HPB Flashcards
(131 cards)
1
Q
at what level of billirubin does jaunice occur?
A
above 50micromol/L
2
Q
what is billirubin the breakdown product of?
A
red blood cells -> haem -> billirubin
3
Q
how is billirubin excreted?
A
billirubin is conjugated by the liver so it becomes water soluble, then it is excreted via the vile into the GI tract through the duodenum. it is egested in the faeces as stercobilin and urobilinogen but 10% of urobilinogen is reabsorbed into blood and excreted via kidneys
4
Q
what are the three types of jaundice?
A
pre hepatic - excess haemolysis…forms unconjugated hyperbillirubinaemia (liver can not cope with quantity to conjugate)
intrahepatic - dysfunction of hepatic cells and can become cirrhotic and compresses billary tree …both conjugated and unconjugated
post hepatic - obstruction of billary drainage …already conjugated by liver
5
Q
give 3 causes of pre hepatic jaundice
A
haemolytic anaemia
gilbert’s syndrome
criggler-naijjar syndrome
6
Q
give 3 causes of intrahepatic jaundice
A
alcoholic liver disease
hepatitis
primary sclerosing cholangitis
hepatocellular carcinoma
7
Q
give 3 causes of post hepatic jaundice
A
intra luminal - gallstones
mural - strictures
extra mural - pancreatic cancerqq
8
Q
how does post hepatic jaundice clinically present?
A
conjugated billirubin can be excreted via urine as water soluble —-dark urine (can also be present in intra hepatic)
and due tn obstruction, reduced stercobilin entering Gi tract which normally colours the stools - pale stools
9
Q
what investigations are required for a patient presenting with jaundice?
A
LFTS
coag screen - PT is marker of liver synthesis function
FBC - anaemia, raised MCV and thrombocytopenia - liver disease
UandE’s
specialist markers
10
Q
what does each LFT mean?
A
billirubin - degree of jaundice
albumin - liver synthesis function
AST and ALT - if ratio >2 then alcoholic liver disease, if around 1 then viral hepatitis
ALP - billary obstruction, bone disease, pregnancy, malignancies
gamma GT - more specific for billary obstruction
11
Q
what are the causes of acute liver injury and what markers would test?
A
hep A, B, C, E
CMV
EBV
-paracetamol lieve, caeruloplasmin, antinuclear antibody and IgG
12
Q
what are the causes of chronic liver injury and what markers would test?
A
hep B and C
- caeruloplasmin, ferritin and transferrin saturation, tissue transglutaminase antibody, alpha 1 antitrypsin, autoantibodies (AMA, anti SMA, ANA - autoimmune)
13
Q
what investigations are required for a patient with jaundice?
A
USS abdomen
MRCP - visualise bil
liver biopsy
14
Q
how is a gallstone managed
A
removal through ERCP or stenting of common bile duct
15
Q
how is hyperbillirubinaemia symptomatically treated
A
pruritus - cholestyramine to increase billary drainage
- anti histamines
16
Q
what complications of hyperbillirubinaemia need to monitored for
A
coagulopathy - with vit K or fresh frozen plasma
hypoglyceamia - give glucose or dextrose
decompensating chronic liver disease (hepatic encephalopathy) - laxatives +/- neomycin to reduce ammonia producing bacteria
17
Q
why do gallstones form?
A
formed from cholesterol, phospholipids, and bile pigments (products of haemoglobin metabolism). It is stored in the gallbladder, before passing into the duodenum upon gallbladder stimulation..gallstones form as a result of supersaturation of bile
18
Q
what are the types of gallstones?
A
Cholesterol stones – composed purely of cholesterol, from excess cholesterol production
There is a well recognised link between poor diet, obesity, and cholesterol stones
Pigment stones – composed purely of bile pigments, from excess bile pigments production
Commonly seen in those with known haemolytic anaemia
Mixed stones – comprised of both cholesterol and bile pigments
19
Q
what are the risk fx for gallstones?
A
5 F’S - fat, female, fertile, forty, family hx
pregnancy, COCP, haemolytic anaemia, malabsorption
20
Q
what are the clinical fx of gallstones?
A
billary colic - impacted gallstone, no inflammation - sudden, dull, colicky pain radiates RUQ to epigastrium, precipitated by fatty foods
N+V
acute cholecystitis - constant pain in RUQ or epigastrium, signs of inflammation, tender in RUQ, positive murphy’s sign, guarding, sepsis
21
Q
what is murphy’s sign?
A
Whilst applying pressure in the RUQ, ask the patient to inspire. Murphy’s sign is positive when there is a halt in inspiration due to pain, indicating an inflamed gallbladder
22
Q
what are the ddx for gallstones?
A
gastro-oesophageal reflux disease, peptic ulcer disease, acute pancreatitis, or inflammatory bowel disease.
23
Q
which investigations are required for gallstones?
A
FBC and CRP – assess for the presence of any inflammatory response, which will be raised in cholecystitis
LFTs – biliary colic and acute cholecystitis are likely to show a raised ALP (indicating ductal occlusion), yet ALT and bilirubin should remain within normal limits (unless a Mirizzi syndrome, discussed below)
Amylase (or lipase) – to check for any evidence of pancreatitis
A urinalysis, including a pregnancy test
imaging -trans-abdo USS - The presence of gallstones or sludge (the start of gallstone formation)
Gallbladder wall thickness (if thick walled, then inflammation is likely)
Bile duct dilatation (indicates a possible stone in the distal bile ducts)
MRCP if not found on USS
24
Q
how is billary colic managed?
A
analgesia
low fat diet, weight loss, increased exercise
high chance of recurrence and may require elective laprascopic cholectomy within 6 weeks of first presentation
25
how is acute cholecystitis managed?
IV abx
analgesia
antiemetics
laprascopic cholecystectomy within 1 week but should be within 72 hrs
if have pain post cholecytsectomy may be a retained CBD
26
what is a complication of gallstones?
mirizzi syndrome - stone located in hartmanns pouch (an outpouching of gallbladder wall at junction with the cystic duct or in cystic duct itself causing compression of CHD..obstructive jaundice...requires laprascopic cholecystectomy
gallbaldder empyema = gallbladder full of pus..laprascopic cholecystectomy
chronic cholecystitis - recurrent or unreated cholecystitis - CT...elective cholecytectomy
bouveret's syndrome - inflammation of gallbladder can cause a fistula from wall to small bowel..cholecystoduodenal fistula sp gallstones passes and impacts in duodenum
gallstone ileus - ^ stone impacts at terminal ileum..SBO
27
define ascending cholangitis
biliary outflow obstruction* and biliary infection. During an obstruction, stasis of fluid combined with elevated intraluminal pressure allows the bacterial colonisation of the biliary tree to become pathological.
28
what are the causes of ascending cholangitis?
gallstones, ERCP, cholangiocarcinoma
pancreatitis, primary sclerosing cholangitis
usually e.coli, klebsiella species, enterococcus
29
what are the clinical fx of ascending cholangitis?
charcot's - RUQ, fever, jaundice
reynolds pentad - jaundice, fever, RUQ, hypotension and confusion
pruritus, pale stools, dark urine
PMH - gallstones, recent ERCP, or previous cholangitis
MHX- COCP, fibrates, lipid rich diet
pyrexia, rigors, confusion, hypotension, tachycardia
30
which investigations are required for ascending cholangitis?
FBC - leukocytosis, LFT's - raised ALP nad gamma Gt and billirubin
blood cultures
USS - bile duct dilation >6mm, or gallstones
ERCP
31
how is ascending cholangitis managed?
sepsis 0 IV access for fluids, bloods, blood cultures, broad spectum IV abx
endoscopic biliary decompression
ERCP - with or without sphincterotomy and stenting
32
what are the complications of ERCP?
pancreatitis, bleeding, perforation
33
define cholangiocarcinoma
malignancy of billiary tree
high incidence in south east asia - chronic endemic parasitic infection from liver flukes can cause
usually adenocarcinomas then rest are squamous cell, sarcomas, lymphomas
34
where is the most common site for a bile duct tumour?
bifurcation of right and left hepatic ducts - klatsin tumour
35
what are the risk fx for cholangiocarcinoma?
Primary sclerosing cholangitis (lifetime risk of 10-20%)
Ulcerative colitis
Infective (Liver flukes, HIV, hepatitis virus)
Toxins (Chemicals in rubber and aircraft industry)
Congenital (Caroli’s disease, choledochal cyst)
Alcohol excess
Diabetes mellitus
36
what are the clinical fx of cholangiocarcinoma?
asx
jaundice
pruritus
steatorrhoea
non speciifc abdo pain
dark urine
weifht loss
lethargy
cachexia
37
define courvoisier's law
in the presence of jaundice and an enlarged or palpable gallbladder, malignancy of the biliary tree or pancreas should be strongly suspected as the cause is unlikely to be gallstones
38
which investigations are required for cholangiocarcinoma?
LFT - billirubin, ALP, gamma GT
tumour markers - CEA, CA19-9
Ultrasound scanning may initially show dilated biliary ducts, however CT imaging or MRI imaging is required for diagnosis.
Endoscopic retrograde cholangiopancreatography (ERCP) is required to obtain a tissue sample, which will delineate the exact location of the lesion and take brushings of the area.
Staging of the disease is best done via CT imaging. Angiography may be used in pre-operative planning to image the hepatic arteries and portal vein.
39
how is cholangiocarcinoma managed?
complete surgical resection
if intrahepatic or klatsin tumours - partial hepatectomy or reconstruction of biliary tree
if distal common duct tumour - pancreaticiduodenectomy
radiotherapy
palliative - stenting, surgical bypass, chemo and radio
40
what is the prognosis of cholangiocarcinomas ?
12-18months from diagnosis as mostly unresectable disease
5 yr survival rates after surgery - 10-40%
41
define simple liver cysts
fluid-filled epithelial-lined sacs within the liver, most commonly occurring in the right lobe. They are relatively common, with a prevalence of 2.5-18%, increasing in incidence with age
due to congenitally malformed bile duct cells, failing to connect to the extrahepatic ducts, which leads to a local dilatation filled with a bile-like fluid, of varying size.
42
what are the clinical fx of simple liver cysts?
normally asx
around 10-15% will have abdo pain, nausea, early satiety
43
which investigations are required for simple liver cysts?
LFTs normal but may have raised gamma GT
tumour markers - CEA, CA19-9 elevated
USS - well defined, thin walled, oval with no septations
44
how are simple liver cysts managed?
mostly no intervention, if >4cm follow up USS, if size unchanged for 2-3 yrs, no further scans until asx
if asx - USS guided aspiration or laprascopic deroofing
45
define polycystic liver disease
presence of ≥20 cysts within the liver parenchyma, each of which are ≥1cm in size.
46
what are the genetic causes of polycystic liver disease?
utosomal dominant polycystic kidney disease (ADPKD)
Caused by mutations in the PKD1 (chromosome 16) and PKD2 (chromosome 4) genes, whereby 10-60% of patients will also develop have liver cysts (as the most common extra-renal manifestation of ADPKD)
Autosomal dominant polycystic liver disease (ADPLD)
Caused by mutations in the PRKCSH (chromosome 19) or SEC63 (chromosome 6) genes; patients with this genotype will not have any renal involvement.
47
what are the clinical fx of polycystic liver disease?
asx
may have abdo pain as cysts grow, and hepatomegaly
can cause liver cirrhosis and portal hypertension
48
which investigations are required for polycystic liver disease?
normal LFT's
USS
49
how are polycstic liver cysts managed?
asx left alone
short term benefit of somatostatin analogues
surgery indicated if -(1) intractable symptoms (2) inability to rule out malignancy on imaging alone (3) prevention of malignancy.
US guided aspiration of laprascopic deroofing
50
define cystic neoplasms
rare
common subtype are cystadenomas (non-invasive mucinous cystic neoplasms). These are premalignant lesions, developing as a result of abnormal proliferation of biliary epithelium and can undergo malignant transformation into cystadenocarcinomas in around 10% of case
51
what are the clinical fx of cystic neoplasms?
asx
if do = abdo pain and anorexia
52
which investigations are required for cystic neoplasms?
LFTS normal
ALP, CEA, CA19-9 can be elevated
CT with contrast
aspiration or biopsy should be avoided as can lead to peritoneal seeding
liver lobe resection
53
define hyatid cysts
Hydatid cysts, or Echinococcal cysts, result from infection by the tapeworm Echinococcus granulosus
The eggs as passed by faceo-oral transmission. After being excreted by carnivores (commonly from dogs), the larvae invade their hosts’ gastrointestinal tract, before passing via the hepatic portal system into the liver, where they continue to grow and form cysts
54
what are the clinical fx of hyatid cysts?
asx
vague abdo pain
jaundice and cholangitis
55
which investigations are required for hyatid cysts?
LFTS normal
FBC - eosinophilia, echinococcal antibody titres are positive in 80% of those with the diseas
USS - calcified spherical lesions with multiple septations
56
how are hyatid cysts managed?
aspiration not recommended as can rupture and cause anaphlactic reaction
cyst deroofing
anti microbials
57
define liver abscesses
polymicrobial bacterial infection spreading from the biliary or gastrointestinal tract, either via contiguous spread or seeding from the portal and hepatic veins.
Common causes include cholecystitis, cholangitis, diverticulitis, appendicitis, or septicaemia
The most commonly isolated organisms are E. Coli, K. pneumoniae, and S. constellatus, although fungal causes may also be present in immunocompromised patients.
58
what are the clinical fx of liver abscess?
ever, rigors, and abdominal pain*. Other symptoms include bloating, nausea, anorexia, weight loss, fatigue and jaundice.
On examination, patients will have RUQ tenderness +/- hepatomegaly. If the abscess ruptures (a rare complication), then patients may present with signs of shock.
59
which investigations are required for liver abscess?
FBC- leukocytosis
LFTS - raised ALP
peripheral blood and fluid cultures for microscopy
USS - poorly defined lesion, potential gas bubbles and septations
CT with contrast
60
how are liver abscesses managed?
fluids
abx
image guided aspiration
underlying cause managed
61
define amoebic abscess
most common extra-intestinal manifestation of amebiasis infection, caused by the organism Entamoeba histolytica.
The infection spreads via faeco-oral route. Once in the colon, the trophozoite begins to invade the mucosa and spread to the liver via the portal system
62
what are the clinical fx of emoebic abscess?
abdo pain, nausea, fever, rigors, weight loss, bloating, recent travel
leucocytsosi with deranged LFTs - peipheral blood and fluid cultures for microscopy
samples to check for E.histolytica
USS - porroly defined lesions
63
how are amoebic abscesses managed?
abx
surgical drainage
luminal agent
64
how common is liver cancer and the types?
Malignant lesions of the liver represent metastasis from other primary cancers in 90% of cases, with primary liver malignancies being relatively rare. Of the primary liver cancers, 90% are hepatocellular carcinoma (HCC), with intrahepatic cholangiocarcinoma making up the remainder.
Hepatocellular carcinoma is the sixth most common cancer worldwide and the second leading cause of cancer death. Incidence rates vary significantly across the globe, mainly determined by the incidence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection
65
what are the risk fx for liver cancer?
Liver cirrhosis
Viral hepatitis infection, mainly hepatitis B virus and hepatitis C virus, alcohol excess, non-alcoholic fatty liver disease, and other rare causes including metabolic (hereditary haemochromatosis, Wilson’s disease) and autoimmune (primary biliary cirrhosis) processes
Aflatoxin exposure
Particularly in combination with HBV infection
Hepatocellular adenoma*
Smoking
Advanced age (>70yrs)
Positive family history
66
what are the clinical fx of liver cancer?
fatigue, weight loss, abdo pain
irregular enlarge liver
ascites, jaundice, confusion
67
whcih investigations are required for liver cancer?
FBC, LFT, Clotting
AFP
USS - hypodense heterogenous lesion
MRI/CT
uss/ct GUIDED percutaneous biopsy
68
how is liver cancer staged?
The Barcelona Clinic Liver Cancer staging system (BCLC) is the most accepted and widely used staging for HCC. It accounts for tumour stage, based on tumour size and number of tumours, as well as liver function*, physical status, and cancer related symptoms. These factors are used to define stage as 0 (very early), A (early), B (intermediate), C (advanced) and D (terminal)
69
how is liver cancer managed?
MDT
liver transplant or resection
ablative techniques - deep sited small tumours
anti-angiogenic agents if metastatic
transarterial chemoembolisation = injecting chemo into arteries
70
what is the criteria for liver transplants?
One lesion < 5cm or up to three lesions all <3cm
There is no vascular infiltration
There are no extra-hepatic manifestations
71
what is the prognosis of liver cancer?
depends on extent of underlying cirrhosis
the expected 5 year survival for each treatment pathway, assuming no or mild cirrhosis, are:
Liver transplantation 60-75%
Liver Resection 45-70%
Ablation 68% (in tumours <2cm)
TACE 26%
72
where is secondary liver metasistai likely to originate from?
mainly colorectal
or panceeas, breast and lung
73
what is the difference between acute and chronic pancreatitis?
its limited damage to the secretory function of the gland, with no gross structural damage developing. Repeated episodes of acute pancreatitis can eventually lead to chronic pancreatitis.
74
what are the causes of acute pancreatitis?
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune - lupus
Scorpion venom
Hypercalcaemia
ERCP
Drugs - azathioprine, NSAIDS, diuretics
75
what is the pathophysiology behind acute pancreatitis?
the causes will trigger a premature and exaggerated activation of the digestive enzymes within the pancreas. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts (often termed “third spacing”).
Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats (resulting in a ‘fat necrosis’) and blood vessels (sometimes leading to haemorrhage in the retroperitoneal space). Fat necrosis can cause the release of free fatty acids, reacting with serum calcium to form chalky deposits in fatty tissue, resulting in hypocalcaemia.
Severe end-stage pancreatitis will eventually result in partial or complete necrosis of the pancreas.
76
what are the clinical fx of acute pancreatitis?
severe epigastric pain radiating to back
N+V
may be haemodynamically unstable
cullens sign - bruising around umbilicus
grey turner's - bruising in flank
tetany from hypocalcaemia
gallstones can cause obstructive jaundice
77
what are the ddx of acute pancreatitis?
abdominal aortic aneurysm, renal calculi, chronic pancreatitis, aortic dissection, or peptic ulcer disease
78
which investigations are required for acute pancreatitis?
serum amylase or serum lipase (lipase better as amy can be raised in bowel perf, ectopic preg or DKA)
LFTS - ALT raised then gallstones
USS - gallstone and duct dilation
abdo x ray - sentinal loop sign - dilated proximal bowel loop adjacent to pancreas due to localised inflammation
contrast CT - oedema and swelling, necrosis
79
how is the severity of acute pancreatitis measured?
within 48 hrs of admission - modified glasgow criteria
PANCREAS: pO2 <8kPa, Age >55yrs, Neutrophils (/WCC) >15×109/L, Calcium <2mmol/L, Renal function (Urea) >16mmol/L, Enzymes LDH>600U/L or AST>200U/L, Albumin <32g/L, Sugar (blood glucose) >10mmol/L
80
how is acute pancreatitis managed?
treat underlying cause
IV fluids, 02
NG tube
catheterisation
opioid analgesia
in high dependency unit
broad spec abx
81
what are the systemic complications of acute pancreatitis?
Disseminated Intravascular Coagulation (DIC)
Acute Respiratory Distress Syndrome (ARDS)
Hypocalcaemia - Fat necrosis from released lipases, results in the release of free fatty acids, which react with serum calcium to form chalky deposits in fatty tissue
Hyperglycaemia - Secondary to destruction of islets of Langerhans and subsequent disturbances to insulin metabolism
82
what are the local complications of acute pancreatitis?
pancreatic necrosis - if clinical deterioration and raised infection markers indicates and fine needle aspiration of necrosis to confirm
pancreatic pseudocyst - collection of fluid containing pancreatic enzymes, blood and necrotic tissue, lack an epithelial lining and have a vascular and fibrotic wall surrounding it, can cause billiary or gastric outlet obstruction. treated usually surgical debridgeemnt of drainage but 50% resolve spontaneously
83
what are the main causes of chronic pancreatitis?
chronic alcohol abuse
idiopathic
metabolic (hyperlipidaemia, hypercalcaemia),
infection (both viral (e.g. HIV, mumps, coxsackie) and bacterial (e.g. Echinococcus),
hereditary (e.g. cystic fibrosis),
autoimmune (e.g. autoimmune pancreatitis (AIP) or SLE),
anatomical (malignancy or stricture formation), or congenital anomalies (e.g. Pancreas divisum or Annular pancreas)
84
what are the clinical fx of chronic pancreatitis?
chronic pain - epigastrium and back
Endocrine insufficiency – diabetes mellitus
exocrine suffiency - malabsorption - weight loss, diarrhoea, stearrhoea
abdo soft and tender
significant cachexia
concurrent pseudocysts - billiary and gastric outlet obstruction
85
which investigations are required for acute pancreatitis?
urine dip
routine bloods - fbc, crp
serum amylase or lipase no raised
blood glucose
LFT's
faecal elastase
CT - atrophy and calcification and pseudocysts
USS or MRCP - billiary tree
86
how is chronic pancreatitis managed?
treating underlying cause
alcohol cessation or statin therapy for hyperlipidaemia
analgesia
enzyme replacement - creon replaces lipas
fat soluble vitamins
insulin regimes and annual surveillance
ERCP
ESWL
duct stones - frey's procedure - involves coring out of the diseased part of the pancreatic head and formation of a lateral pancreaticojejunostomy; this allows better drainage of the main pancreatic duct into the jejunum
whipple's
87
what is a complication of chronic pancreatitis?
pancreatic malignancy
88
how common is pancreatic cancer?
4th most common cause of cancer-related deaths in the UK. It is rare under 40 years of age, with 80% of cases occurring between 60-80yrs, and unfortunately it is uncommon to be diagnosed early enough for curative treatment.
89
what are the types of pancreatic cancer?
ductal carcinoma - most common
exocrine tumours - pancreatic cyst carcinoma
endocrine tumours - islet cells
90
where is the most common location is pancreatic cancer?
head of pancreas
91
what are the risk fx of pancreatic cancer?
moking, chronic pancreatitis, and dietary factors (high red meat intake, low fruit and vegetables intake). There may also be a hereditary element, as 7% of patients have a family history of the disease.
92
what are the clinical fx of pancreatic cancer?
obstructive jaundice – due to compression of the common bile duct (present in 90% of cases at time of diagnosis), typically painless
Weight loss – due to the metabolic effects of the cancer, or secondary to exocrine dysfunction
Abdominal pain (non-specific) – due to invasion of the coeliac plexus or secondary to pancreatitis
acute pancreatitis or thrombophlebitis migrans (a recurrent migratory superficial thrombophlebitis, caused by a paraneoplastic hypercoagulable state).
Late onset diabetes mellitus
cachectic, malnourished, jaundice
93
what are the ddx for pancreatic cancer?
Causes of obstructive jaundice – gallstone disease, cholangiocarcinoma
Causes of epigastric abdominal pain – gallstone disease, peptic ulcer disease, gastric cancer, acute coronary syndrome
94
which investigations are required for pancreatic cancer?
FBC - anaemia and thrombocytopenia
LFT - raised bilirubin, ALP, gamma GT
CA19-9 - assess response to tx
abdo USS - pancreatic mass or dilated billiary tree
CT TAP
EUS for staging of adenocarcinoma
95
how is pancreatic cancer managed?
radical resection + adjuvant chemo-
Head of the pancreas typically undergo a pancreaticoduodenectomy (termed a Whipple’s procedure) with regional lymphadenectomy
Body or tail of pancreas typically undergo a distal pancreatectomy +/- splenectomy with regional lymphadenectomy
if non resectable - chemo - FOLFIRINOX, insertion of billiary stent, enzyme replacement
96
how are pancreatic tumours classified?
resectable, borderline resectable, or locally advanced*, depending on the degree of contact between the tumour and surrounding vessels (namely the portal vein, superior mesenteric artery or vein, coeliac trunk, and common hepatic artery), and metastatic diseas
97
what are the complications of surgery?
pancreatic fistula, delayed gastric emptying, and pancreatic insufficiency.
98
definf whipples procedure
A Whipple’s procedure involves the removal of the head of the pancreas, the antrum of the stomach, the 1st and 2nd parts of the duodenum, the common bile duct, and the gallbladder.
All viscera removed in the operation are done so due to their common arterial supply (the gastroduodenal artery), shared by the head of the pancreas and the duodenum.
Following this, the tail of the pancreas and the hepatic duct are attached to the jejunum, allowing bile and pancreatic juices to drain into the gut, whilst the stomach is subsequently anastomosed with the jejunum allowing for the passage of food.
99
how are endocrine tumours of the pancreas classified?
functional or non-functional tumours, based on their hormone secretion status.
Functional tumours actively secrete hormones and their signs and symptoms are related to this, whilst non-functional tumours do not secrete active hormones and clinical features are related purely to their malignant spread
100
G cell tumour
gastrin(gastrinoma) Stimulates the release of gastric acid Zollinger-Ellison syndrome, resulting in severe peptic ulcers, refractory to medical treatment, with diarrhoea and steatorrhoea
101
alpha cells
Glucagon
(glucagonoma) Increase blood glucose concentration Hyperglycaemia, diabetes mellitus, and necrolytic migratory erythema
102
beta cells
Insulin
(insulinoma) Decrease blood glucose concentration Symptomatic hypoglycaemia, such as sweating or changed mental state, improving with consumption of carbohydrates
103
delta cells
Somatostatin
(Somatostatinoma) Inhibits the release of GH, TSH and prolactin from the anterior pituitary, and of gastrin Diabetes mellitus, steatorrhoea, gallstones (due to inhibition of cholecystokinin), weight loss, and achlorhydria (due to gastrin inhibition)
104
non islet cells
Vasoactive intestinal peptide
(VIPoma) Secretion of water and electrolytes into the gut. Relaxation of enteric smooth muscle. Prolonged profuse watery diarrhoea, severe hypokalaemia, and dehydration (also known as Verner-Morrison syndrome)
105
how are endocrine tumours investigated and managed?
CT imaging, MRI imaging, and EUS. Small non-functional well differentiated pancreatic NETs (<1cm) can simply be observed, whilst larger or functioning tumours need resection, with any distant metastatic disease also resected if the tumour is low grade and the metastases is low volume.
Somatostatin analogues can be used to control and ameliorate the effects of hormonal hypersecretion
106
define pancreatic cysts
fluid filled lesions within pancreas
majority are benign
usually asx
107
how can pancreatic cysts be classified?
mucinous (lined with mucin-producing epithelium) or non-mucinous (namely simple cysts, pseudocysts, and serous cystadenomas). As a general rule, serous cysts are lower risk and mucinous cysts are higher risk.
Mucinous cysts include intraductal papillary mucinous neoplasms (IPMNs) and mucinous cystic neoplasms (MCNs)*, pancreatic neuroendocrine tumours with a cystic component, and pancreatic adenocarcinoma with cystic degeneration
108
what are the clinical fx of pancreatic cysts?
asx 70%
non specific abdo pain or back pain, post obstructive jaudnice and vomit
can become infected - systemic fx
malignant transformation - obstructive jaundice, weight loss
tender badomen, abdo mass
109
what are the high risk sx of pancreatic cysts?
obstructive jaundice without alternative explanation, new onset diabetes mellitus, recurrent pancreatitis due to a pancreatic cyst, a substantially elevated serum CA19-9 level, or cytology suggesting the presence of high-grade dysplasia or neoplasia
110
what are the ddx of pancreatic cysts?
cancer and pseudocysts
111
which investigations are required for pancreatic cysts?
pancreatic protocol CT scan or MRCP
Endoscopic US scan with Fine Needle Aspiration (EUS-FNA) for cytology and biomarker assessment (e.g. amylase). In those with concerning features, CA19-9 serum levels
112
how is risk stratified of pancreatic cysts?
Low risk features – cyst diameter <3cm, cystic morphology with central calcification, or asymptomatic
High risk features – main pancreatic duct dilatation greater than 10mm, any enhancing solid component, or non-enhancing mural nodule
113
how are pancreatic cysts managed?
high risk of malignancy and symptomatic - resection
MRI for surveillance
114
define splenic infarct
occlusion of splenic artery or one of its branches...necrosis
As the spleen is supplied by the splenic artery (from the coeliac axis) and the short gastric arteries (from left gastroepiploic artery), infarction is often not complete due to collateral circulation.
115
what are the causes of splenic infarcts?
Haematological disorders* such as lymphoma, myelofibrosis, Sickle Cell Disease, Chronic Myeloid Leukaemia, Polycythaemia Rubra Vera, or hypercoagulable states
Embolic disorders such as endocarditis, atrial fibrillation, infected aneurysm grafts, or post-MI mural thrombus
Other rarer causes include vasculitis, trauma (including blunt trauma or torsion of a ‘wandering’ splenic artery), collagen tissue diseases, or surgery (pancreatectomy or liver transplantation).
116
what are the clinical fx of splenic infarcts?
left upper quadrant abdominal pain, which may radiate to the left shoulder.
fever, nausea and vomit
can be asx
LUQ tenderness
117
what are the ddx for splenic infarct?
peptic ulcer disease, pyelonephritis or ureteric colic, and a left sided basal pneumonia
118
which investigations are required for splenic infarct?
abdo scan with IV contrast
FBC, UE,LFT, coag screen - raised WCC and d dimer
119
how is splenic infarcts pictured on ct?
segmental wedge of hypoattenuated tissue
apex of wedge points to hilum of spleen
120
how are splenic infarcts managed?
analgesia
IV fluids
underyling condition
long term anticoag
splenectomy with vacciniation against capsulated bacteria and low dose abx
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what is a consequence of a splenectomy??
overwhelming post-splenectomy infection (OPSI) syndrome
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what are the most common complications of splenic infarctions?
splenic rupture, abscess and pseudocyst
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define splenic abscess
if cause of embolus was non sterile eg: endocarditis
CT - but hard to diagnose
usually exploratory surgery
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define auto-splenectomy
rare conditions that results in asplenism..repeated infarction results in fibrosis and atrophy if spleen
usually caused by sickle cell anameia
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what is a consequence of splenic rupture?
intraperitoneal haemorrhage
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what is the most common cause of splenic rupture?
abdominal trauma- seat belt injuries and falls onto the left side
iatrogenic or secondary due to splenomegaly from haematological malignancy or infective causes - EBV
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what are the clinical fx of splenic rupture>
abdo pain
hypovolaemic shock
LUQ tenderness
peritonism
radiating left shoulder pain - kehr's sign
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which investigations are required for splenic rupture?
if haemodynamically unstable and peritonitic -immediate laparatomy
CT TAP with IV contrast
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how are splenic infarcts graded?
American Association for Surgery of Trauma -
1
– Capsular tear <1cm parenchymal depth
– Subcapsular haematoma <10% surface area
2
– Capsular tear 1-3cm parenchymal depth
– Subcapsular 10-50% surface area, or intraparenchymal <5cm
3
– Capsular tear >3cm parenchymal depth, or any tear involving trabecular vessels
– Subcapsular >50% surface area, or intraparenchymal >5cm, or any expanding or ruptured haematoma.
4
– Laceration involving segmental or hilar vessels, devascularising >25% of the spleen
5
– Completely shattered spleen or hilar vascular injury, devascularising the entire spleen
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how is splenic rupture managed?
atients who are haemodynamically unstable* or with a grade 5 injury (a shattered spleen or major hilar vascular injury) need urgent laparotomy.
Haemodynamically stable patients with grade 1–3 injuries without active extravasation can be treated conservatively. They should be resuscitated using the principle of permissive hypotension, admitted to a high dependency area for observation, and have serial abdominal examinations for any evidence of deterioration. The patient should be placed on strict bed rest and have a repeat CT scan at 1-week post-injury.
With any evidence of increasing tenderness or peritonitis, there should be a low threshold for re-imaging and / or laparotomy (as associated injuries such as small bowel injuries are easily missed on initial CT imaging).
All patients who are treated conservatively should receive prophylactic vaccinations (against Strep Pneumoniae, Haemophilus Influenzae B (HIB) and Meningococcus) at discharge
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what are the complications of treatment of splenic rupture?
Ongoing bleeding
Splenic necrosis
Splenic abscess or cyst formation
Thrombocytosis
