HPB Flashcards

1
Q

What is the aetiology of a splenic infarct?

A

A
- Haemotological Disease: Lymphoma, Myelofibrosis, Sickle cell, CML, Polycythemia Vera, Hypercoagulable states
- Thromboembolism: endocarditis, AF, post MI mural thrombus,
- Rare causes: trauma, vasculitis, liver surgery, panreatectomy

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2
Q

What are the clinical features of a splenic infarct?

A

Often asymptomatic
LUQ pain/tenderness that radiates to the left shoulder (Kehr’s sign)
Fever
N+V
Pleuritic chest pain

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3
Q

What differential diagnoses can be considered when a patient presents with symptoms of a splenic infarct?

A

Peptic ulcer disease
Pyelonephritis
Ureteric colic
Left sided basal pneumonia

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4
Q

What is the immediate and long term management for a patient with a splenic infarct?

A

Immediate:

Analgesia
IV fluids
Manage underlying condition
Consider long term anticoagulation
Avoid splenectomy due to OPSI
Long-term:

  • Vaccination against encapsulated bacteria NHS

Prophylatic low dose abx (Penicillin V)

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5
Q

What are the complications of a splenic infarct?

A

A
- Splenic rupture: do splenectomy
- Splenic abscess: when cause of infarct was non-sterile embolus e.g infective endocarditis. May be seen on CT scan but confirmed with explorative surgery
- Pseudocyst formation
- Autosplenectomy: causes asplenism. Repeated splenic infarcts leads to progressive fibrosis and atrophy of the spleen. Common in sickle cell as when crises there is splenic artery occlusion. Leaves patient susceptible to infection

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6
Q

What are the clinical features of splenic rupture?

A

Abdominal pain
Hypovolemic shock
LUQ tenderness/Peritonism
Kehr’s sign due to diaphragm irritation

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7
Q

What investigations do you do for a suspected splenic rupture?

A

Haemodynamically unstable with peritonism: immediate laparotomy

Haemodynamically stable: urgent CT chest-abdomen-pelvis with IV contrast

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8
Q

What are the main complications of conservative treatment and embolisation treatment for splenic rupture?

A

Ongoing bleeding
Splenic necrosis
Splenic abscess or cyst formation
Thrombocytosis (give aspirin if platelet count rises)
- OPSI so give prophylatic Penicillin V and vaccinations to prevent sepsis

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9
Q

What would you see on ultrasound with gallstone pathology?

A

Gallstones or sludge
Thickened gallbladder wall if inflamed
Bile duct dilatation (stone in the distal bile ducts)

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10
Q

What is the difference between MRCP and ERCP?

A

MRCP - Identifies any biliary obstruction

ERCP - Identifies any biliary obstruction and allows for intervention

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11
Q

What are some complications of gallstones?

A

Mirizzi Syndrome
Gallbladder empyema
Chronic cholecystitis
Bouveret’s Syndrome
Gallstone ileus

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12
Q

What is Mirizzi Syndrome and how is it managed?

A

Stone located in Hartmann’s pouch or the cystic duct, that compresses the common hepatic duct
Causes obstructive jaundice
Confirmed with MRCP and manage by laparoscopic cholecystectomy

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13
Q

What is chronic cholecystitis, what are the complications of this and how is it managed?

A

History of recurrent or untreated cholecystitis
Ongoing RUQ or epigastric pain w/wo N+V
- Complications: gallblader carcinoma, biliary enteric fistula

  • Diagnose with CT or often histologically post-cholecystectomy.

Treat with elective cholecystectomy

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14
Q

What is Bouveret’s Syndrome and Gallstone Ileus?

A

A
Inflammation of gallbladder can form cholecystoduodenal fistula allowing gallstones into small bowel, resulting in bowel obstruction
- Bouveret’s Syndrome – stone impacts proximal duodenum, causing a gastric outlet obstruction
- Gallstone Ileus – stone impacts terminal ileum (narrowest part of small bowel), causing a small bowel obstruction

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15
Q

What is a cholangiocarcinoma and what is the common histology and location of these?

A

Cancer in the biliary system but usually extrahepatic
- Common location: bifurcation of right and left hepatic ducts (Klatskin tumour).
Slow growing that invades locally and metastases to lymph nodes then peritoneal cavity, liver, lung
- Histology: 95% adenocarcinoma, SCC, lymphoma, sarcomas, small cell cancers

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16
Q

What is Courvoisier’s Law?

A

In the presence of painless jaundice and an enlarged gallbladder/RUQ mass, there is likely an obstructing pancreatic or gallbladder malignancy not gallstones
Sign only present if tumour obstructing distal to cystic duct

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17
Q

What are some differentials for cholangiocarcinoma?

A

A
Think of other causes of post-hepatic jaundice:

obstructive choledocholithiasis
bile duct strictures
external compression from extra-biliary tumour
benign biliary tumours
pancreatic tumours
primary biliary cirrhosis
primary sclerosing cholangitis.

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18
Q

Most patients with cholangiocarcinoma will require palliative treatment. What are some of the options for this?

A

Stenting: with ERCP to relieve obstructing symptoms but may need to be replaced every few months as prone to occlusion

Surgical bypass: if obstruction not relieved by stenting

Palliative radiotherapy and chemotherapy to slow tumour growth e.g cisplatin

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19
Q

How are simple liver cysts managed?

A

<4cm asymptomatic: no intervention

> 4cm asymptomatic: follow up US scans at 3,6,12 months to check for growth. If size of cyst remains unchanged for 2-3 years no intervention unless becomes asymptomatic
- Symptomatic: ultrasound-guided aspiration or laparoscopic de-roofing (lower rates of recurrence)

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20
Q

What are the clinical features of cystic neoplasms in the liver and what is the histology of these?

A

Features: asymptomatic as grow very slowly, abdominal pain, anorexia, bloating, fullness, nausea

Histology: cystadenomas (non-invasive mucinous cystic neoplasms). Premalignant biliary epithelium that can become cystadenocarcinomas

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21
Q

What investigative procedure should you avoid if you suspect a cystic neoplasm of the liver?

A

Aspiration or biopsy should be avoided as can cause peritoneal seeding

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22
Q

What are hyatid cysts?

A

A
Liver cysts formed by infection by the tapeworm Echinococcus granulosus.

Eggs are passed faeco-orally (dogs) and pass into the hepatic portal system where they form cysts

High prevalence in South America, North Africa, Central Asia

23
Q

How are hyatid cysts managed?

A

If asymptomatic can monitor
- Surgical cyst deroofing

  • Antiparasitics e.g albendazole, mebendazole and/or praziquantel

DO NOT ASPIRATE AS RUPTURE CAN CAUSE ANAPHYLAXIS

24
Q

What is the pathophysiology of a liver abscess?

A

Polymicrobial bacterial infection spreading from the biliary or gastrointestinal tract, either via contiguous spread or seeding from portal and hepatic veins

Common organsims: E. Coli, K. pneumoniae, and S. constellatus, Fungal in immunocompromised

Causes: cholecystitis, cholangitis, diverticulitis, appendicitis, or septicaemia

25
Q

What are the clinical features of a liver abscess?

A

Fever, rigors, abdominal pain

Bloating, nausea, anorexia, weight loss, fatigue and jaundice
On examination will have RUQ pain with hepatomegaly
If ruptures may have signs of sepsis

26
Q

How are liver abscesses managed?

A

DEPENDS ON SIZE

Fluid resuscitation
- Antibiotics

  • US/CT guided aspiration w or w/o catheter drainage
  • Cyst deroofing

Surgery if ruptures
TREAT ANY UNDERLYING CAUSE TOO

27
Q

What is an amoebic abscess?

A

Most common extra-intestinal manifestation of Entomoeba Histiolytica (from spread via portal system)

Spreads faeco-oral and once in colon invades mucosa to get to portal system. Common in developing world e.g South America, India

28
Q

What are the clinical features of an amoebic abscess?

A
  • Vague symptoms of abdominal pain, nausea, fever or rigors, weight loss, and bloating

May have prodrome of abdominal pain and diarrhoea
- History of recent travel (<6 months) to an endemic area

29
Q

What are some of the causes of HCC?

A
  • Viral hepatitis (most common)

Chronic alcoholism
Hereditary haemochromatosis
PBS
Aflatoxin (cereals and nuts)

30
Q

What are two risk assessment tools used once a diagnosis of HCC has been made?

A

Child-Pugh: calculates prognosis of patients with liver cirrhosis.

Looks at serum bilirubin, albumin, INR, degree of ascites, and evidence of encephalopathy

MELD: calculates same prognosis but better and also predicts likelihood of patient tolerating a liver transplant.

Looks at creatinine, bilirubin, INR, sodium, and the use of dialysis (at least twice per week)

31
Q

What malignancies metastasise to the liver and how do they present?

A

Bowel (via the portal circulation), breast, pancreas, stomach, and lung
Hepatomegaly and ascites
Jaundice and upper abdominal pain

32
Q

How can you tell the difference between acute and chronic pancreatitis?

A

Limited damage to the secretory function of the gland, with no gross structural damage developing.

Repeated acute can lead to chronic

33
Q

What is the pathophysiology of acute pancreatitis?

A

Premature and exaggerated activation of digestive enzymes
Pancreatic inflammatory response (Increasing vascular permeability and fluid shifts, third spacing)
Pancreatic enzymes in blood stream cause fat autodigestion leading to fat necrosis and hameorraghe into retroperitoneal space
Free fatty acids react with calcium to form chalky deposits and hypocalcaemia
End stage is complete necrosis of the pancreas

34
Q

Other than aucte pancreatitis, what may cause a raised serum amylase?

A

Bowel perforation
Ectopic pregnancy
DKA

35
Q

What are some of the risk tools used to assess the severity of pancreatitis?

A

PANCREAS
Pa02
age
neutrophils
calcium
renal function
enzymes
albumin
sugar

36
Q

What are some systemic complications of acute pancreatitis?

A

DIC
ARDS
Hypocalcaemia
Hyperglycaemia as Islets of Langerhan’s destroyed and insulin production halted

37
Q

What are some local complications of acute pancreatitis and how are they managed?

A

Pancreatic Necrosis

Suspect if patient has signs of persistent systemic inflammation for more than 7-10 days after onset
Necrosis prone to infection so suspect if patient deteriorates and raised inflammatory markers
Confirm by CT imaging then fine needle aspiration biopsy
Treat with pancreatic necrosectomy 3-5 weeks after onset so walled off necrosis
Pancreatic Pseudocyst

Collection of fluid containing pancreatic enzymes, necrotic material and blood. Lack epithelial lining but surrounded by vascular and fibrous that’s why psuedo
Often in lesser sac blocking gastro-epiploic foramen
Often found incidentally on image or mass effect e.g biliary or gastric outlet obstruction
Can haemorraghe, rupture or become infected
May resolve spontaneously but if still there after 6 weeks surgical debridement or endoscopic drainage

38
Q

How is chronic pancreatitis managed?

A
  • Treat reversible underlying cause e.g alcohol cessation or statins for hyperlipidaemia
  • Analgesics (neuropathic not opiates like acute)

Exocrine dysfunction give enzyme replacement (like Creon) and fat soluble vitamins
Endocrine dysfunction may need insulin regimes and annual check of HbA1c
- ERCP for diagnostic and stone removal/sphincterotomy

Endosonography-guided celiac plexus blockade or thoracoscopic splanchnicectomy for analgesia
- Steroids to reduce symptoms of autoimmune pancreas. High dose prednisolone then low dose maintenance

39
Q

What is the pathophysiology of pancreatic cancer?

A

90% are ductal carcinoma of the pancreas.
10% Exocrine (Pancreatic Cystic Carcinoma) or Endocrine (Derived from Islet Cells of Pancreas)
- Direct invasion of local structures typically involves the spleen, transverse colon, and adrenal glands.

  • Lymphatic metastasis typically involves regional lymph nodes, liver, lungs, and peritoneum and common at diagnosis
40
Q

What is the clinical presentation of pancreatic cancer?

A

Features depend on site of tumour, at tail insidious onset + not symptomatic until late

*- Obstructive Jaundice**
*- Abdo Pain** (Secondary to invasion of coeliac plexus)
*- Weight loss/**Cachetic
Acute Pancreatitis
Thrombophlebitis Migrans
Abdominal mass/enlarged gallbladder

41
Q

What investigations are done when we suspect pancreatic cancer?

A

Lab

  • FBC (anaemia and thrombocytopenia)
  • LFTs (raised bilirubin, ALP and gamma GT showing obstructive jaundice)
  • CA19-9 not to diagnose but to measure response

Imaging

Initial USS to look for bile duct dilatation or pancreatic mass
- CT to diagnose followed by chest-abdomen-pelvis CT scan or PET to stage

  • Endoscopic US for fine needle aspiration biopsy or ERCP for biopsy
42
Q

What is a Whipple’s procedure and what are some complications of this procedure?

A

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

All share blood supply of gastroduodenal artery

Tail of the pancreas and the hepatic duct are anastomosed to the jejunum to drain bile and stomach anastomosed too

Complications: pancreatic fistula, delayed gastric emptying, and pancreatic insufficiency

43
Q

Pancreatic cancer has a very poor prognosis as it is a highly metastatic cancer. What are the palliative care options with pancreatic cancer?

A

Percutaneous or ERCP Biliary stent: to relieve obstructive jaundice and pruitis

Palliative chemotherapy: gemcitabine based. used if good performance status

Enzyme replacements (inc Lipases e.g Creon): for exocrine insufficiency to stop malnourishment and steatorrhea

44
Q

What are some endocrine tumours of the pancreas?

A

Functional (symptoms due to secretion) or Non-functional (symptoms due to metastatic spread)

Gastrinoma (Zollinger-Ellison)
Insulinoma
Somatostatinoma
Glucagonoma
VIPoma

45
Q

What is multiple endocrine neoplasia 1 syndrome (MEN1)?

A

Hereditary condition associated with tumours of the endocrine. Used to be called Wermer syndrome

Hyperparathyroidism due to parathyroid tumours
Endocrine pancreatic tumours
Pituitary tumours

46
Q

How are endocrine tumours of the pancreas investigated and managed?

A

Ix:

Combination of CT, MRI and/or Endoscopic Ultrasound.
Intra-arterial calcium with digital subtraction angiography
Mx:

If small non-functioning just observed
If large functioning then primary tumour and metastases resected
Somatostatin analgoues can help control effects of hormone oversecretion

47
Q

What are some low risk and high risk pancreatic cysts?

A

In general mucinous cysts are high risk and serous cysts are low risk

48
Q

What are pancreatic pseudocysts?

A

Often following pancreatitis

The inflammatory reaction produces a necrotic space in the pancreas that fills with pancreatic fluid, however this lacks an epithelial lining

Often asymptomatic

49
Q

How are pancreatic cysts investigated and how do we stratify them as low risk/high risk?

A

Often picked up on imaging. If found do pancreatic protocol CT scan or magnetic resonance cholangiopancreatography to further assess.

May then do Endoscopic US scan with Fine Needle Aspiration (EUS-FNA) to further assess and work out low risk/high risk

50
Q

How are pancreatic cysts managed and what is the prognosis?

A

Low risk: left alone with surveillence every 5 years due to malignancy risk

High risk: resection is first line with follow up MRI every 2 years

If non-malignant excellent prognosis but if malignant 60% 5 year survivial

51
Q

How long after acute pancreatitis caused by gallstones should there be a cholecystectomy?

A

2 Weeks

52
Q

What can cause air in the billiary tree?

A

Post ERCP due to sphincterotomy
Following passage of gallstone
Scarring from acute pancreatitis

53
Q
A