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General Surgery > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

Hepatic causes of increased conjugated bilirubin

A

Decreased secretion from liver from:
1. Drug interactions
2. Cirrhosis
3. Hepatitis
4. Cholestasis
5. Dubin Johnson syndrome

Biliary obstruction (more common)
Excess conjugated in the urine resulting from extra or intrahepatic biliary obstruction produces dark urine and absence of conjugated in the gut produces white stools (typical of conjugated obstructive jaundice)

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2
Q

Which LFTs will be elevated in biliary obstruction

A

ALP
GGT

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3
Q

What can cause raised ALP in LFTs

A

Biliary obstruction
Space occupying lesions of liver

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4
Q

Venous return directions

  1. Away from umbilicus
  2. Towards umbilicus (in all directions)
  3. Upwards towards IVC
A
  1. Portal hypertension
  2. Portal vein thrombosis
  3. IVC obstruction
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5
Q

LFTs elevated in hepatic injury

A

GGT
ALT
AST

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6
Q

Tumour markers in the liver

A

AFP
CEA (carcinoembryonic antigen)
CA 19-9 (carbohydrate antigen)
CGA (chromogranin level)

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7
Q

Tumour markers in the liver

A

AFP
CEA (carcinoembryonic antigen)
CA 19-9 (carbohydrate antigen)
CGA (chromogranin level)

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8
Q

Diff between hepatocellular cancer and cirrhotic liver

A

Hepatocellular is enlarged, hard and nodular
Cirrhotic can be enlarged, normal or small, with blunt, libulated and firm edges

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9
Q

Side effects of Albendazole or Mebendaole

A

Bone marrow suppression
Liver toxicity
Renal toxicity

Do FBC and LFT every two weeks

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10
Q

Symptoms of portal hypertension

A

Haematemesis
Blood in stool or melena
Peripheral oedema
Ascites
Mental confusion or disorientation (Encephalopathy?)
Caput Medusa

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11
Q

What are causes of portal hypertension

A

Pre-hepatic:
1. PVT
2. SVT
3. Congenital atresia and stenosis

Hepatic
1. Cirrhosis (Hep B&C, Alcohol, MAFLD)
2. Acute alcohol liver disease
3. Schistosomiasis
4. Idiopathic

Posthepatic
1. Budd Chiari
2. Veno occlusive disease
3. Constructive pericarditis

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12
Q

Management of oesophageal varices

A

Most preferred: band ligation

Pharmacotherapy
Octereotide
Terlipressin

Endoscopic therapy
Band ligation
Injection sclerotherapy: scleroscent

Tamponade
Balloon temponade
Stent temponade

Endovascular
TIPS
Trans venous obliteration of varices

Surgical therapy
Shunt procedures
Gastric devascularisation

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13
Q

Management of gastric varices

A

Endoscopic control with cyanoacrylate (sclerotherapy)

Bleeding from portal hypertensive gastropathy (PHG) tx: b blockers or TIPS

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14
Q

Complications of Portal hypertension

A

Gastric Varices
Portal hypertensive gastropathy (diffuse, precludes endoscopy)
Hepatic encephalopathy
Hepatorenal syndrome
Ascites
Spontaneous bacterial Peritonitis

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15
Q

Symptoms of encephalopathy

A

Monotonous speech
Flat affect
Metabolic tremor
Muscular uncoordination
Impaired handwriting
Asterixis
Coma
Upgoing plantar responses
Hypo/hyperactive reflexes
Decerebrate posture
Retort hepaticus

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16
Q

Events that precipitated hepatic encephalopathy in cirrhotic patients

A

Electrolyte disturbance: hypokalemia
Gastrointestinal bleeding: oesophageal and gastric varices, duodenal erosions
Drugs: alcohol withdrawal, benzos
Infection: SBP, UTI, pneumonia
Colonic content: dietary protein overload, constipation

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17
Q

Differentials for hepatic encephalopathy

A

Intracranial Space occupying and vascular lesions
Trauma
Infection
Metabolic
Endocrine
Drug induced
Post epileptic coma

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18
Q

Hormones produced by pancrease

A

Pancreatic juice

Insulin
Glucagon
Somatostatin (regulated islet cell secretion)
Pancreatic polypeptide (regulated GI function)

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19
Q

Pathogenesis of Acute Pancreatitis

A

Inappropriate active of trypsinogen to trypsin in the pancreatic cells (normally happens in duodenum).
Once activated these enzymes are responsible for auto digestion of pancreatic tissues resulting in
1. necrosis
2. SIRS in severe case

SIRS occurs when these enzymes stimulate production of inflammatory cytokines which triggers an inflammatory cascade. It may develop into ARDS (acute Resp distress syndrome), multi organ dysfunction syndrome or organ failure.

Mechanism in which trypsin is activated is unclear
Gallstone pancreatitis the trigger results from gallstone passing into bile duct causing temporary obstruction in sphincter of oddi. Pancreatitis enzymes are maybe caused by increased pancreatic duct pressure or due to bile reflux into pancreatic duct

2 pathological entities
Acute intestinal adematous pancreatitis (IOP)
Acute Necrotising pancreatitis

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20
Q

Manifestations of SIRS

A

ARDS
Multi organ dysfunction syndrome
Organ failure

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21
Q

How to diagnose pancreatitis

A

2 of the following

  1. Abdo pain: Epigastric pain, radiates to the back, acute onset, severe
    2.Serum Lipase or amylase >3* normal
    Characteristic fin
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22
Q

Differentials for acute pancreatitis

A

Alcohol induced pancreatitis
Gall stones
Pancreatitis carcinoma

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23
Q

Criteria for SIRS or how is it diagnosed

A

2 of following
HR >90
Temp >38 or <36
WCC >12000or <4000
Resp >20breaths or PCO2 <32mmHg

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24
Q

Criteria for organ failure

A

2 or more for one of the organ systems

Resp
Renal
CVS

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25
Q

Classification of Acute Pancreatitis

A

Mild Acute Pancreatitis (MAP)
-no organ failure
-no systemic sx

Moderately severe Acute Pancreatitis (MSAP)
-transient organ failure resolves wishing 48h
-local/systemic sx w/o multiple organ failure

Severe Acute Pancreatitis (SAP)
-persistent single or multiple organ failure lasting >48h

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26
Q

What other conditions cause elevated serum lipase or amylase

A

Perforated peptic ulcer
Small bowel infarction

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27
Q

Investigations for pancreatitis

A

Serum amylase and lipase: >3*normal
Bloods: Calcium and Lipid profile. Blood gas and full biochemistry.
CXR and AXR: pleural effusion on L side,ileus with sentinel loop and colon cutoff sign, pancreatic calcifications
U/S: gall stones
ERCP: contraindicated in acute settings unless as a therapeutic procedure in pt with gallstone pancreatitis associated with/w jaundice and cholangitis

28
Q

Aetiology of pancreatitis

A

Alcohol
Gallstones
Idiopathic

Miscellaneous
Obstructive: postERCP, pancreatic carcinoma, congenital Choledochal cysts and pancreas division
Metabolic: hyperlipidemia, hyperparathyroidism, aminoaciduria, porphyria
Drugs: Anti-TB, Anti-biotics, Anti-retrovirals, thiazide diuretics
Trauma : blunt or postoperative

Viral infections
Pregnancy (ass/w gall stones)
Collagen disease

29
Q

Treatment of pancreatitis

A

General treatment
Mild pancreatitis
Supportive: hospitalisation with supportive measures such as bedrest, nil per mouth, IV fluids and analgesia
Counselling on alcohol if it’s the main cause
Nasogastric suction if there is an ileus or severe pain
US for gallstones. Hypertriglycerides and rarely hypercalcemia need to be excluded

Gallstones Pancreatitis on US: Initial conservative, then elective cholecystectomy 1-4 weeks after the acute attack. Early intervention in progressive jaundice w/ or w/o chalangitis, Do ERCP or Papillectomy (prevents recurrence of pancreatitis)

Management of Severe Acute Pancreatitis
ICU management
Volume replacement for hypovolemic shock
Respiratory failure management with ventilation
Metabolic: hyperglycaemia, Hypocalcemia, renal failure
Ensure patient nutrition via NGT
No surgery in early phases of severe pancreatitis unless bowel is ischemic or if there’s abdo compartment syndrome

Poor prognosis in : obese, age >60, multiple organ failure

Local complications
Acute peipancreatic fluid collections and necrosis on US, endoscopic US, CT and MRI
Drainage indicated in symptomatic collections or infected necrosis after 2weeks of onset of severe pancreatitis
1. Percutaneously under US or CT
2. Endoscopic using endoscopic US, stents are placed between stomach/duodenum to allow drainage
3. Surgery, at laparotomy a communication is placed between cyst and enteral lumen

Bleeding from false aneurysm: selective angiographic embolisation

30
Q

Parameters for severe pancreatitis

A

Haemodynamic instability
Hypoxic confusion
Pleural effusion and pulmonary infiltrates on CXR
SIRS response (2or more criteria)

31
Q

Fictions of the liver

A

Synthesis
-clotting factors synthesis
-Lipoprotein -Cholesterol transport
-Globulin - immune function
-Albumin -oncotic pressure
-Ceruloplasmin -Copper bioavailability

Storage
Micronutients
-Minerals (copper, zinc, magnesium, Iron)
-Vitamins (A,D,E,K,B12)
Glycogen for Blood sugar balance

Secretion
Bile needed for digestion and GI anti-microbial
Cholesterol- precursor of sex hormones , vit D

Detoxification
Drugs/alcohol
Fatty acids
Steroid hormones
Ammonia-urea
Environmental toxins or allergens

Metabolism
Detoxification of fat
T4-T3

Immune system
Contains viruses adn pathogens
Maintain hepatic and portal being immune system

32
Q

Functions of LFTs or liver enzymes

A

ALP is an enzyme associated with/w cholestasis
Bilirubin measure of bile conjugation and excretion
yGGT is a measure of enzyme induction
ALT and AST are increased in hepatocyte injury
Albumin measure synthetic capability of liver and is a product of hepatocellular protein synthesis

33
Q

Pathophysiology of chronic pancreatitis

A

Alcohol is the most common cause
During acute exacerbation there is increased interstitial oedema, necrosis, and inflammatory infiltration. Introductal calcification seen in alcohol induced, tropical pancreatitis and is commonly seen in advanced disease.

Alcohol induced pancreatitis hypothesis: Necrosis-Inflammation-Fibrosis sequence.
This sequence once established may be self perpetuating.
Smoking is an important co-factor in pathological processes precipitated by alcohol.
Formation of calcified stones: As a result of bicarbonate and water secretion on one hand and protein and calcium on the other.

Pain, what causes it:
1. Inflammatory process and calcified ductal protein plugs leading to parenchyma fibrosis and ductal epithelium damage, ductal changes lead to strictures and obstruction with tissue and ductal hypertension. Ductal dilatation often occurs.
2. Interaction between products of inflammation and damaged neural structures
3. Toxin metabolism and the generation of excessive oxygen derived free radicals which exceed normal protective mechanisms
4. Parenchyma fibrosis leads to a form of compartment syndrome with micro vascular eschemia and pain

34
Q

Symptoms of chronic pancreatitis

A

Pain
Nausea and vomiting
Palpable cyst mass
Ascites
obstructive jaundice
GI bleeding from false aneurysm
DM requiring insilun
Hypoglycaemia during to lack of control by glucagon to insulin
Steatorrhea from fat malabsorption

Pain is the predominant symptom.
Pain in the epigastrium and radiates to the back, worse after meals and May be relieved by sitting upright or leaning forward. May be relieved by hot water bottles also.

First attack of alcohol is usually preceded by long period (+- 10yrs) of excessive alcohol intake. Attack usually induced by binge drinking and present on on the afternoon on the night before

Pain may be persist despite pt being abstinent

35
Q

Complications of chronic pancreatitis

A

Pancreatic destruction with endocrine and/or exocrine insufficiency with development of DM and fat malabsorption.
Psedocysts and Ascites (from inflammation, necrosis and ductal hypertension )
False aneurysms, with subsequent haemorrhage in relation to a pseudocys
SVT (leading to Portal hypertension)
Portal hypertension
Biliary stenosis
Duodenal stenosis
Mortality

36
Q

Investigations for pancreatitis

A

Bloods:
1. Serum amylase/lipase
2. Random/Fasting glucose or HBA1C
3. Albumin (L)
4. LFTs (bili, ALP, GGT)

Pancreatic Function Tests
Faecal Acid steatocrit and Elastase

Imaging
Endoscopic US
CT Scan
MRI/MRCP
ERCP has limited diagnostic but offers therapeutic benefits

37
Q

Management of chronic pancreatitis

A

Abstinence from alcohol
Low fat diet
Non narcotic analgesics Paracetamolor NSAID
Trial of high dose pancreatic enzymes together with acid suppression
Narcotic analgesia, progressing in potency as necessary
Antidepressants

38
Q

What are gall stones Meade up of

A

Cholesterol
Bilirubin
Calcium salts

39
Q

What are gall stones Meade up of

A

Cholesterol
Bilirubin
Calcium salts

40
Q

Risk factors for gallstones

A

Age
BMI/obese
Child bearing or pregnancy
Drugs (oestrogen, somatostatin analogue)
Ethnicity
Family hx
Gender (female
Hypercholestrolemia

41
Q

What is bile made up of

A

Cholesterol
Water
Bile salts
Phospholipid

42
Q

Differences between black and brown stones

A

Black stones= bilirubin and large amounts of mucin glycoproteins. Common in chronic haemolytic disorders and cirrhosis. Form in gallbladder.
Brown stones = calcium bilirubinate stones occur in presence of infected bile and may be related to worm manifestations. Ass/w stasis and anaerobic infections. Form in bile ducts, within biliary tree.

43
Q

Risk factors for pancreatic cancer

A
  1. Family history
  2. Smoking
    3.Cancer predisposing syndromes: hereditary nonpolyposis colon cancer, familial denomatous polyposis (FAP), familial breast cancer BRCA2, Peutz-Jehers syndrome.
    4.Chronic Pancreatitis
    5.DM
  3. Obesity
44
Q

Clinical presentation of pancreatic cancer

A

Painless obstructive jaundice
Upper abdo pain radiating to the back
Abdominal mass
Weight loss
Late onset DM
Gastric outlet obstruction
Dyspepsia
Ascites
Thrombophlebitis migrants

45
Q

Significance of Lewis blood group antigen in pancreatic cancer

A

C A- 19-9 (tumour markers for pancreatic cancer) expression requires presence of Lewis blood group antigen

46
Q

How is diagnosis of gastrinomas made

A

Clues:
Peptic ulcer refractory to medical therapy
Peptic ulcers at unusual sites
Absence of risk factors to peptic ulcers
Secretory diarrhea that resolves on NGT or PPIs

Confirmatory
Gastric acid hypersecretion
Hypergastrinaemia (fasting level high)
Pt should have stopped PPIs a week prior to testing

47
Q

What is the gastronomy triangle

A

Edges
The cystic duct
Boarders of 2nd and 3rd part of duodenum
Junction of the neck and body of pancreas

Triangle where most gsstrinomas are found

48
Q

What is the gastronomy triangle

A

Edges
The cystic duct
Boarders of 2nd and 3rd part of duodenum
Junction of the neck and body of pancreas

Triangle where most gsstrinomas are found

49
Q

Management of gastronomas

A

If not localised, Longitudinal Duodenotomy.
Small well encapsulated pancreas tumour= enuclation
Large poorly encapsulated: distal pancreatectomy

50
Q

Clinical Features of glucagonoma syndrome

A

Cachexia
Malnutrition
Protein depletion
Vesicopustular rash on groins (necrotic migratory erythema)
Glucose intolerance
DVTs

51
Q

Features of VIPoma

A

Watery diarrhea
Hypokalemia
Hypochlorhydia/ achlorhydia

(Tumours often in body or tail than head

52
Q

Functions of the spleen

A

Haematological
1. Removal of aged and deformed RBC from circulation by phagocytosis
2. Removal of platelets and leukocytes from circulation if abnormal or coated with antibodies
3. Extramedullary haematopoiesis in certain pathologies eg myeloproliferative conditions
4. Platelet reservoir

Immunological
1. Removal of bacteria from circulation (after phagocytosis antigens are presented to lymphocytes leading to specific and amplified immune response
2. Opsonin production
3. Antibody production
4. Lymphocyte proliferation

53
Q

Indications for splenectomy

A

Trauma/disease involving spleen or it’s blood supply
Splenic cysts
Splenic abscesses
Splenic artery aneurysms
Benign or malignant tumours related to spleen
Staging of non-Hodgkin
Left sided Portal HPT
Haematological conditions which are potentially curable or ameliorated by splenectomy
e.g Haemolytic anaemia (haemolysis)
Symptomatic anaemia requiring persistent transfusion
Symptoms of splenomegaly
Hypersplenism and symptomatic cholelithiasis
Myeloproliferative disorders
As part of another surgical condition ed distal pancreatectomy
Purpura
Hereditary: Hereditary spherocytosis, hereditary elliptocytosis, Thalassaemia major.

54
Q

Splenic disorders

A

Benign and Tumours (benign&Malignant)

Benign
1. Splenic cysts:
-Congenital: have an epithelial lining, can be simple cysts, dermoid or epidermoid cysts
-Hydatid from echinococcus granulosis, can enlarge and rupture or 2nd infection
-pseudocysts have no epithelial lining form after resolution of haematoma
2. Splenic abscess from haematogenous seeding, penetrating trauma or extension from adjacent structure, ID drug use, immune compromised.
3. Splenic artery aneurysm seen in older people with atherosclerosis, young female as congenital, complication of pancreatitis or pancreatic pseudocyst

Tumours
Benign: Haemangiomas and Lymphangiomas

Malignant
1. Nonhodgkins
2. Nonlymphoid malignancies eg angiosarcoma, plasmacytoma
3. Metastatic

55
Q

Causes of splenic artery aneurysms

A

Atherosclerosis in older people
Congenital lesions in young females
Acute or chronic pancreatitis of pancreatic pseudo aneurysm

56
Q

Complications of splenic tumours

A

Rupture
Hypersplenism

57
Q

Secondary causes of hypersplenism

A

Inflammatory/Infective: RA, SLE, Sarcoidosis
Malaria, TB, Syphilis
Portal HPT
Chronic haemolytic anaemias: spherocytosis, thalassaemia
Malignancy: lymphoma, leukaemia, mets carcinoma, myeloproliferative
Storage diseases: gauchers, amyloidosis

58
Q

Secondary causes of hypersplenism

A

Inflammatory/Infective: RA, SLE, Sarcoidosis
Malaria, TB, Syphilis
Portal HPT
Chronic haemolytic anaemias: spherocytosis, thalassaemia
Malignancy: lymphoma, leukaemia, mets carcinoma, myeloproliferative
Storage diseases: gauchers, amyloidosis

59
Q

Post op complications of splenectomy

A

Early
Haemorrhage
Gastric perforation
Injury to tail of pancrease
Subphrenic abscess
Atelectasis on lower L lung
PVT

Late
Thrombotic events (from rise in platelet)
Overwhelming post splenectomy infection (OPSI)

60
Q

Which organisms are risky for post-splenectomy patients

A

Streptococcus pneumonia
Haemophilus influenza
Nisseria meningitidis

Vaccinate them atleast 14days post op or before d/c in emergency splenectomy
Vaccinated against in 5years

61
Q

Preventative strategies to decrease incidence of OPSI

A
  1. Patient education: aware of increased risk of infection, should present as soon as possible in acute febrile illness.
  2. Immunisation every 5years (Strep pneumonia, haemophilus influenza, NisseriaMeningitidis)
  3. Antibiotic prophylaxis
62
Q

Preventative strategies to decrease incidence of OPSI

A
  1. Patient education: aware of increased risk of infection, should present as soon as possible in acute febrile illness.
  2. Immunisation every 5years (Strep pneumonia, haemophilus influenza, NisseriaMeningitidis)
  3. Antibiotic prophylaxis
63
Q

Tumoursin the liver

A

Benign
-Haematoma
-Hepatic Adenoma
-FNH

Malignant
-HCC
-Cholangiocarcinoma
Colorectal
Neuroendocrine

64
Q

How do pyogenic abscesses get in the liver? (5)

A

Biliary
Via Portal vein
Haematogenous via hepatic artery
Direct from adjacent organ
Trauma

65
Q

Treatment of amoebic abscess

A

Metronidazole

Operate if risk of rupture

66
Q

Surgical indications in adenomas

A

Men
Bleeding
Risk of malignant transformation (screenshot )

General Surgery (6 decks)

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