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5th Year Revision > Surgery - HPB > Flashcards

Surgery - HPB Flashcards

1
Q

How are gallstones made, what are they made of, what is bile made of?

What are some risk factors for gallstones?

A
  • Bile = c_holesterol, phospholipids, bile pigments_
  • Bile is stored in the gallbladder then passes into duodenum
  • Gallstones form when bile is supersaturated
    • Cholesterol stones = purely cholesterol
    • Pigment stones = purely bile pigments
    • Mixed stones = cholesterol +bile pigments

Risk factors = Fat, Female, Fertile (pregnancy), Forty, Fhx

And Oral contraceptives, haemolytic anaemia, malabsorption (crohns)

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2
Q

What are the 2 presentations associated with gallstones?

A

Presentations are biliary colic or acute cholecystitis

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3
Q

How does biliary colic present?

A
  • When gallbladder neck is impacted by a gallstone
  • No inflammatory response but the contraction of the occluded gallbladder neck causes pain
  • Presentation
  • Dull sudden colicky pain in RUQ
    • can radiate to epigastrium and back
    • precipitated by eating fatty foods (fatty acids stimulate Cholecystokinin release which causes contraction of gallbladder)
  • nausea and vomiting
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4
Q

How does acute cholecystitis present?

A
  • constant pain in RUQ or epigastrium
  • signs of inflammation eg. fever, lethargy
  • tender in RUQ and +ve Murphys sign
    • Murphys sign = press RUQ and get pt to breathe in. +ve when there is a halt in inspiration due to pain (shows inflamed gallbladder)
  • guarding can indicate gallbladder perf
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5
Q

How would you investigate gallstones?

A
  • Routine bloods (crp is raised in cholecystitis)
  • Lfts (raised alp showing occlusion, but normal alt and bilirubin)
  • Amylase to rule out pancreatitis
  • Urinalysis and pregnancy test
  • 1st line = Trans abdo US
    • Presence of gallstones
    • Thick gallbladder wall = inflammation
    • Bile duct dilation = possible stone
  • If US inconclusive, do Magnetic Resonance Cholangiopancreatography (MRCP)
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6
Q

How would you manage gallstones?

A

Biliary Colic

  • Analgesia
  • Lifestyle = low fat diet, weight loss, exercise
  • Elective laparoscopic cholecystectomy within 6 weeks due to high risk of recurrence

Acute Cholecystitis

  • IV antibiotics (coamoxi + metronidazole)
  • Analgesia and antiemetics
  • Laparoscopic cholecystectomy within 1 week
    • If readmitted post chole with RUQ pain, do an US abdo or MRCP to rule out retained CBD stone
  • If not fit for surgery or unresponsive to antibiotics do a percutaneous cholecystostomy
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7
Q

What are some complications of gallstones?

A

Mirizzi syndrome

  • a stone in hartmanns pouch or in cystic duct can compress the adjacent common hepatic duct = obstructive jaundice even with no stone in common hepatic or cbd
  • Confirm with mrcp
  • Manage with lap chole

Gallbladder empyema

  • Gallbladder fills with pus
  • Similar to acute chole but more septic
  • Diagnose with US or CT and treat with lap chole

Chronic cholecystitis

  • Hx of recurrent or untreated cholecystitis resulting in persistent inflammation of gallbladder
  • Ongoing RUQ or epigastric pain + N/V
  • Diagnose with CT and manage with elective chole

Cholecystoduodenal fistula

  • Fistula between gallbladder wall and small bowel due to recurrent inflammation of gallbladder
  • Lets gallstones pass into small bowel and cause bowel obstruction eg. gallstone ileus (terminal ileum) or bouverets syndrome (prox duodenum)
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8
Q

What is acute cholangitis?

How does it happen?

A

Infection of biliary tract

  • Due to biliary outflow obstruction + biliary infection (bacterial colonisation due to fluid stasis)
    • In a pt without outflow obstruction, bacterial colonisation would probably not cause cholangitis. It is this combo that is pathological

Causes of obstruction = gallstones, ercp, cholangiocarcinoma, pancreatitis, PSC, etc

Causes of infection = EColi, Klebsiella, Enterococcus

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9
Q

How does acute cholangitis present?

A
  • Charcots Triad = RUQ pain, fever, jaundice
  • Reynolds Pentad = RUQ pain, fever, jaundice, hypotension, confusion
  • Pruritus due to bile accumulation
  • Pale stool and dark urine (obstructive jaundice)
  • Mhx of gallstones or recent ercp or prev cholangitis
  • Dhx of oral contraceptives and fibrates increase risk
  • Hx of Lipid rich diet could suggest gallstones
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10
Q

How would you investigate and manage acute cholangitis?

A

Investigations

  • Routine bloods
    • leucocytosis typically found
    • also raised alp and ggt
    • raised bilirubin
  • Blood cultures
  • US of biliary tract shows bile duct dilation (CBD dilation is >6mm) and any underlying cause like gallstones
  • ERCP is gold standard** as it is also therapeutic (most do **MRCP first)

Management

  • Sepsis 6 if necessary
  • Endoscopic biliary decompression to remove obstruction
    • 1st line = ERCP
      • Ercp complications = pancreatitis, bleeding, perf, repeated cholangitis
    • 2nd line = percutaneous transhepatic cholangiography
  • Long term = elective cholecystectomy if gallstones are the cause
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11
Q

What is a cholangiocarcinoma?

What are some risk factors?

A
  • Cancer of the biliary system
  • Most commonly at bifurcation of right and left hepatic ducts
  • 95% are adenocarcinomas, others are squamous cell etc
  • Risks = psc, uc, infection like hiv or hepatitis, toxins in rubber and aircrafts, congenital, alcohol, diabetes mellitus
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12
Q

How does a cholangiocarcinoma present?

A
  • Asymptomatic until late stage
  • Post hepatic jaundice, pruritus, pale stools, dark urine
  • Jaundice and cachexia o/e
  • Less commonly RUQ pain, early satiety, weight loss, malaise

Courvoisiers law = Jaundice + Enlarged Gallbladder is unlikely to be gallstones. so think malignancy of biliary tree or pancreas

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13
Q

How would you investigate and manage a cholangiocarcinoma?

A

Investigations

  • Routine bloods (obstructive jaundice = high bili, alp, ggt)
  • Tumour markers CEA and CA19-9 can be elevated
  • US to confirm obstruction
  • MRCP is gold standard for diagnosis
  • CT CAP for staging and mets

Management

  • Radiotherapy as neoadjunct or adjunct to surgery
    • Cure is complete surgical resection but majority are inoperable at presentation
    • Partial hepatectomy and reconstruction of biliary tree for intrahepatic or klatskin tumours
    • Pancreaticoduodenectomy for distal common duct tumours
  • Palliative for majority
    • Stenting via ERCP to relieve obstructive symptoms
    • Surgical bypass procedures if stenting doesn’t work
    • Palliative radiotherapy
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14
Q

What is a simple liver cyst?

A

Simple cysts = fluid filled epithelial lined sacs in the liver (commonly Right lobe)

  • Generally asymptomatic
  • Otherwise abdo pain, nausea, early satiety due to mass effect

Investigations =

  • raised ggt, raised cea and ca19-9
  • US is gold standard imaging

Management =

  • For cysts >4cm do follow up US at 3,6,12 months to check for growth.
  • For symptomatic cysts do US guided aspiration or laparoscopic deroofing.
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15
Q

What is polycystic liver disease?

A

Polycystic liver disease = >=20 cysts within liver parenchyma, each >= 1cm

  • Due to…
    • autosomal dominant polycystic kidney disease (PKD1 and PKD2 mutations)
    • Or autosomal dominant polycystic liver disease (PRKCSH and SEC63 mutations)
  • Asymptomatic otherwise abdo pain and cysts grow
  • Hepatomegaly
  • US shows multiple cysts
  • Asymptomatic = monitor and leave it
  • Symptomatic or query malignancy then do surgery
    • US guided aspiration
    • Laparoscopic deroofing of cysts
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16
Q

What is a hydatid cyst?

A

due to tapeworm infection

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17
Q

What is a liver abscess?

How would it present?

A
  • Due to polymicrobial bacterial infection typically spread from biliary or gi tract (eg cholecystitis, cholangitis, diverticulitis, appendicitis)
  • Commonly EColi, K pneumonia, S constellatus
  • Presentation
    • Fever, rigors, abdo pain
    • Bloating, nausea, anorexia, weight loss, fatigue, jaundice
    • O/E RUQ tenderness and hepatomegaly
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18
Q

How would you investigate and manage a liver abscess?

A

Investigations

  • Routine bloods (leucocytosis, raised alp, deranged alt and bili)
  • Peripheral blood and fluid cultures for microscopy
  • US = poorly defined lesions with hypo and hyperechoic areas
  • CT imaging with contrast can also be used

Management

  • A-e, fluid resus etc
  • Antibiotic therapy
  • Us or ct guided aspiration of abscess
  • Be aware of amoebic abscesses that spread to liver via portal system
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19
Q

What is liver cancer and what are some risk factors?

A
  • Hepatocellular carcinoma happens as a result of a chronic inflammatory process affecting the liver
  • Most commonly due to viral hepatitis
    • also due to chronic alcoholism, hereditary haemochromatosis, PBC etc
  • Risks
    • Hep b, hep c
    • High alcohol
    • Smoking
    • >70years old
    • Aflatoxin exposure
    • Fhx of liver disease
20
Q

How would liver cancer present?

A
  • Liver cirrhosis
  • RUQ dull ache
  • o/e irregular enlarged craggy and tender liver
21
Q

How would you investigate and manage liver cancer?

A

Investigations

  • Lfts usually deranged with low platelets or prolonged clotting
    • ast:alt ratio>2 likely alcoholic liver disease
    • ast:alt around 1 likely viral hepatitis
  • alpha fetoprotein usually raised (used to monitor response to treatment)
  • US
    • a mass >2cm + raised afp this is pretty diagnostic
  • Then do staging CT and CTCAP
  • MRI liver scan and contrast ct angio can also be done
    • demonstrates a mass with arterial hypervascularisation (characteristic of HCC)
  • Barcelona Clinic Liver Cancer staging system
  • Child Pugh and MELD score risk assessment tools
    • Child pugh to calculate prognosis of cirrhosis pateints
    • MELD to predict likelihood of pt tolerating liver transplant

Management

  • Mdt, oncologist, radiologist, hepatobiliary surgeons, etc
  • Surgical
    • Surgical resection
    • Transplantation if patients fulfil Milan criteria
  • Non surgical
    • Ultrasound guided ablation for early disease
    • Alcohol ablation for small inoperable cancers
    • Transarterial Chemoembolisation for BCLC stage B
22
Q

Bowel (portal circulation), breast, pancreas, stomach, lung commonly mets to liver.

How would you manage mets to the liver?

A

Investigations

  • Deranged lfts
  • US scan first line
  • CT staging
  • Biopsy not advised as can lead to seeding of tumour

Management is more complex as disease has already metastasised

  • Oncology and palliative services involved
  • Transarterial chemoembolization
  • Selective internal radiotherapy etc
23
Q

What are some causes of acute pancreatitis?

A

GET SMASHED

  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune (eg SLE)
  • Scorpion venom
  • Hypercalcaemia
  • Endoscopic Retrograde CholangioPancreatography
  • Drugs (azathioprine, nsaids, diuretics)
24
Q

What is the pathophysiology of acute pancreatitis?

A
  • All these causes cause an exaggerated activation of digestive enzymes in the pancreas
  • The resulting pancreatic inflammatory response causes increased vascular permeability and fluid shifts (third spacing)
  • Enzymes are released into systemic circulation causing autodigestion of fats (results in fat necrosis) and blood vessels (can result in haemorrhage in retroperitoneal space)
  • Fat necrosis can cause free fatty acids to be released and bind with serum calcium to make chalky deposits in fatty tissue = hypocalcaemia
  • Severe end stage pancreatitis = necrosis of pancreas
25
Q

How does acute pancreatitis present?

A
  • Severe sudden epigastric pain that radiates to back
  • Nausea and vomiting
  • O/E epigastric tenderness
  • Cullens sign (bruising around umbilicus)
  • Grey turners sign (bruising in flanks due to retroperitoneal haemorrhage)
  • Tetany due to hypocalcaemia
  • Underlying cause is Gallstones? Obstructive jaundice
26
Q

How would you investigate and manage acute pancreatitis?

A

Investigations

  • Routine bloods
  • Serum amylase (3x normal upper limit is diagnostic)
  • LFTS (alt >150u/l usually indicates gallstones is the cause)
  • Serum lipase remains elevated longer than amylase
  • Modified Glasgow Criteria
  • Abdo US to identify gallstones too
  • AXR shows sentinel loop sign (dilated prox bowel loop adjacent to pancreas due to localised inflammation)
  • CT imaging later on to confirm pancreatic necrosis if necessary
    • Definitive confirmation = fine needle aspiration of necrosis

Management

  • Treat underlying cause
  • IV fluids resus
  • Ng for vomiting
  • Catheterisation and fluid balance chart
  • Opioid analgesia
  • ITU or HDU admission
  • Broad spec antibiotics
  • If Gallstones is underlying cause = early laparoscopic cholecystectomy
  • If alcohol is underlying cause then refer to appropriate services
27
Q

What is chronic pancreatitis?

A
  • Causes progressive and irreversible damage to pancreatic parenchyma
  • Main cause is chronic alcohol abuse or idiopathic
    • Less common = hyperlipidaemia, hypercalcaemia, infection, hereditary like CF, autoimmune like SLE, anatomical like malignancy or strictures, congenital like pancreas divisum
28
Q

How would chronic pancreatitis present?

A
  • Chronic pain and recurring attacks of acute pancreatitis (acute on chronic pancreatitis)
    • Pain is epigastric and radiates to back
  • Nausea and vomiting
  • Damage to pancreatic parenchyma results in endocrine and exocrine insufficiency
    • Damage to islets of Langerhans = failure to produce insulin = impaired glucose regulation = eventual DM
    • Damage to acinar cells = failure to produce digestive enzymes = malabsorption = weight loss, cachexia, diarrhoea, steatorrhea
  • Pseudocysts can be present due to the recurrent acute pancreatitis attacks = mass effect symptoms of biliary obstruction or gastric outlet obstruction
29
Q

How would you investigate and manage chronic pancreatitis?

A

Investigations

  • Routine bloods
  • Urine dip
  • Amylase and Lipase would not usually be raised in chronic disease
  • Blood glucose
  • Faecal elastase level can be low if there is exocrine insufficiency
  • CT shows pancreatic atrophy/calcification and pseudocysts if there are
  • US or MRCP for anatomy of pancreas and biliary tree

Management

  • Treat any reversible underlying cause eg alcohol cessation
  • Analgesia
  • Exocrine dysfunction = enzyme replacements like Creon that can be taken with meals
    • Also give fat soluble vitamins ADEK
  • Pancreatogenic diabetes = insulin regimes and hba1c surveillance
  • ERCP sometimes indicated
  • Steroids (high dose prednisolone to control, then low dose to maintain) can be used for autoimmune cause
  • Those with chronic pancreatitis >20 years are at risk of pancreatic malignancy
30
Q

What is pancreatic cancer?

What are some risk factors?

A
  • Ductal carcinoma is most common, then exocrine and endocrine tumours
  • 60-70% are in the pancreatic head, then 20% in the body and tail and others only diffusely involve the pancreas
    • Head is prognostically better as they will present with obstructive symptoms more early on than body/tail

Risks = smoking, chronic pancreatitis, diet (high meat, low fruit and veg), fhx, late onset DM >50yo

31
Q

How would you investigate and manage pancreatic cancer?

A

Investigations

  • Routine bloods (lfts = raised bili, alp, ggt)
  • Ca19-9 to assess response to treatment
  • Abdo US shows pancreatic mass or dilated biliary tree
  • CT is gold standard for diagnosis as it also stages it
  • CTCAP for mets

Management

  • Surgery = radical resection
    • but <20% have a resectable tumour at diagnosis
    • SE = pancreatic fistula, delayed gastric emptying, pancreatic insufficiency
    • Adjuvant chemotherapy
  • Non surgical
    • Locally advanced disease = chemotherapy (gemcitabine)
    • Metastatic disease = palliative chemo (FOLFIRINOX or gemcitabine for those who cannot tolerate)
    • Symptomatic management
      • Biliary stent for obstructive jaundice and pruritus
      • Exocrine insufficiency = enzyme replacements like creon
32
Q

What are the endocrine tumours of the pancreas?

A
  • Usually associated with Multiple Endocrine Neoplasia 1 Syndrome
  • Tumours that arise from the endocrine cells
  • They are either functional (they secrete hormones) or non functional (present as just their mass effect or malignant spread)

Different tumours

  • G cells secrete gastrin (gastrinoma)
  • A cells secrete glucagon (glucagonoma)
  • B cells secrete insulin (insulinoma)
  • δ cells secrete somatostatin (somatostatinoma)
  • non islet cells secrete vasoactive intestinal peptide
33
Q

How would you investigate and manage endocrine tumours of the pancreas?

A
  • Blood tests to identify specific subtype
  • CT imaging, Endoscopic US, MRI
  • <1cm are observed otherwise larger need resection
  • Somatostatin analogues are used to control effects of hormonal hypersecretion
34
Q

What is a pancreatic cyst?

What are high and low risk?

A
  • Collections of fluid in the pancreas, typically incidentally identified on imaging

Examples of high risk cysts (malignant) = intraductal papillary mucinous neoplasm, mucinous cystic neoplasm, etc

Examples of low risk cysts = serous cystic adenoma, simple cyst, mucinous non neoplastic cyst

35
Q

How would pancreatic cysts present?

A
  • 70% are asymptomatic
  • Abdo pain or back pain (mass effect)
  • Post obstructive jaundice
  • Vomiting
  • Cysts that are infected have systemic features
  • Some become malignant and metastasise (weight loss, appetite loss, etc)
36
Q

How would you investigate and manage pancreatic cysts?

A

Investigations

  • Routine bloods
  • Ca19-9 to monitor progression
  • Pancreatic protocol CT scan or MRCP is required to fully assess pancreatic cysts = NICE guidelines
    • High risk = >3cm diameter, main pancreatic duct dilation >10mm, enhancing solid component, non enhancing mural nodule
  • If high risk, complete resection may be warranted or Endoscopic US scan with Fine Needle Aspiration (for a biopsy)

Management

  • Majority are benign so just need to be under surveillance every 5 years
  • High risk = resection 1st line
    • Then MRI follow up scan every 2 years
37
Q

What is a splenic infarct?

What are some causes?

A
  • Occurs due to occlusion of the splenic artery or one of its branches = tissue necrosis
  • Spleen is supplied by splenic artery and short gastric arteries so infarction is usually not complete (collateral circulation)

Causes

  • Haematological disorders eg. lymphoma, myelofibrosis, sickle cell, CML, Polycythaemia vera, hypercoagulable states
  • Embolic disorders eg. endocarditis, AF, infected aneurysm grafts
  • Rarely Vasculitis, trauma, collagen tissue disease, etc
38
Q

How would a splenic infarct present?

A
  • LUQ abdo pain which radiates to left shoulder
  • Fever, nausea, vomiting, pleuritic chest pain
39
Q

How would you investigate and manage a splenic infarct?

A

Investigations

  • CT abdo with IV contrast = gold standard
  • Routine bloods (fbc, u&es, lfts, coagulation)

Management

  • Analgesia, iv hydration
  • Identify the cause of the infarction = haematologist, ECHO scan, long term anticoagulation
  • Long term management
    • Avoid splenectomy due to risk of overwhelming post splenectomy infection syndrome (OPSI)
    • Vaccine against S pneumonia, N meningitidis, H influenza
    • Low dose antibiotics (Pen V) to clear encapsulated bacteria
40
Q

What are some complications of a splenic infarct?

A
  • Splenic abscess if cause was eg. non-sterile embolus (eg. infective endocarditis)
  • Auto-splenectomy due to repeated splenic infarction and progressive fibrosis and atrophy
    • Common cause of auto-splenectomy is sickle cell anaemia
41
Q

When would splenic rupture happen?

A
  • The spleen is incredibly vascular so rupture can lead to large intraperitoneal haemorrhage and haemorrhagic shock
  • Usually due to blunt abdo trauma eg. seat belt injuries
    • Rarely iatrogenic or secondary to underlying splenomegaly in things like infections (like EBV) or haematological malignancies
42
Q

How would splenic rupture present?

A
  • Abdo pain following blunt trauma
  • Hypovolaemia shock
  • O/E LUQ tenderness and peritonism as blood loss increases
    • Left shoulder pain (Kehr’s sign) as blood irritates diaphragm
43
Q

How would you investigate and manage splenic rupture?

A

Investigations

  • Anyone haemodynamically unstable + peritonism following trauma is Abdo bleeding until proven otherwise
    • Do a laparotomy immediately
  • Haemodynamically stable with suspected abdo injury
    • Urgent CT CAP with iv contrast
    • FAST scans are useful but should not delay CT or laparotomy
  • Organ injury scale = American Association for the Surgery of Trauma (AAST) Splenic Injury Scale to grade splenic trauma

Management

  • A-e resus
  • Haemodynamically unstable or Grade 5 injury = Urgent Laparotomy
    • Often With splenectomy
    • Some patients may benefit from embolization of splenic vessels if they have vascular abnormalities or higher grade splenic injuries
      • This is to reduce the rate of those that need a splenectomy
  • Haemodynamically stable (Grade 1-3) = Conservative
    • Serial abdo examinations
    • Resus
    • Strict bed rest
    • Repeat ct scan 1 week later
    • Prophylactic vaccinations (strep pneumonia, h influenzae B, meningococcus) after discharge
44
Q

What is overwhelming post splenectomy infection?

A
  • Spleen plays a role in destroying encapsulated organisms like pneumococcus, meningococcus, h influenzae
  • Therefore patients need vaccinations against these organisms and prophylactic Penicillin V
45
Q
A

5th Year Revision (14 decks)

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