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Surgery > HPB > Flashcards

HPB Flashcards

1
Q

hyperbilirubinaemia occurs at bilirubin levels roughly greater than what?

A

50 umol/L

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2
Q

what are the three main types of jaundice?

A

pre-hepatic

hepatocellular

post-hepatic

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3
Q

what occurs in pre-hepatic jaundice?

A

excessive red cell breakdown

liver is overwhelmed and cannot conjugate bilirubin-this causes unconjugated hyperbilirubinaemia

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4
Q

what occurs in hepatocelluar jaundice?

A

dysfunction of the hepatic cells

liver loses ability to conjugate bilirubin as well as habing some degree of obstruction

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5
Q

what occurs in post hepatic jaundice?

A

obstruction of biliary drainage

bilirubin is not all excreted

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6
Q

what happens to the levels of unconjugated and conjugated bilirubin in pre-hepatocellular and post- hepatic jaundice?

A

pre-hepatic: inc in unconjugated bilirubin

hepatocellular: inc in both unconjugated and conjuagted bilirubin

post-hepatic: inc in conjugated bilirubin

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7
Q

causes of pre-hepatic jaundice?

A

haemolytic anaemia

gilberts syndrome

criggler-najjar syndrome

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8
Q

causes of hepatocellular jaundice?

A

alcoholic liver disease

viral hepatitis/ autoimmune hepatitis

hereditary haemochromatosis

primary biliary cirrhosis/ primary sclerosing cholangitis

hepatocellular carcinoma

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9
Q

causes of post- hepatic jaundice?

A

gallstones

cholangiocarcinoma

strictures

pancreatic cancer

abdo masses

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10
Q

unconjuagted or conjugated bilirubin is excreted via the urine?

A

conjugated as it is water soluble

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11
Q

darker urine will be seen in which kind of jaundice?

A

hepatocellular or post-heaptic

normal urine is seen in unconjugated disease

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12
Q

pts presenting with jaundice should have which routine bloods done?

A

LFTS

coag studies

FBC

U&Es

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13
Q

pts presenting with jaundice should have which specialist bloods done? what do they indicate?

A

Bilirubin- degree of jaundice

Albumin- liver synthesis function

AST/ ALT- hepatocellular injury

ALP- raised in biliary obstruction

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14
Q

which blood marker is more specific for biliary obstruction than ALP but not routinely carried out?

A

Gamma-GT

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15
Q

which imaging is performed when investigating liver obstruction or gross pathology?

A

US abdo

Magnetic Resonance Choliangography (MRCP)

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16
Q

if bleeding or rapid coagulopathy presents in a pt with jaundice which management is required promptly?

A

Vitamin K or FFP

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17
Q

which complications are importnant to look for when dealing with a jaundiced patient?

A

coagulopathy

encephalopathy

infection (bowels)

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18
Q

what forms bile?

A

cholesterol, phospholipids, bile pigments (haem)

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19
Q

what are the three main types of gallstone?

A

Cholesterol stones

Pigment stones

Mixed stones

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20
Q

what are the risk factors for gallstone disease? (5 Fs)

A

Fat

Female

Fertile

Forty

Family History

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21
Q

of those who are symptomatic with gallstones how do these people present?

A

50% with biliary colic (impacted stone in neck of gallbladder)

35% as acute cholecystitis (inflammatory)

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22
Q

how does the pain differ in biliary colic and acute cholecystitis?

A

biliary colic- sudden, dull and colicky (can be precipitated by fatty foods)

acute cholecystitis- constant pain, signs of inflammation

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23
Q

what is murphys sign?

A

Apply pressure to RUQ and ask patient to inspire- Murphys sign +ve if this causes pain

indicates inflammed gallbladder

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24
Q

what are some differentials for RUQ pain?

A

Cholecystitis

GORD

peptic ulcer disease

acute pancreatitis

IBD

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25
Q

which blood tests should be carried out in suspected cholecystitis?

A

FBC and CRP (inflammation)

LFTs (raised ALP likely)

Amylase (rule out pancreatitis)

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26
Q

what imaging should be performed in suspected gallstone pathologies?

A

trans-abdominal ultrasound

MRCP

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27
Q

how is biliary colic managed?

A

lifestye advice- wgt loss, no fatty foods

elective laparoscopic cholecystectomy

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28
Q

how are cases of acute cholecystitis managed?

A

IV antibiotics (co-amoxiclav +/- metronidazole)

laparoscopic cholescytectomy

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29
Q

what is important to exclude in any patient presenting with RUQ pain post cholecystectomy?

A

a retained CBD stone

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30
Q

what is Mirizzi syndrome?

A

stone in Hartmanns pouch or in cystic duct causes compression on common hepatic duct

results in obstructive jaundice- confirm diagnosis with MRCP

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31
Q

inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between which structures?

A

gallbladder and small bowel

stones can pass directly into small bowel typically duodenum from gallbladder

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32
Q

fistula formation between the gallbladder and small bowel following inflammation can result in which two complications?

A

Bouverets syndrome- stone impacts in proximal duodenum causing gastric outlet obstruction

Gallstone Ileus- stone impacts in terminal ileum causing small bowel obstruction

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33
Q

inflammation of the biliary tract is referred to as?

A

cholangitis

combination of obstruction and subsequent infection

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34
Q

cuases of cholangitis?

A

galstones

ERCP

choliangocarcinoma

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35
Q

what are the most common causitive organisms of cholangitis?

A

E. coli

Klevsiella

enterococcus

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36
Q

what are the common presenting symptoms of cholangitis?

A

RUQ pain, fever, jaundice

(may also have pruritis)

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37
Q

what are the two syndromes associated with cholangitis?

A

Charcots triad: Jaundice, fever, RU pain

Retnolds Pentad: Jaundice, fever, RUQ pain, hypotension, confusion

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38
Q

which investigations should be carried out in suspected cholangitis?

A

Routine bloods: FBC, LFTs, Blood cultures

US scan

ERCP (therapeutic and diagnosis)

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39
Q

how are patients with cholangitis managed?

A

may present with spesis- sepsis 6

endoscopic biliary decompression or ERCP

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40
Q

cancers of the biliary system are termed what?

A

cholangiocarcinoma

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41
Q

where is the most common site for bile duct cancers?

A

bifurcation of right and left hepatic ducts

typically slow-growing and invade locally

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42
Q

cholangiocarcinoma occurs more frequently in which patient populations?

A

>65yr olds

south-east asia due to association with chronic endemic parasitic infections

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43
Q

cholangiocarcinomas arise from which cells?

A

95% are adenocarcinomas from cholangiocytes

rarer- sqaumous cells carcinomas

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44
Q

what are the main risk factors for cholangiocarcinoma?

A

Primary sclerosing cholangitis

UC

infective- hepatitis. HIV

TOxins

Congenital

alcohol excess

diabetes mellitus

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45
Q

liver abscesses typically result from what?

A

polymicrobial bacterial infection spreading from biliary or GI tract

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46
Q

list common causes of liver abscesses?

A

cholecystitis, cholangitis diverticulitis, appendicitis, septicaemia

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47
Q

what are the most commonly isolated organisms in liver abscesses?

A

E.coli

K. pneumoniae

S. constellatus

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48
Q

how do patients with a liver abscess typically present?

A

fever, abdo pain, rigors

also: bloating, anorexia, wgt loss, fatigue, jaundice

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49
Q

what shoul dbe considered in all pts presenting with pyrexia of unknown origin assoc with abdo pain or bloating?

A

pyogenic liver abscess

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50
Q

what blood results will be seen in a pt with a liver abscess?

A

FBC- leucocytosis

LFTS- abnormal

ALP- raised

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51
Q

in addition to routine bloods pts with suspected liver abscess should have which investigations sent for mictoscopy?

A

peripheral blood and fluid cultures

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52
Q

what will be seen on US in pt with liver abscess?

A

poor defined lesion with hypo and hyper echoic areas

similar pic seen on CT with contrast

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53
Q

how are patients with liver abscesses managed?

A

fluid resuscitation

start antibitoic therapy

image guided aspiration of abscess

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54
Q

what is the causitive organism of an amoebic abscess and how does this infection spread?

A

entamoeba histolytica

faecal- oral spread- once in colon the tropozite invade the mucosa and spread to liver via portal system

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55
Q

how do patients present with an amoebic abscess?

A

vague symtpoms of abdo pain, fever, rigors, wgt loss, bloating

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56
Q

when would you suspect an amoebic abscess in a patient?

A

history of recent travel (<6 months) to an endemic region

(South America, Indian subcontinent, Africa)

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57
Q

whta will bloods show in patients with an amoebic abscess?

A

leucocytosis with deranged LFTS

Peripheral blood and fluid culture should also be sent for microscopy

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58
Q

in addition to bloods and microscopy what else shoudl be tested in patients with suspected amoebic abscess?

A

Blood and stool samples sent for Entamoeba histolytica antbodies

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59
Q

how are patients with an amoebic abscess managed?

A

most pts treated with antibiotics alone

surgivcal drainage may be required in larger cysts

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60
Q

what are the only two antimicrobials of choice to treat an Entamoeba histolytca in amoebic abscess?

A

metronidazole

tinidazole

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61
Q

how do simple liver cysts appear on US imaging?

A

anechoic (no echo, black on US), well-defined, thin-walled, oal/spherical lesions

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62
Q

define a simple liver cyst and where they msot commonly occur?

A

fluid-filled epithelial-lined sacs withint the liver most commonly the right lobe

63
Q

what may be raised in pts with simple liver cysts?

A

rasied GGT

LFTs are typically normal

64
Q

how are simple liver cysts managed?

A

most require no intervention

>4cm, follow up US at 3, 6, 12 months

US aspiration if symptomatic

65
Q

how is polycystic liver disease characterised?

A

presence of >20 cysts of which each are >1cm

66
Q

which two autosomal dominant conditions cause polycystic liver cysts?

A

autosomal dominant polycystic kidney disease (ADPKD)

autosomal dominant polycystic liver disease (ADPLD)

67
Q

what % of liver cysts are true cystic neoplasms?

A

5%- most common type are cystadenomas, premalignant lesions

68
Q

why should aspiration/ biopsy be avoided in suspected cystic neoplasms?

A

risk of seeding

69
Q

what is the management choice for cystadenomas and cystadenocarcinomas of the liver?

A

liver lobe resection

samples then sent to histopathology for diagnosis confirmation

70
Q

hydatid cysts result from which infection?

A

tapeworm, Echnococcus granulosus

71
Q

what will show in US if Hydatid cyst?

A

calcified, spherical lesion with multiple septations

Cyst deroofing to manage

72
Q

how does hepatocellular carcinoma arise?

A

result of chronic inflammation affecting the liver

most common causes include: viral hepatitis, chronic alcoholism

73
Q

what are the risk factors for hepatocellular carcinoma?

A
74
Q

in developing countries what accounts for around 90% of HCC cases?

A

Viral hepatitis

HCC much more common in asian individuals secondary to hep B infections in childhood

75
Q

what are the main presenting symtpoms of HCC?

A

similar to that of liver cirrhosis: vague symtpoms such as fatigue, wgt loss, fever

dull ache in RUQ is uncommon but if present should raise suspicion in those with known cirrhosis

76
Q

what will be seen on examination that is highly suggestive of liver malignancy i.e. HCC?

A

irregular, enlarged, craggy and tender liver

Ascites if indicator of late stage liver disease also

77
Q

differtials for pt presenting with liver failure or non-specific liver signs?

A

infectious hepatitis

cardiac failure (smooth hepatomegaly)

benign hepatocellular adenoma

lother causes of liver cirrohsis

78
Q

how sre suspected cases of liver malignancy investigated?

A

LFTs- may be deranged

FBC- may show low platelets

AFP (raised in 70% cases)

US scan

79
Q

which ratio of AST:ALT is suggestive of alcoholic liver disease rather than viral hepatitis?

A

AST:ALT >2 alcoholic liver disease

AST:ALT around 1 viral hepatitis

80
Q

what on US combined with raised AFP is virtually diagnostic of liver malignancy?

A

mass >2cm

Biopsy can be perfromed if still unsure

81
Q

what system is used to stage liver cancers?

A

Barcelona Clinic Liver cancer staging system

82
Q

which score isused to asses pts with liver cirrhosis and calculate prognosis?

A

Child-Pugh score

MELD score also used to predict mortality and likelihood of pt tolerating transplant

83
Q

what is the surgical management for liver cancer?

A

surgical resection

transplantation

(limited by tumour size and liver function alongside comorbidities)

84
Q

liver transplant in liver cancer pts can only be carried out if they fulfill which criteria?

A

Milan Critera

one lesion is <5cm or three lesions <3cm

no extrahepatic manifestations

no vascular infiltration

85
Q

what non-surgical management options are available for liver cancer?

A

image guided ablation

TACE- transarterial chemoembolisation

86
Q

what is the median survival time of pts with HCC from time of daignosis?

A

aroudn 6 months

extent of underlying cirrhosis is main prognostic factor

87
Q

what are the most common cancers to metastise to the liver?

A

bowel, breast, pancreas, stomach, lung

88
Q

can you biospy liver mets secondary to a primary cancer originiating elsewhere in the body?

A

no- risk of seeding cancer

89
Q

what is the GET SMASHED mneumonic?

A

Gallstones

Ethanol

Trauma

Steroids

Mumps

Autoimmune disease i.e. SLE

Scorpion venom

Hypercalcaemia

ERCP

Drugs (azathioprine, NSAIDs, Diuretics)

90
Q

what happens pathologically in acute pancreatitis?

A

exaggerated inflammatory response causing inc in vascular permeability and subsewuent fluid shifts

enzymes released from pancreas causing autodigestion of fats (fat necrosis) and blood vessels which could lead to haemorrhage

91
Q

fat necrosis in pancreatitis releases fatty acids which eventually causes which biochemical abnormality?

A

hypocalcaemia

fatty acids react with serum calcium to form chalky depositis in fatty tissue

92
Q

how do patients with pancreatitis typically present?

A

severe epigastric pain which can radiate to the back

nausea and vomiting

93
Q

which bruising signs can sometimes be seen in pancreatitis?

A

Cullens sign-bruising around umbilicus

Grey Turners sign- bruising in the flanks

94
Q

differentials for acute abdominal pain that radiates to the back other than pancreatitis?

A

AAA

renal calculi

chronic pancreatitis

aortic dissection

peptic ulcer disease

95
Q

in addition to rountine bloods which investigations are specific to acute pancreatits?

A

serum amylase- 3x upper limit is diagnostic

LFTs- if raised can indicate gallstones as cause

serum lipase- more accurate than amylase but not routinely available

96
Q

what are the current UK guidelines for CT imaging used to asses severity of a disease i.e. pancreatitis?

A

should be performed 6-10 days after admission in patients with features of persistent inflammatory response

97
Q

how is acute pancreatits managed?

A

IV fluid resuscitation

Nasogastric tube

Cathetirisation + fluid balance chart

Opioid analgesia

broad spectrum antibiotic if pancreatic necrosis

98
Q

what are the potential systemic complications of pancreatitis?

A

Disseminated Intravascular Coagulation (DIC)

Acute Respiratory Distres Syndrome (ARDS)

Hypocalcaemia (from fat necrosis)

Hyperglycaemia (islet destruction and subsequent insulin disturbance)

99
Q

what are the potential local complications of pancreatitis?

A

pancreatic necrosis- persistent inflammation for >7/10 days, confirm with CT

pancreatic pseudocyst- collection of fluid containg pancreatic enzymes blood and necrotic tissue (usually found couple of weeks later)

100
Q

what imaging is used in suspected cases of acute pancreatitis?

A

US to investigate underlying cause i.e. gallstones

CT only used if complications are suspected or diagnosis uncertain

101
Q

what are the two most common causes of acute pancreatitis?

A

gallstones

alcohol

102
Q

which level of serum amylase is daignostic of acute pancreatitis?

A

3x upper limit of normal

103
Q

what is the M:F ratio of chronic pancreatitis?

A

4:1

average onset > 40yrs

104
Q

what are the main causes of chronic pancreatitis?

A

chronic alcohol abuse (60%)

idiopathic (30%)

105
Q

in addition to the typical epigastric pain and N&V pts with chronic pancreatits what may patients may also present with?

A

endocrine insufficiency- damage to islet of langerhans cells causes insulin disruption and impaired glucose regulation

exocrine insufficiency- damage to acinar cells causes failed digestive enzyme production leading to malabsoprtion

106
Q

in addition to routine bloods and investigations which two tests can be helpful in diagnosing chronic pancreatitis?

A

blood glucose- second to endocrine insufficiency

faecal elastase- will be low second to exocrine insufficiency

107
Q

how are cases of chronic pancreatitis managed?

A

analgesia

enzyme replacement if exocrine dysfunction i.e. Creon

vitamin supplements (fat soluble: A, D, E, K)

108
Q

what makes up 90% of pancreatic cancers?

A

ductal carcinoma of the pancreas

exocrine tumours and endocrine tumours make up remainder

109
Q

direct invasion of pancreatic cancers involves which structures?

A

spleen, transverse colon, adrenal glands

lymphatic invasion: regional lymph nodes, liver, lungs, peritoneum

*metastasis is common at time of diagnosis*

110
Q

risk factors for pancreatic cancer?

A

smoking, chronic pancreatitis

late onset diabetes, diagnosis >50yrs = 8x greater risk of developing carcinoma

111
Q

what % of cases of pancreatic cancer are unresectable at diagnosis?

A

80%- due to vague and non-specific symtpoms

112
Q

what is Courvoisier’s Law?

A

in the presence of jaundice and an enlarged/ palpable gallbladder, malignancy of the biliary tree or pancreas fhould be strongly suspected

113
Q

which tumour marker has a high sensitivity and specificty for pancreatic cancer?

A

CA19-9

assesses repsonse to treatment rather than initial diagnosis

114
Q

what imaging is used for pancreatic cancer?

A

US for initial imaging

CT is most important for diagnosis and staging

*chest-abdomen-pelvis CT following diagnosis and potentialy PET-CT*

115
Q

how are cases of pancreatic cancer managed?

A

only curative management is radical resection

whipples (pancreaticoduodenectomy)- tumour of head of pancreas

dital pancreatectomy

116
Q

what is removed during a Whipples procedure?

A

head of the pancreas, antrum of stomach, 1st and 2nd parts of duodenum, the common bile duct and the gallbladder

all removed due to shared supply of gastroduodenal artery

117
Q

adjuvant chemotherapy with which drug is commonly used following surgery in pancreatic cancer?

A

5-flourouracil

FOLFIRINOX and Gemcitabien therpay are alternatives

118
Q

how are patients with pancreartic cancer palliatively managed?

A

palliative chemo i.e gemcitabine

enzyme replacements i.e. Creon for exocrine insificiency

119
Q

what is the prognosis in pancreatic cancer?

A

5-year survival rate <5%

120
Q

how can endocrine tumours of the pancreas be described?

A

functional- actively secreting enzymes with symtpoms related to this

non-functional- clinical features relate purely to malignant spread

121
Q

endocrine tumours of the pancreas are associated with which syndrome?

A

MEN1 (multiple endocrine neoplasia 1)

122
Q

what are the endocrine tumours of the pancreas?

A

Gastrinoma (G cells)

Glucagonoma (a cells)

Insulinoma (ß cells)

Somatostatinoma (σ cells)

VIPoma (non-islet cells)

123
Q

how are pancreatic cysts divided?

A

true cysts (non-inflammatory)

pseudocysts (inflammatory)

124
Q

name the parts of the pancreas?

A
125
Q

how can true pancreatic cysts be classified?

A

secretions, histology, risk of malignancy

126
Q

as a rule are serous or mucinous pancreatic cysts higher risk for malignancy?

A

serous cyst are low risk

muccinous are high risk

127
Q

how are those with low and high risk pancreatic cysts typically followed up?

A

high risk- follow up MRI every 3 years

low risk- every 5 years

128
Q

what are the msot common causes of splenic infarction?

A

Haematological disease*: lymphoma, sickle cell, CML

Thromboembolism

*cause infarction through congestion of splenic circulation by abnormal cells

129
Q

what are important differentials of LUQ pain?

A

splenic rupture

peptic ulcer disease

pyelonephritis

left sided basal pneumonia

130
Q

what is the gold standard investigation for splenic rupture?

A

CT abdo scan with IV contrast

segmental wedge of hypoattenuated tissue will be visible with the apex of the wedge pointign to hilum o fspleen from the segmental branchig of splenic artery

131
Q

what are the complications of splenic infarction?

A

splenic rupture

splenic abscess

pseudocyst formation

Most cases will warrant splenectomy

132
Q

what follows splenic rupture?

A

large intraperitoneal haemorrhage rapidly leading to haemorrhagic shock

133
Q

msot cases of splenic rupture are secondary to what?

A

abdominal trauma- particularly blunt trauma

minority of cases are iatrogenic or second to underlying splenomegaly

134
Q

how is splenic rupture managed?

A

those who are haemodynamically unstable or with grade 5 injury (shattered spleen) require urgent laparotomy

haemodynaically stable pts can be treated conservatively

135
Q

what is OPSI?

A

Overwhelming Post-Splenectomy Infection

asplenic pts cannot mount normal immunological response

136
Q

asplenic pts including those post-splenectomy shoudl receive vaccinations against which three organisms?

A

Pneumococcus

Meningococcus

H. Influenzae

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Surgery (3 decks)

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