/c hepatitis (>6/12) —> cirrhosis, HCC

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103
Q

Features of c/c HCV infection

A

C/c persistent hepatitis
Cirrhosis
HCC
Extrahepatic disease - mixed essential cryoglobulinaemia, Glomerulonephritis, sporadic porphyria cutanea tarda

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104
Q

Mx of HCV

A

Directly acting antiviral - used in combination (given for 8/52 to 12/52)

Protease inhibitors - telaprevir, simeprevir
NS5 A/B inhibitors - Elbasavir, Velpatasivir

hCBV is totally curable

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105
Q

Hep D virus

A

Defective RNA virus requiring hep B for replicate

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106
Q

Types of infection of HDV

A

Coinfection - HBV and HDV at same time
Superinfection - development of HDV in pt w/ pre-existing HBV

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107
Q

Decompensated cirrhosis

A

Inability of liver to carry out normal functions

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108
Q

Features of decompensated cirrhosis

A

Development of ascites
Encephalopathy
Jaundice
Coagulopathy
GI bleeding

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109
Q

HDV clinical progression

A

Most severe form of viral hep
C/c infection –> cirrhosis –> HCC

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110
Q

Mx of HDV

A

Only treatment for c/c HDV
Pegylated IFNa

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111
Q

Testing for HCV

A

Hep C antibody screen
Hep C RNA confirms dx, csalulate viral load, assess genotype

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112
Q

Features of HEV

A

RNA virus transmitted by faecal oral route
Normally produces only mild illness, except in immunocompromised and pregnant
No vaccination

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113
Q

Characteristics of a/c liver failure

A

Confusion (i.e. encephalopathy)
Jaundice
Asterixis
GI bleeding
Ascites
Bruising (high INR)

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114
Q

What is cirrhosis

A

Severe, irreversible fibrosis of liver

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115
Q

Which complications are cirrhosis associated w/

A

HCC
GI bleeding
Spontaneous bacterial peritonitis

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116
Q

What is c/c liver disease characterised by

A

Caput medusae
Splenomegaly
Palmar erythema
Dupuytren’s
Leuconychia
Gynaecomastia
Spider naevi

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117
Q

Features of HBV

A

2nd most important carcinogen
DNA virus
Causes 1 million deaths/ yrs
100x more contagious than HIV

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118
Q

modes of transmission of HBV

A

Sexual
Parenteral - HCWs at increased risk
Perinatal
Transfusion

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119
Q

Nature of HBV infection

A

Most people recover within 2/12
Only 10% are symptomatic
10% become c/c HBV carriers

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120
Q

Viral markers of HBV

A

HBsAg
HBeAg
HbcAg
HbsAb
HBV DNA

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121
Q

HBsAg for HBV

A

Surface antigen
Used as general marker of active infection

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122
Q

HBeAg for HBV

A

E antigen
Marker of viral load and implies high infectivity

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123
Q

HBcAg for HBV

A

Core antibodies
Implies past or current infection

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124
Q

HBsAb for HBV

A

Surface antibody
Implies vaccination or past or current infection

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125
Q

HBV DNA for HBV

A

Direct count of viral load

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126
Q

Vaccination for HBV

A

Involves injecting Hep B surface antigen - 3 doses
Vaccinated pts are tested to confirm response to vaccine

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127
Q

Prevention of HBV infection

A

UK antenatal screening
Exposure-prone procedure for HBV infected HCW
Global eradication programme (immunisation)
Prophylaxis

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128
Q

Prophylaxis for HBV

A

Pre exposure is active immunisation
Post-exposure is accelerated active immunisation

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129
Q

Approach to c/c HBV infection therapy

A

Treat when they enter the immune elimination phase and develop active hepatitis
(ALT elevation and bx evidence of c/c hepatitis and fibrosis)

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130
Q

Treatment for c/c HBV infection

A

Immunomodulators - pegylated IFNa
Nucleoside analogues - lamivudine
Nucleotide analogues - adefovir, tenofovir

Given for 48/52

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131
Q

Features of HAV

A

Most common viral hep
RNA virus transmitted by faecal-oral route
Rarely, fulminant hep ensues but never c/c liver disease

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132
Q

HAV transmission

A

Close personal contact (e.g. household contact, sexual contact)
Homeless person - poor hygiene
Drug use
Contaminated food
Blood exposure

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133
Q

Px of HAV

A

Nausea
Vomiting
Anorexia
Jaundice

Can cause cholestasis

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134
Q

Mx and vaccination for HAV

A

Resolves without mx - 1-3 months
Mx is usually basic analgesia
Vaccination is available to reduce chance of developing infection

135
Q

Types of autoimmune hepatitis

A

Type 1
Type 2

136
Q

Type 1 AI hepatitis

A

Occurs in women in late 40s/50s
Presents around menopause w/ fatigue and features of liver disease on examination
Less a/c course that Type 2

137
Q

Type 2 AI hepatitis

A

Occurs in pts in their teenage/ early twenties w/ a/c hepatitis
High transmianases and jaundice

138
Q

Ix for AI hepatitis

A

Raised transaminases
IgG levels
Associated w/ many autoantibodies

139
Q

Autoantibodies for Type 1 AI hepatitis

A

ANA
Anti-actin
Anti-soluble liver antigen (anti-SLA/LP)

140
Q

Autoantibodies for Type 2 AI hepatitis

A

anti-LKM1
anti-LC1

141
Q

Dx for AI hep

A

Confimed w/ liver bx

142
Q

Mx for AI hepatitis

A

High dose steroids e.g. pred, that are tapered over time as immunosuppressants are introduced e.g. azathioprine
Liver transplant may be required end stage however can recur n transplanted liver

143
Q

What is liver cirrhosis

A

Result of c/c infl and damage to hepatocyte - permannaet architectural change

144
Q

Main causes of crrhosis

A

HCV
Alcohol
NAFLD
Hep B

145
Q

Rarer cases of cirrhosis

A

AI hepatitis
PSC
PBS
Wilson’s disease
Haemochromatosis
Cytogenic
Drug induced
A1AT deficiency

146
Q

Relevance of hepatic stellate cels in fibrosis

A

Can cause wither progression or regression of liver fibrosis

147
Q

What is portal HTN

A

Increased resistance in the blood bessie leading INTO the liver cause by fibrosis

148
Q

Different approaches to treating liver fibrosis

A

Control or curve primary disease
Target receptor-ligand interactions
Inhibit fibrpgenesis
Promote resolution of fibrosis

149
Q

Why does portal HTN cause a lot of morbidlity vs mortality

A

Poor synthetic function

150
Q

Fixed and dynamic component of portal HTN

A

Fixed - localised HTN in portal system due yo architectural change bin liver
Dynamic - triggered by infl, toxin, causes a/c rise in pHTN and vascular issues

151
Q

Classification of aetiologies of PHTN

A

Pre-hepatic
Intra-hepatic
Post-hepatic

152
Q

Pre-hepatic aetiologies of PHTN

A

Budd-Chiari syndrome
Cardiac causes

153
Q

Intra-hepatic causes of PHTN

A

Pre-sinusoidal - schistomaniasis
Sinusoidal - cirrhosis, alcohol hepatitis
Post-sinusidal - venoocclusive syndrome

154
Q

Signs of cirrhosis

A

Jaundice
Hepatosplenomegaly
Spider naevi
Palmar erythema
Gynaecomastia
Bruising
Ascites
Caput medusae
Asterixis

155
Q

Hepatosplenomegaly in cirrhosis

A

However liver may shrink as it becomes more cirrhotic
Splenomegaly due to PHTN

156
Q

Spider naevi

A

Telangiectasia with a central arteriole and small vessels radiating away

157
Q

Palmar erythema in cirrhosis

A

Red discolouration on palm, typically hypothenar eminence
Caused by hyper dynamic circulation

158
Q

Why do we see gynaecomastia and testicular atrophy in cirrhosis

A

Endocrine dysfunction

159
Q

Caput medusae

A

Distended paraumbilical veins due to PHTN

160
Q

Asterxixis in cirrhosis

A

Flapping tremor as a result of toxic metabolic encephalopathy - decompensated cirrhosis

161
Q

Bloods for liver cirrhosis

A

LFT - usually normal unless decompensated (deranged)
Low albumin and increased PT (INR)
Hyponatreamia
Deranged U&Es
Enhanced liver fibrosis test - 1st line for NAFLD

162
Q

Ix for liver cirrhosis

A

Bloods
Ultrasound
Fibroscan - transient electrography
Endoscopy
CT/ MRI
Liver bx

163
Q

What might you see on an ultrasound for liver cirrhosis

A

Nodularity on surface of liver
‘Corkscrew’ appearance of arteries
Enlarged portal vein
Ascites

164
Q

Endocsopy for cirrhosis

A

Assess for and treat oesophageal varices when PHTN is suspected

165
Q

CT/MRI for liver cirrhosis

A

Useful when looking for:
HCC
Hepatosplenomegaly
Ascites

166
Q

Liver bx for cirrhosis

A

Used to conform dx

167
Q

Gading of cirrhosis

A

Child-Pugh score
From 5 - 15
Takes into account: bilirubin, albumin, INR, ascites, encephalopathy
Provides estimated one-year survival

168
Q

MELD score

A

Used every 6/12 for pts w/ compensated cirrhosis
Represents 3/12 mortality in %

169
Q

General mx of cirrhosis

A

Screening for HCC every 6/12
Endoscopy every 3 years
High protein, low sodium diet
Mx of complications
HAV and HBV imunistaion to prent viral superinfection

170
Q

Screening for HCC in cirrhosis pts

A

Ultrasound
Alpha-fetoportein - tumour marker for HCC

171
Q

Complications of cirrhosis

A

Malnutrition
PHTN, variceal bleeding
Ascites*
HCC
Hepatic encephalopathy
Hepatorenal syndrome

172
Q

How does cirrhosis cause malnutrition

A

Increased use of muscle tissue as food
Affected metabolism of proteins in liver and reduced production of proteins
Disrupted ability to store and release glycogen

173
Q

How does PHTN cause varices

A

Back pressure from portal system causes vessels at the sites where the portal system anastomoses w/ systemic venous system to become swollen and tortuous

174
Q

Where can varices occur

A

GOJ
Ileocaecal junction
Rectum
Anterior abdominal wall (caput medusae)

175
Q

Treatment of stable varices

A

Non-selective beta blocker e.g. propanolol
Elastic band ligation
Sclerotherpay - less effective
TIPS if all else fails

176
Q

TIPS for varices

A

Transjugular Intra-hepatic portosystemic shunt
Stent placed in connection made between hepatic and portal vein
Allows blood to flow from portal vein into hepatic and relieve pressure

177
Q

Treatment for bleeding oesophageal varices

A

Resusc
Endoscopy - injection of sclerosant, elastic band ligation
Sengstaken Blakemore tube

178
Q

Resus for bleeding varices

A

Vasopressin analogue e..g terlipressin
Corect coagulopathy w/ vit K and FFP
Prophylactic BSAbx
Consider ITU as pts may exsanguinate

179
Q

Sengstaken Blakemore tube for bleeding varices

A

Inflatable tube inserted into oesphagus to tamponade bleeding varices
Used when endoscopy fails

180
Q

When are pts typically listed for a liver transplant

A

MELD > 15
Point at which survival w/ transplant is higher than w/out

181
Q

What is ascites

A

Excess fluid in peritoneal cavity

182
Q

Pathophys of ascites in c/c liver disease

A

Increased portal venous pressure –> increased vasodilators –> fluid leaks out of capillaries and bowel –> decreased blood pressure entering kidneys, activates RAAS –> Na+ and fluid retention
Low albumin also decreases oncotic pressure

183
Q

Causes of ascites

A

Portal HTN
HCC
Infection or infl - TB, pancreatitis
Decreased albumin - nephrotic syndrome, IBD (protein losing enteropathy)
Myxoedema

184
Q

Ix for ascites

A

Diagnostic paracentesis
RBC and WBC count
Culture - SBP suspected
Glucose
LDH
Amylase - increased in pancreatitis

185
Q

Diagnostic paracentesis for ascites

A

Allows calculation of serum-ascites albumin gradien
SAAG = serum albumin - ascites albumin

High gradient (>11) = transudate: portal HTN
Low gradient (<11) = exudative: HCC, pancreatitis, TB

186
Q

Mx of ascites

A

Low sodium diet
Diuretics - spiro, furosemide
Paracentesis
Prophylactic abx for SBP
Consider TIPS and liver transplant in refractory ascites

187
Q

SBP

A

Spontaneous Bacterial Peritonitis
Infection developing in ascitic fluid and peritoneal lining w/out any clear cause

188
Q

Px of SBP

A

May be asymptomatic - have low threshold fro ascitic fluid culture
Fever
Abdo pain
Vomiting

189
Q

Dx of SBP

A

Neutrophils >250 per micro litre

190
Q

Common causative organisms for SBP

A

E. coli
Klebs penumoniae
Gram +ve cocci

191
Q

Mx for SBP

A

Abx - co-amoxi, cephalosporins

192
Q

What is hepatorenal syndrome

A

Kidney failure w/out known cause in presence of severe liver disease
Dx of exclusion

193
Q

Pathophys of hepatorenal syndrome

A

RAAS seen in portal HTN leads to regional vasoconstriction –> renal hypoperfusion
Tjis causes rapid deterioration of kidney function, may be fatal

194
Q

Mx of hepatorenal syndmrome

A

Terlipressin
Refer for liver transplant

195
Q

Hepatic encephalopathy (a/c decompensated liver disease) px

A

Jaundice
Coagulopathy
Ascites
Confusion/ Asterixis
GI bleeding

196
Q

Grading for hepatic encephalopathy

A

0 - 4
0 is minimal HE - no clinical manifestation
1 is mild - alteration in behaviour, mild confusion
2 is moderate - lethargy, moderate confusion
3 - severe - stupor, incoherent speech
4 - coma

197
Q

Pathophys of hepatic encephalopathy

A

Build up toxins affecting brain
Ammonia is produced by intestinal bacteria when breaking down protein, usually absorbed
Liver cannot metabolise ammonia and collateral vessels allow ammonia to pass directly into systemic system

198
Q

Ppting factors for HE

A

Constipation*
Infection
Medications
High protein diet

199
Q

Mx of hepatic encephalopathy

A

Laxatives e.g. lactulose
Long-term bx e.g. rifaxim
Supportive - basic airway support, NG feeding, stop bleeding into gut
Liver transplant

200
Q

Why are laxative given in the mx of hepatic encephalopathy

A

Promotes excretion of ammonia
Alters gut pH favouring bacteria that produce less urea

201
Q

Prognosis of hepatic encephalopathy

A

1 yr if not given liver transplant

202
Q

Px of Budd-Chiari syndrome

A

Triad of hepatomegaly, abdominal pain and ascites due to hepatic venous obstruction

203
Q

Stages in alcoholic and fatty liver disease

A

Steathosis - fatty liver
Steatohepatitis - fatty liver plus progressive infl, characterised by Mallory bodies
Cirrhosis
HCC

Similar pattern seen in A1AD and drug-induced

204
Q

Clinical states of cirrhosis

A

Compensated - pts are asymptomatic and small amount of residual function remains
Decompensated - liver no longer has capacity to carry out normal function. If insult is removed, liver may ‘recompensate’

205
Q

What is PBC

A

Primary biliary cirrhosis - AI cholestatic liver disease that can lead to cirrhosis

206
Q

Pathophys of PBC

A

AI destruction of small, INTRAhepatic bile ducts –> cholestasis —> progressive fibrosis —> cirrhosis

207
Q

Epidemiology of PBC

A

Seen in older women, 40+
F: M is 10:1
Increased incidnecr of other AI disorder e.g. thyroid, coeliac

208
Q

Auto-antibodies for PBC

A

Anti-mitochondrial - hallmark
ANA
Anti-gp210 and anti-sp100

209
Q

Blood results for PBC

A

Raised ESR
Raised IgM

210
Q

Sx of PBC

A

Most pts are asymptomatic at dx
Fatigue
Pruritus
RUQ pain

211
Q

Dx of PBC

A

AMA +ve in 95%
Cholestatic picture on LFTs
Imaging - liver USS and MRCP

212
Q

When should PBC be considered

A

In any pt that has unexplained rise in ALP

213
Q

Mx of PBC

A

Urseodeoxycholic acid - helps flow of bile
Asses response after 12/12
2nd line is oecticholic acid
Liver transplant
Treat pruritus

214
Q

Drugs to treat pruritus in PBC

A

Sertraline
Gabapentin
Rifampicin

215
Q

Complications of PBC

A

Mainly due to cirrhosis and cholestasis

Hypercholesterolaemia
Malabsorption of fat-soluble vits
Malabsorption
Osteoporosis

216
Q

PSC

A

Primary sclerosing cholangitis
Immune-mediated disease charcterised by cholestasis, bile duct structures and hepatic fibrosis

217
Q

Pathophys of PSC

A

Progressive infl, fibrosis and destruction of BOTH intra- and extra-hepatic bile ducts

218
Q

Intra vs extra-hepatic bole ducts

A

Intra - small ducts proximal to R and L hepatic duct
Extra - large bile ducts starting at R and L hepatic ducts

219
Q

Types of sclerosing cholangitis

A

Primary - referes to PSC
Secondary - any condn causing bile duct damage and biliary obstruction

220
Q

Secondary causes of sclerosing cholangitis

A

Infl - Ig4-sclerosng cholangitis, pancreatitis
Malignancy - cholangiocarcinoma
Infection
Choledocholithiasis
Drugs
Papillary stenosis

221
Q

Epidemiology of PSC

A

More commonly seen in men
Avg age is 40
IBD is seen in 80% of pts w/ PSC but only 4% of pts with IBD have PSC

222
Q

Sx of PSC

A

Fatigue
Pruritus
Features of cholangitis

223
Q

Signs of PSC

A

Hepatomegaly
Splenomegaly
Excoriation
Stigmata of c/c liver disease

224
Q

Dx of PSC

A

Liver biochem - cholestatic pattern
MRCP - biliary stricturing or dilatation
ERCP

225
Q

When is ERCP used in dx of PSC

A

Pts who also need therapeutic interventions (e.g. treat duct stricture) or who cannot undergo MRI

226
Q

Tumour marker for cholangiocarcinoma

A

CA19.9

227
Q

Mx for PSC

A

Only effective treatment is liver transplant
Lifestyle and preventative

228
Q

Complications

A

Cholangitis
Cholangiocarcinoma (10%)
Osteoporosis

229
Q

Surveillance for PSC

A

Annual colonoscopy for colorectal cancer
Annual USS of gallbladder for biliary malignancy

230
Q

Pathophys of autoimmune hepatitis (AIH)

A

AI hepatocyte damage
Minority of cases triggered by drugs e.g. minocycline

231
Q

Clinical features of AIH

A

Asymptomatic
A/c or c/c presentation
PMH or Fhx of AI disease

232
Q

Ix for AIH

A

Bloods - increased ANA, ASMA and IgG
LFTs - hepatitic picture
Bx is always needed

233
Q

1st line treatment for AIH

A

Pred +/- azathioprine
Continue mx until LFTs normlaise then maintain on reduced dose

234
Q

Prognosis of AIH

A

Excellent on treatment - 95% survival in 10 yrs

235
Q

Px pf alcholic hepatitis

A

Jaundice
Fever
Tender hepatomegaly
Worsening of underlying cirrhosis if present

236
Q

Blood for alcoholic hepatitis

A

Neutrophilia
Increased AST/ALT
AST:ALT ratio >2
Increased bilirubin
Increased PT/ INR

237
Q

Layers of GB

A

Mucosa
Muscularis propria
Lamina propria
Serosa
No mucosa

238
Q

Physiology of GB emptying

A

Bile stored and concentrated up to 15x in GB
Vagal stimulation causes weak contraction of GB
Bile acids via blood stimulate parenchymal secretion
Secretin via blood stream stimulates liver ductal secretion
CCK in blood stream

239
Q

Effects of CCK on GB

A

Gallbladder contraction
Relaxation of Sphincter of Oddi

240
Q

Types of gallstones (cholelithiasis)

A

Cholesterol stones
Pigment stones
Mixed stones
Stones w/ Ca content

241
Q

Types of pigment stones

A

Black - cirrhosis risk factor
Brown

242
Q

Cause of black pigment gallstones

A

C/c haemolysis

243
Q

Where do brown pigment stones typically dvelop

A

In obstructed and infected bile ducts

244
Q

Factors associated w/ cholelithiasis formation

A

Impaired GB function - emptying, absorbing
Superstaurated bile - age, diet
Absorption/ enterohepatic circulation of bile acids
Cholesterol nucleating factors

245
Q

Where can gallstones cause complicatiosn

A

In GB
In bile ducts
In intetsine

246
Q

Complications of gallstones in GB

A

Biliary colic
A/c or c/c cholecystitis
Empyema of GB
Mucocele
Perforation

247
Q

Complications of gallstones in bile ducts

A

Biliary obstruction
A/c cholangitis
A/c pancreatitis

248
Q

Complication of gallstones in intestine

A

Intestinal obstruction - gallstone ileus

249
Q

Risk factors for gallstones

A

Fat
Forties
Female
Fair

250
Q

Biliary colic pain

A

Intermietent - occurs in waves
Seen in RUQ
Typically squeezing pain, pt unable to get comfortable

251
Q

Pathophys of biliary colci

A

Biliary obstruction w/ OUT infection, causing pain as GB contracts against it
Due to stone impaction in GB neck or cystic duct

252
Q

Structures in GB

A

Neck Body
Fundus
Cystic duct

253
Q

Signs and sx of biliary colic

A

Continuous RUQ/ epigastric pain - may radiate to back (below scapular), worse after fatty meal
N & V
Usually resolves 20mins - 6 hrs

254
Q

Important -ve findings in biliary colic

A

No fever
No peritonism
Normal WBC
Murphy’s sign -ve

255
Q

Ix for biliary colic

A

Abdo US - looking for stone and duct dilation
LFTs
Consider MRCP if duct dilation and/or abnormal LFTs

256
Q

Conservative mx for biliary colic

A

Analgesia
Avoid triggering foods i.e. low fat diet

257
Q

Surgical mx for biliary colic

A

Laporoscopic cholecystectomy

258
Q

A/c cholecystitis

A

A/c infl of GB, typically caused by cholelithiasis impaction
Usually sterile chemical infl but becomes infective in 1/3

259
Q

Clinical features of a/c cholecystitis

A

Continuous RUQ pain, may raidate
Fever and local peritonism - pts lying still (not writhing)
+ve Murphy’s sign
Vomiting

260
Q

Murphy’s sign

A

Ask pt to deep breath and use 2 fingers to press on RUQ
Pain/ arrest of inspiration but NO pain in LUQ

261
Q

Bloods for a/c cholecystitis

A

Icreased WBC
Increased CRP
Deranged LFTs in 1/3

262
Q

US for a/c cholecystitis

A

4hrs NBM as this will distend GB
May show stones, thick-walled GB and normal bile ducts

263
Q

Extra options of imaging in a/c cholecytsitis

A

HIDA cholescintigraphy (nuclear med) - cystic duct obstruction
CT abdo for ddx or complications

264
Q

Mx for a/c cholecystitis

A

Conservative - fluids, anagelsia, IV abx (ITU if perforation)
Surgical - lap chole (done before abx if v a/c)

265
Q

Complications of a/c cholecystitis

A

Perforation (presnsts as shock)
GB empyema
C/c cholecystitis - leads to fibrosed and shrunken GB

266
Q

Mirrizzi syndrome

A

Syndrome where impacted stone in cystic duct or neck of GB causes extrinsic compression of CBD

267
Q

GB mucocele

A

Overdistended GB filled with mucous
Usually non-infl
Caused by impaction of stone in cystic duct or neck of GB
Px is same as cholecystitis

268
Q

Empyema of GB

A

Most severe complication of a/c cholecystitis
Results from progression of a/c cholecystitis and in background of bile stasis and cystic duct obstruction

269
Q

Mx of GB empyema

A

Surgical emergency
Prompt treatment w/ IV abx and surgical removal or aspiration (cholecystotomy)

270
Q

Caustaive organism for a/c cholecystitis

A

E. coli
Klebsiella
Clostridia

271
Q

What is ascending cholangitis

A

Infection of CBD secondary to choledocholithiasis

272
Q

Risk factors for ascending cholangitis

A

Biliary malignancy
Post ERCP

273
Q

Px of ascending cholangitis

A

Charcot’s triad - fever, RUQ pain, jaundice
Raynuad’s pentad - add confusion, hypotension (sepsis)

274
Q

Ix for ascending cholangitis

A

Deranged LFTs (typically indication for MRCP)
Raised WBC/ CRP

275
Q

Imaging for a/c cholangitis

A

USS - stones, dilation and thickening bile ducts
MRCP

276
Q

Mx of ascending cholangitis

A

IV abx and fluid
ERCP once stable - sphincterotomy and stone clearance
Consider stone exploration as an alternative

277
Q

How is a lap chole performed

A

Using 4 ports w/ 2 ports at least 10mm in size and 2 ports at least 5mm in size
Must see critical view of safety - identified cystic duct and artery

278
Q

Complications of lap chole

A

Bleeding - bleeding disorders are CI
CBD injury
Missed CBD stones
Bowel injury
Potetnial seeding of tumour if GB cancer is present (CI)

279
Q

ERCP

A

Endoscopic retrograde cholangiopancreatography
Upper GI endoscopy w/ injection of contrast in biliary tree and pancreas, can then proceed to sphincterotomy, stone clearance and stenting

280
Q

Infl complications of ERCP

A

A/c pancreatitis
Cholangitis

281
Q

Traumatic complications of ERCP

A

Bleeding
GI perforation
Bile duct injury

282
Q

What is gallstone ileus

A

Gallstone eroded through GB and duodenum (fistula formed)
Typically impact in terminal ileum (narrowest part of small intestine) to cause SBO

283
Q

Imaging for gallstone ileus

A

Air in biliary system (pneumobiliary) - Mercedes Benz sign
Dilated loops of bowel

Both seen on AXR

284
Q

Sx of gallstone ileus

A

Nausea and vomiting
Biliary colic
Absolute contipation

285
Q

What type of jaundice is caused by choledocholithiasis

A

Obstructive
Unconjugated bilirubin unable to GIT - backing up in system, then kidneys

286
Q

At which size do we operate on GB polyps

A

> 10mm - 8% chance of cancer
Can be dismissed if <6mm

287
Q

Types of adenomas (GB polyps)

A

Pyloric gland type
Intestinal type
Foveolar papillary type
Tubopapillary type

288
Q

When are adenomas in the GB significant

A

PSC
Any size maters as there’s a higher risk of cancer

289
Q

Cholangiocarcinoma

A

Cancer of bile ducts

290
Q

Epidemiology of GB cancer

A

2.5:1 F:M
Presents in older age, 70 yrs
Normally adenocarcinoma

291
Q

Lifestyle risk factors for GB cancer

A

DM
DMI
Sweetened beverages

292
Q

Environmental risk factors for GB cancer

A

C/c bacterial infections
Arsenic
Aflatoxins

293
Q

Genetic risk factors for GB cancer

A

Female sex
Age
PSC
Anomalous pancreaticobiliary ductal junction

294
Q

Associated diseases with GB cancer

A

GB polyps
Crohn’s disease
Sjorgrens syndrome (decreased risk)

295
Q

GB cancer px

A

Presents at late stage
Invading liver mass
Obstructive jaundice
Wt loss/ anorexia/ RUQ pain

296
Q

Biliary atresia

A

Condn in infants where bile ducts inside and outside liver are scarred so bile cannot ENTER intestine
Bile builds up in liver and damages it –> cirrhosis

297
Q

Px of biliary atresia

A

Jaundice in children 3-6 weeks old

298
Q

Mx of biliary atresia

A

Kasai procedure - intestine attaches to liver to allow bile to drain
Eventually liver transplant

299
Q

Choledochal cyts

A

Congenital dilation of bile ducts
Can be classified in 5 types - Type 1 is most common

300
Q

Natural hx of choledochal cysts

A

Choledochal cysts are infl in nature
Can lead to cholangitis or pancreatitis

301
Q

Key difference in pathology - IgG4 sclerosing cholangitis vs PSC

A

Lymphoplasmacytic infiktration
Storiform firbosis
Obliterative fibrosis
Lymphoplasmacytic-type psuedotumors in hilar bile duct

302
Q

Tropical infections affecting biliary system

A

Clonirchis sinesis
Opisthorcis viverrini
Opisthorchis felineus

303
Q

Risk factors for cholangiocarcinoma

A

Cholestatic liver disease - PSC, choledochal cysts
Liver cirrhosis
Biliary stone disease
Infections
Infl disorders
Toxins - alcohol, drugs
Metabolic condn
Genetic disorder - Lynch syndrome

304
Q

Infections as risk factors for cholangiocarcinoma

A

Liver flukes
Hep B/C
Typhoid
Recurrent pyogenic cholangitis
HIV

305
Q

Infl disorders as risk factors for cholangiocarcinoma

A

IBD
C/c pancreatitis
Gout
Thyrotoxicosis

306
Q

Prognosis of cholangiocarcinoma

A

5 yesr survival is 5%

307
Q

Where is cholangiocarcinoma endemic in

A

Thailand
Vietnam
Cambodia
Laos

308
Q

Choledocholithiasis

A

Gallstones within billiary tree

309
Q

Biliary tree

A

Ductal system that transmits bile produced by hepatocytes to 2nd part of duodenum (via ampulla of Vater and sphincter of Oddi)

310
Q

Biliary tree anatomy

A

R & L hepatic ducts converge to form the common hepatic duct
GB is drained by cystic duct
Cystic duct and common hepatic duct converge to form CBD
Pancreatic duct also joins common bile duct, proximal to ampulla of Vater

311
Q

How can gallstones cause a/c pancreatitis

A

Stones get impacted distally in biliiopancreatic duct causing disruption to flow of pancreatic enzymes

312
Q

What is post cholecystectomy syndrome attributed to

A

Changes in bile flow after removal

313
Q

Sx of post cholecystectomy syndrome

A

Diarrhoea
Indigestion
Epigastric or RUQ pain and discomfort
Nausea
Intolerance of fatty foods
Flatulence

314
Q

Types of contrast in MRI for liver lesions

A

Gadovist stays in vascular sytsem
Primovist gets taken up liver cell and excreted in biliary system

If there’s a lesion and it takes up primovist, means there are functioning hepatocytes. If the lesion is metastatic, it WONT take up primovist dye

315
Q

Haemangiomas in liver

A

Non-cancerous mass in liver made up of blood vessels
Most common benign liver lesion

316
Q

Haemangioma features on MRI

A

Appears hyperchoic (looks white compared to greyness of liver)
Lights up to T2 image, lightbulb sign

317
Q

Giant haemangioma in liver

A

Can trap platelets and cause thrombocytopenia

318
Q

Giant haemangioma features on MRI

A

Seen on T1
Sharply marginates, hypointense mass

319
Q

Focal nodular hyperplasia

A

2nd most common benign liver tumour

320
Q

Focal nodular hyperplasia features on MRI

A

Hypoechoic mass
Arterially enhancing lesion, if given primovist
Results of increased hepatocyte numbers caused by hypo perfusion or hyperperfusion from anomalous arteries within the hepatic lobule

321
Q

What can adenomas turn into

A

Adenomas can bleed and turn into HCCs

322
Q

What does the type of adenoma its classified as, depended on

A

What protein is mutated: beta catenin and HNF 1 alpha

323
Q

Who are adenomas most common in

A

Males who use anabolic steroids
Can also be driven by oestrogen

324
Q

Histopathology of HCC

A

Takes most of its supply from hepatic artery
Often fat calcification, may have necrosis and multiple masses of variable attenuation

325
Q

HCC features on MRI

A

Hypointense compared to surrounding iver
Rapid washout - supply to HCC is predominantly from hepatic artery rather than portal veins
Diffusion restriction/ rim enhancement on post-contrast images causing a capsule

326
Q

Px of HCC

A

Constitutional sx
Jaundice
Portal HTN
Hepatomegaly

327
Q

Mx of HCC

A

If lesion is small, resect
If not, liver transplant
Trans arterial chemo embolism (TACE) and trans arterial radioembolism, thermal/ cryo ablation can be used

328
Q

LI-RAD classoifictaion

A

Used to score liver lesions

LR1-2 : benign
LR 3-4: proability for HCC
LR5: 100% HCC

329
Q

Risk factors for HCC

A

HBV and HCV infection
Alcoholism
Biliary cholangitis
Food toxins
Congenital biliary atresia
Wilson disease, A1AT deficiency

330
Q

How does uncojugated bilirubin enter the circulation

A

RBCs enter senescence after 120 days
Macrophages in spleen and bone marrow engulf and degrade RBC and Hb into heme and globin
Globin is broken down into iron and unconjugated bilirubin

331
Q

How do we go from unconjugated bilirubin to conjugated

A

Glucuronic acids are added

332
Q

How is conjugated bilirubin excreted

A

By the liver in bile through CBD
Conjugated bilirubin is water soluble

Conjugated bilirubin travels through terminal ileum and start of large intestine
Bacteria converts conjugated bilirubin into urobilinogen by removing gluronic acid
Urobilinogen is lipid soluble

333
Q

How is conjugated bilirubin distributed

A

15% re absorbed by blood bound to albumin
80% oxidised by intestinal bacteria to stercobilinogen - excreted in the faeces
5% to kidney - converted to urobilinogen - gives urine its yellow colour

MBBS - Year 3 (9 decks)

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