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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which LFTs will be elevated in biliary obstruction

A

ALP
GGT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can cause raised ALP in LFTs

A

Biliary obstruction
Space occupying lesions of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

LFTs elevated in hepatic injury

A

GGT
ALT
AST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tumour markers in the liver

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tumour markers in the liver

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Side effects of Albendazole or Mebendaole

A

Bone marrow suppression
Liver toxicity
Renal toxicity

Do FBC and LFT every two weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Symptoms of portal hypertension

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of gastric varices

A

Endoscopic control with cyanoacrylate (sclerotherapy)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of Portal hypertension

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Differentials for hepatic encephalopathy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hormones produced by pancrease

A

Pancreatic juice

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Manifestations of SIRS

A

ARDS
Multi organ dysfunction syndrome
Organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Differentials for acute pancreatitis

A

Alcohol induced pancreatitis
Gall stones
Pancreatitis carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Criteria for organ failure

A

2 or more for one of the organ systems

Resp
Renal
CVS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Classification of Acute Pancreatitis
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
26
What other conditions cause elevated serum lipase or amylase
Perforated peptic ulcer Small bowel infarction
27
Investigations for pancreatitis
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
Aetiology of pancreatitis
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
Treatment of pancreatitis
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
Parameters for severe pancreatitis
Haemodynamic instability Hypoxic confusion Pleural effusion and pulmonary infiltrates on CXR SIRS response (2or more criteria)
31
Fictions of the liver
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
Functions of LFTs or liver enzymes
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
Pathophysiology of chronic pancreatitis
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
Symptoms of chronic pancreatitis
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
Complications of chronic pancreatitis
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
Investigations for pancreatitis
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
Management of chronic pancreatitis
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
What are gall stones Meade up of
Cholesterol Bilirubin Calcium salts
39
What are gall stones Meade up of
Cholesterol Bilirubin Calcium salts
40
Risk factors for gallstones
Age BMI/obese Child bearing or pregnancy Drugs (oestrogen, somatostatin analogue) Ethnicity Family hx Gender (female Hypercholestrolemia
41
What is bile made up of
Cholesterol Water Bile salts Phospholipid
42
Differences between black and brown stones
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
Risk factors for pancreatic cancer
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 6. Obesity
44
Clinical presentation of pancreatic cancer
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
Significance of Lewis blood group antigen in pancreatic cancer
C A- 19-9 (tumour markers for pancreatic cancer) expression requires presence of Lewis blood group antigen
46
How is diagnosis of gastrinomas made
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
What is the gastronomy triangle
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
What is the gastronomy triangle
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
Management of gastronomas
If not localised, Longitudinal Duodenotomy. Small well encapsulated pancreas tumour= enuclation Large poorly encapsulated: distal pancreatectomy
50
Clinical Features of glucagonoma syndrome
Cachexia Malnutrition Protein depletion Vesicopustular rash on groins (necrotic migratory erythema) Glucose intolerance DVTs
51
Features of VIPoma
Watery diarrhea Hypokalemia Hypochlorhydia/ achlorhydia (Tumours often in body or tail than head
52
Functions of the spleen
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
Indications for splenectomy
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
Splenic disorders
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
Causes of splenic artery aneurysms
Atherosclerosis in older people Congenital lesions in young females Acute or chronic pancreatitis of pancreatic pseudo aneurysm
56
Complications of splenic tumours
Rupture Hypersplenism
57
Secondary causes of hypersplenism
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
Secondary causes of hypersplenism
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
Post op complications of splenectomy
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
Which organisms are risky for post-splenectomy patients
Streptococcus pneumonia Haemophilus influenza Nisseria meningitidis Vaccinate them atleast 14days post op or before d/c in emergency splenectomy Vaccinated against in 5years
61
Preventative strategies to decrease incidence of OPSI
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
Preventative strategies to decrease incidence of OPSI
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
Tumoursin the liver
Benign -Haematoma -Hepatic Adenoma -FNH Malignant -HCC -Cholangiocarcinoma Colorectal Neuroendocrine
64
How do pyogenic abscesses get in the liver? (5)
Biliary Via Portal vein Haematogenous via hepatic artery Direct from adjacent organ Trauma
65
Treatment of amoebic abscess
Metronidazole Operate if risk of rupture
66
Surgical indications in adenomas
Men Bleeding Risk of malignant transformation (screenshot )