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Liver & Idiot friends Flashcards

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1
Q

What are examples of pancreatic exocrine secretions?

A

Acinar cells release:

Amylase,
Lipase,
colipase,
phospholipase

proteases (trypsinogen, chymotrypsinogen)

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2
Q

What are examples of pancreatic endocrine secretions? What cells are responsible?

A

Endocrine component is in the form of the pancreatic islets of Langerhans

Alpha cell - glucagon

Beta cell - insulin

D cell - somatostatin

PP cells - pancreatic polypeptide

Enterochrommaffin cells - serotonin

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3
Q

What are causes of acute pancreatitis?

A

IGETSMASHED

Idiopathic
Gallstones (60%)
Ethanol (30%)
Trauma
Steroids
Mumps
Autoimmune
Scorpion Venom
Hyperlipidaemia
ERCP
Drugs (azathioprine, furosemide,corticosteroids)
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4
Q

How would acute pancreatitis present?

A

differential for anyone with upper abdo pain

gradual or sudden severe epigastric or central abdo pain that radiates to the back
- sitting forward may relieve

Anorexia, nausea and vomiting
Tachycardia
Fever
Jaundice
Dehydration
Hypotension
Abdominal guarding and tenderness

Cullen’s sign - periumbilical ecchymosis

Grey Turner’s sign - Left flank bruising

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5
Q

How would you investigate acute pancreatitis?

A

serum lipase/amylase - 3 times the upper limit of the normal

aspartate aminotransferase/alanine aminotransferase - 3x upper limit of normal

FBC - leucocytosis

CRP

haematocrit - indicator of severity

ABG

Abdo plain film

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6
Q

What can be used to assess severity of acute pancreatitis?

A

APACHE II (acute physiology and chronic health evaluation)

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7
Q

How would you manage acute pancreatitis?

A 
Iv fluids
Morhpine/fentanyl
nutritional support
supplementary oxygen
ondansetron
calcium gluconate
magnesium sulfate
insulin

with gall stones - cholecystectomy
ERCP

alcohol induced - counselling + alcohol withdrawal prophylaxis

infected pancreatic necrosis - IV abx (imipenem), catheter drainage, necrosectomy

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8
Q

What is a major concern for a patient with acute pancreatitis? What criteria would you look out for?

A

Systemic Inflammatory response syndrome (sepsis syndrome)

tachycardia > 90 bpm
tachypnoea > 20bpm
pyrexia >38 degrees
high white cell count

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9
Q

What are the causes of chronic pancreatitis?

A

long-term alcohol excess

chronic kidney disease

defects in trypsinogen gene

cystic fibrosis

autoimmune pancreatitis

trauma

recurrent acute pancreatitis

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10
Q

How does chronic pancreatitis present?

A

epigastric pain that bores through to the back (relieved by sitting forward)

exarcebated by alcohol

N&V

exocrine dysfunction - malabsorption, weight loss, diarrhoea, steatorrhoea, protein deficiency

endocrine dyfunction - diabetes

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11
Q

How would you investigate chronic pancreatitis?

A

blood glucose - glucose intolerance/diabetes

CT scan - pancreatic calcifications

Abdo USS -

Abdo Xray

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12
Q

how would you manage chronic pancreatitis?

A

analgesia

pancreatin + omeprazole

enteral feeding

octreotide

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13
Q

What are the functions of the liver?

A

Glucose and fat metabolism

Detox and excretion : bilirubin, ammonia, drugs/hormones/pollutants

Protein synthesis : albumin, clotting factors

Defence against infection : reticulo-endothelial system

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14
Q

What is ALT an indicator of?

A

found in high concentration within hepatocytes - useful marker of hepatocellular injury

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15
Q

What is ALP an indicator of?

A

concentrated in the liver, bile duct and bone tissues

often raised in liver due to increased synthesis in response to cholestasis

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16
Q

What could cause an isolated rise in ALP?

A

bony metastases/primary bone tumours
vit d deficiency

recent bone fractures

renal osteodystrophy

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17
Q

When would you review GGT? What is it an indicator of?

A

When ALP raised = review GGT

raised GGT = biliary epithelial damage and bile flow obstruction, also raised in response to alcohol and drugs such a phenytoin

raised GGT + ALP = highly suggestive of cholestasis

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18
Q

What is indicative of, if patient if jaundiced but ALT and ALP levels are normal?

A

isolated rise in bilirubin suggestive of pre-hepatic cause of jaundice

gilberts syndrome
hemolysis

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19
Q

If patient is jaundiced, but normal urine and normal stools? What does this mean?

A

Pre-hepatic cause

as unconjugated bilirubin is water-soluble and wont affect urine or stools

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20
Q

If patient is jaundiced, but dark urine and normal stools ? What does this mean?

A

hepatic cause

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21
Q

If patient has dark urine and pale stools? What does this mean?

A

post-hepatic (obstructive)

bile and pancreatic lipases can’t reach fat = steatorrhoea

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22
Q

What are some causes of decreased albumin?

A

liver disease e.g. cirrhosis

Inflammation triggering an acute phase response = reduced albumin production

Protein-losing enteropathies or nephrotic syndrome

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23
Q

What does the ALT/AST ratio show?

A

ALT>AST seen in chronic liver disease

AST>ALT seen in cirrhosis and acute alcoholic hepatitis

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24
Q

What is biliary colic? How would you describe it?

A

Pain associate with temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder

Pain is of sudden onset, severe but constant and has a crescendo characteristic

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25
What is cholecystitis?
gallbladder inflammation
26
What are some risk factors for gall stones?
- obesity and rapid weight loss - diet high in animal fat and low in fibre - diabetes mellitus - contraceptive pill - liver cirrhosis - multiparity - smoking
27
What are they types of gallstones? Which more common
Cholesterol gallstone (80%) Bile pigment stones
28
What are the causes of cholesterol gallstones?
cholesterol crystallisation in bile which has an excess of cholesterol - relative deficiency in bile salts and phospholipids - excess cholesterol in diabetes or high cholesterol diet other causes - reduced gallbladder motility and stasis (pregnancy and diabetes)
29
What are the two types of bile pigment stones? What are they made up of?
Black - calcium bilirubinate and a network of mucin glycoproteins that interlace with salts such as calcium bicarbonate Brown - calcium salts (calcium bicarbonate), fatty acids and calcium bilirubinate
30
How do gallstones present?
majority asymptomatic biliary/gallstone colic - sudden onset pain, severe but constant and has a crescendo related to over-indulgence of fatty food normally mid-evening till early hours of morning epigastrium pain - radiation to shoulder and right sub scapular nausea and vomiting
31
What are the causes of cholecystitis?
gallstones - 95%, that completely obstruct the cystic duct bile inspissation (dehydration) bile stasis (trauma or severe systemic illness)
32
How would cholecystitis present?
continuous epigastric pain severe localised right upper quadrant abdominal pain tenderness, muscle guarding or rigidity vomiting, fever and local peritonitis
33
How would you differentiate acute cholecystitis and biliary colic?
Inflammatory component of acute cholecystitis (local peritonitis, fever and raised WBC)
34
What would happen if a gallstone moved from the cystic duct to the common bile duct?
obstructive jaundice and cholangitis
35
How would you investigate cholecystitis?
RUQ USS - distended gallbladder, thickened gallbladder wall, gallstones, positive Murphy's sign FBC - elevated WBC CRP - raised LFTs - elevated Alk Phos, gamma-GT and bilirubin
36
How would you treat cholecystitis?
Abx - cefuroxime + metronidazole NSAIDs - diclofenac laparoscopic cholecystectomy percutaneous cholecystostomy tube
37
How would you investigate suspected gallstones?
FBC - normal in simple biliary colic LFTs - cholelithiasis = normal, choledocholithiasis = elevated alk phos, elevated bilirubin Lipase and amylase - elevated in acute pancreatitis Abdo USS
38
How would you treat gallstones?
cholecystectomy | ERCP
39
What is ascending cholangitis? What are its causes?
infection of the biliary tree - common bile duct obstructed by gallstones - benign biliary stricture following biliary surgery - cancer of head of pancreas = bile duct obstruction - parasites
40
How would ascending cholangitis present?
``` biliary colic fever with rigors jaundice RUQ pain Jaundice is cholestatic - dark urine, pale stools and skin may itch ```
41
How would you investigate ascending cholangitis?
FBC - wbc raised Serum urea - raised in patients with severe disease Serum creatinine - raised in patients with severe disease ABG - metabolic acidosis LFTs - hyperbilirubinaemia, raised serum transaminases and alk phos CRP blood culture ERCP Transabdominal USS
42
How would you manage ascending cholangitis?
IV tazobactam/imipenem biliary decompression lithotripsy morphine sulfate
43
What is Mirizzi's syndrome?
stone in gallbladder presses on bile duct causing jaundice
44
What are some causes of acute hepatitis?
Infection - viral (hepatitis A & E, herpes viruses), non-viral (leptospirosis, toxoplasmosis) Non-infective - alcohol, durgs, toxins, pregnancy, autoimmune, hereditary metabolic
45
How does acute hepatitis present?
``` general malaise myalgia GI upset Abdo pain - RUQ with/without cholestatic jaundice tender hepatomegaly ```
46
How does chronic hepatitis present?
clubbing palmar erythema dupuytrens contracture spider naevi
47
What are some causes of chronic hepatitis?
Infection (hep B/C) Alcohol Drugs Autoimmine Hereditary metabolic
48
What may misleading about LFTs in chronic hepatitis?
AST and ALT can be normal compensated liver function can be maintained with cirrhosis
49
What is Hepatitis A? How is it spread? What are some risk factors?
It is an RNA, picorna virus spread via faeco-oral route RFs - shellfish, travellers and food handlers
50
How would Hep A present?
Viraemia - unwell (nausea, fever, malaise) Jaundice Urine dark and stools pale = intrahepatic cholestasis hepatosplenomegaly
51
How would you diagnose Hep A?
IgM anti-hepatitis A virus Transaminases - elevated Bilirubin - elevated Serum creatinine/urea - renal failure uncommon but well recognised with Hep A
52
How would you manage Hep A?
in unvaccinated people - normal immunoglobulin or hepatitis A vaccine otherwise - supportive care
53
What is Hepatitis B? How is it transmitted?
DNA virus blood borne transmission
54
What ways can Hep B be transmitted?
``` IV drug abuse Needle stick Tattoos Sexual Blood products IV drug abusers Mother to child in-utero ```
55
How would Hep B present?
Incubation 1-6 months Viraemia - unwell, nausea, fever, malaise, anorexia and arthralgia Rashes - urticaria, polyarthritis after 1-2 weeks patients can become jaundiced urine dark and stools pale = intrahepatic cholestasis hepatosplenomegaly
56
How would you investigate Hep B?
HBsAg - appears 2-10 weeks after exposure anti-HBs - appears several weeks after HBaAg - suggestive of resolved infection, also detectable in those immunised with HBV vaccine anti-HBc (IgM + IgG) - detectable in all patients who have been exposed to HBV - best single test for screening household contacts of HBV- infected individiuals
57
How to manage Hepatitis B?
Supportive Anti-viral (lamivudine/entecavir/tenofovir) FOR CHRONIC - Peginterferon alfa 2a weekly
58
What is Hepatitis D? How is it spread?
incomplete RNA virus requires HBV for assembly Blood-borne transmission Acquired simultaneously with HBV
59
What are some complications associated with Hep D?
superinfection - someone with chronic HBV gets Hep BD - secondary acute hepatitis and increased rate of liver fibrosis progression increase risk of fulminant hepatitis - VERY BAD can result in chronic hepatitis = hepatocellular carcinoma
60
What is Hep C? How is it spread?
RNA flavivirus transmitted by blood and blood products - common in haemophiliacs before screening of blood products was introduced
61
How would Hep C present?
most acute infections = asymptomatic 10% = mild influenza-like illness with jaundice and rise in ALT and AST can lead to cirrhosis, liver failure and HCC
62
How would you investigate Hepatitis C?
enzyme immunoassay or hepatitis antibodies nucleic acid amplification tests serum aminotransferases viral genotyping
63
How would you treat Hep C?
Anti-viral - elbasvir + grazoprevir SC PEGylated interferon-alpha2A/B
64
What is cirrhosis?
End stage of all progressive chronic liver diseases - once fully developed is irreversible and may be associated clinically with symptoms and signs of liver failure and portal hypertension
65
What are some causes of cirrhosis?
Chronic alcohol abuse non-alcoholic fatty liver disease Hep B+/- D Hep C Primary biliary cirrhosis Autoimmune hepatitis Wilson's Alpha-antitrypsin deficiency Drugs
66
What are the two types of cirrhosis? What are their causes?
Micronodular - regenerating <3mm in size - alcohol or biliary tract disease Macronodular - varying size may be seen within larger noules - chronic viral hepatits
67
How would cirrhosis present?
Leucochynia - white discolourations on nails ``` Clubbing Palmar Erythema Dupuytrens contracture Spider naevi Xanthelasma Loss of body hair Hepatomegaly Bruising Ankle swelling and oedema ``` Abdo pain due to ascites
68
What is the the Child-Pugh classification of cirrhosis?
Ascites, encephalopathy, bilirubin, albumin and prothrombin = given 1-3 and added up <7 is best and >10 is bad prognosis Can be used to predict chance of variceal bleed, mortality and need for liver transplant
69
How would you investigate cirrhosis?
``` Liver Biopsy LFTs GGT Albumin PT platelet count antibodies to hepatitis C hepatitis B antigen ```
70
What are some complications associated with Cirrhosis?
Coagulopathy - fall in clotting factors II, VII, IX & X Encephalopathy - liver flap, confusion/coma Hypoalbuminaemia - oedema Portal hypertension - ascites, oesophageal varices
71
How would you manage cirrhosis?
treatment of underlying chronic liver disease monitoring of complications - abdo USS Sodium restriction and diuretic for ascites Liver transplantation
72
What are pre-hepatic causes of Portal Hypertension?
Portal Vein Thrombosis Portal Vein occlusion (malignancy) Primary Biliary Cirrhosis
73
What are some intra-hepatic causes portal hypertension?
cirrhosis (80%) schistosomiasis sarcoidosis acute hepatitis
74
What are some post-hepatic causes of portal hypertension?
right heart failure constrictive pericarditis IVC obstruction Budd-chiari
75
How would a patient with portal hypertension present?
hematemesis and melena from ruptured gastro-oesophageal varice clubbing palmar erythema dupuytrens contracture spider naevi
76
How would you manage a variceal haemorrhage?
resuscitate until hemodynamically stable if anaemic = blood transfusion Vit K + platelet transfusion Vasopressin - IV terlipressin Prophylatic Abx - cephalosporin Variceal banding Balloon tamponade to reduce bleeding Transjugular intrahepatic portoclaval shunt (TIPS)
77
What is Primary Biliary Cirrhosis? What are some risk factors?
Chronic disorder with progressive destruction of small bile ducts, leading to cirrhosis ``` Fam Hx Many UTIs Smoking Past Pregnancy Use of nail polish/hair dye Other Autoimmune ```
78
How would someone with primary biliary cirrhosis present?
``` asymp normally pruritus lethargy and fatigue jaundice hepatomegaly pigmented xanthelasma ```
79
How would you investigate primary biliary cirrhosis?
increased alkaline phosphate gamma-GT - elevated bilirubin - elevated antimitochondrial antibody immunofluorescence liver biopsy abdo USS - obstructive duct lesions must be excluded before PBC diagnosis
80
How would you treat primary biliary cirrhosis?
ursodeoxycholic acid prednisolone antipruritic - colestyramine
81
What would a liver biopsy show in PBC?
portal tract infiltrate, mainly of lymphocytes and plasma cells granulomas damage to and loss of small bile ducts and ductular proliferation portal tract fibrosis and eventually cirrhosis
82
What are the stages of alcoholic liver disease?
Fatty Liver disease Alcoholic hepatitis Alcoholic cirrhosis
83
How would fatty liver, alcoholic hepatitis and alcoholic cirrhosis present?
Fatty liver - often no symptoms and signs, nausea, vomiting, diarrhoea hepatomegaly Alcoholic Hepatitis - patient may be well, mild to moderate symptoms of ill health, mild jaundice, signs of chronic liver disease, deranged LFTs Alcoholic Cirrhosis - can be very well with a few symptoms, ascites, bruising, clubbing and dupuytrens
84
How would you investigate alcoholic liver disease?
AST, ALT - elevated AST/ALT ratio - >2 seen in 70% of cases, ALT>AST suggests viral hep or non-alcoholic fatty liver alk phos - elevated bilirubin - elevated gamma-gt - elevated FBC U&Es hepatic USS
85
What are some hepatotoxic drugs?
Abx - augmentin, flucloxacillin, TB drugs, erythromycin CNS drugs - chlorpromazine, carbamazepine immunosuppresants analgesic - diclofenac GI drugs - PPIs
86
What is hereditary haemochromatosis?
inherited disorder of iron metabolism in which there is increased intestinal iron absorption - leads to iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin - leads to eventual fibrosis and functional organ failure - most common signle gene disorder in caucasians
87
What is the cause of hereditary haemochromatosis?
HFE gene mutation on chromosome 6 - autosomal recessive high intake of iron and chelating agents alcoholics
88
What is the clinical presentation of haemochromatosis?
men more affected - no menstruation and increased dietary iron tiredness and arthralgia hypogonadism slate-grey skin pigmentation chronic liver disease - ascites, oedema, bruising heart failure and arrythmias
89
What is the classic triad in haemochromatosis?
bronze skin pigmentation hepatomegaly diabetes mellitus
90
How would you investigate haemochromatosis?
serum transferrin saturation - >45% serum ferritin - raised
91
How would you treat haemochromatosis?
avoid iron or iron containing supplements hep A and B vaccination phlebotomy iron chelation - desferrioxamine
92
What is Wilson's disease?
Disorder of biliary copper excretion with too much copper in the liver and CNS Autosomal recessive disorder of gene chromosome 13 Occurs more often in cultures with consanguinity
93
What is the presentation of Wilson's disease?
children with hepatic problems - hepatitis, cirrhosis and fulminant liver failure young adults with CNS problems - tremor, dysarthria, involuntary movements, dysphagia, dyskinesia reduced memory Kayser-Fleischer ring - copper deposition in cornea - greenish-brown pigment
94
How would you investigate Wilson's disease?
LFTs 24 hour urine copper slit-lamp examination - Kayser-Fleischer rings
95
How would you treat Wilson's disease?
Zinc Trientine Penicillamine
96
What are some signs of liver failure?
Hepatic Encephalopathy - confusion, coma, liver flap Abnormal bleeding Ascites jaundice
97
What is fulminant hepatic failure?
Clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function
98
What are risk factors for hepatocellular carcinoma?
HBV and HCV Cirrhosis Haemochromatosis
99
How would HCC present?
Weight loss Anorexia ``` Fever Fatigue Jaundice Ache Ascites ``` Rapid development of these in cirrhotic patients = HCC
100
How would you investigate HCC?
``` alpha fetoprotein - elevated USS of liver FBC U&Es LFTs - elevated aminotransferases, alk phos and bilirubin prothrombin time ```
101
What are the components of the Barcelona clinic liver cancer?
Tumor function - number, size , vascular invasion Liver function - portal htn, bilirubin Chris-Pugh score
102
How would you manage HCC?
chemo liver transplant
103
What are risk factors for cholangiocarcinomas?
Parasitic worms Biliary cysts Inflammatory bowel disease
104
Where are the most common liver mets from?
GI tract Breast Bronchus
105
What kind of cancers are pancreatic? Which part of the pancreas normally affected?
adenocarcinoma | exocrine component of pancreas normally affected
106
What are risk factors for pancreatic adenocarcinomas?
``` smoking alcohol aspirin diabetes chronic pancreatitis genetic mutation - PRSS-1 fam hx ```
107
How would a pancreatic cancer present?
``` Anorexia Weight loss diabetes Acute pancreatitis painless obstructive jaundice ``` epigastric pain that radiates to the back - relieved by sitting forward

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