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Gastro > Liver & Idiot friends > Flashcards

Liver & Idiot friends Flashcards

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
Q

What is cholecystitis?

A

gallbladder inflammation

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26
Q

What are some risk factors for gall stones?

A
  • obesity and rapid weight loss
  • diet high in animal fat and low in fibre
  • diabetes mellitus
  • contraceptive pill
  • liver cirrhosis
  • multiparity
  • smoking
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27
Q

What are they types of gallstones? Which more common

A

Cholesterol gallstone (80%)

Bile pigment stones

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28
Q

What are the causes of cholesterol gallstones?

A

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)

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29
Q

What are the two types of bile pigment stones? What are they made up of?

A

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

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30
Q

How do gallstones present?

A

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

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31
Q

What are the causes of cholecystitis?

A

gallstones - 95%, that completely obstruct the cystic duct

bile inspissation (dehydration)

bile stasis (trauma or severe systemic illness)

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32
Q

How would cholecystitis present?

A

continuous epigastric pain

severe localised right upper quadrant abdominal pain

tenderness, muscle guarding or rigidity

vomiting, fever and local peritonitis

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33
Q

How would you differentiate acute cholecystitis and biliary colic?

A

Inflammatory component of acute cholecystitis (local peritonitis, fever and raised WBC)

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34
Q

What would happen if a gallstone moved from the cystic duct to the common bile duct?

A

obstructive jaundice and cholangitis

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35
Q

How would you investigate cholecystitis?

A

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

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36
Q

How would you treat cholecystitis?

A

Abx - cefuroxime + metronidazole

NSAIDs - diclofenac

laparoscopic cholecystectomy

percutaneous cholecystostomy tube

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37
Q

How would you investigate suspected gallstones?

A

FBC - normal in simple biliary colic

LFTs - cholelithiasis = normal, choledocholithiasis = elevated alk phos, elevated bilirubin

Lipase and amylase - elevated in acute pancreatitis

Abdo USS

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38
Q

How would you treat gallstones?

A

cholecystectomy

ERCP

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39
Q

What is ascending cholangitis? What are its causes?

A

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
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40
Q

How would ascending cholangitis present?

A 
biliary colic
fever with rigors
jaundice
RUQ pain
Jaundice is cholestatic - dark urine, pale stools and skin may itch
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41
Q

How would you investigate ascending cholangitis?

A

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

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42
Q

How would you manage ascending cholangitis?

A

IV tazobactam/imipenem

biliary decompression

lithotripsy

morphine sulfate

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43
Q

What is Mirizzi’s syndrome?

A

stone in gallbladder presses on bile duct causing jaundice

44
Q

What are some causes of acute hepatitis?

A

Infection - viral (hepatitis A & E, herpes viruses), non-viral (leptospirosis, toxoplasmosis)

Non-infective - alcohol, durgs, toxins, pregnancy, autoimmune, hereditary metabolic

45
Q

How does acute hepatitis present?

A 
general malaise
myalgia
GI upset
Abdo pain - RUQ
with/without cholestatic jaundice
tender hepatomegaly
46
Q

How does chronic hepatitis present?

A

clubbing
palmar erythema
dupuytrens contracture
spider naevi

47
Q

What are some causes of chronic hepatitis?

A

Infection (hep B/C)

Alcohol
Drugs
Autoimmine
Hereditary metabolic

48
Q

What may misleading about LFTs in chronic hepatitis?

A

AST and ALT can be normal

compensated liver function can be maintained with cirrhosis

49
Q

What is Hepatitis A? How is it spread? What are some risk factors?

A

It is an RNA, picorna virus

spread via faeco-oral route

RFs - shellfish, travellers and food handlers

50
Q

How would Hep A present?

A

Viraemia - unwell (nausea, fever, malaise)

Jaundice

Urine dark and stools pale = intrahepatic cholestasis

hepatosplenomegaly

51
Q

How would you diagnose Hep A?

A

IgM anti-hepatitis A virus

Transaminases - elevated

Bilirubin - elevated

Serum creatinine/urea - renal failure uncommon but well recognised with Hep A

52
Q

How would you manage Hep A?

A

in unvaccinated people - normal immunoglobulin or hepatitis A vaccine

otherwise - supportive care

53
Q

What is Hepatitis B? How is it transmitted?

A

DNA virus

blood borne transmission

54
Q

What ways can Hep B be transmitted?

A 
IV drug abuse
Needle stick
Tattoos
Sexual
Blood products
IV drug abusers
Mother to child in-utero
55
Q

How would Hep B present?

A

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
Q

How would you investigate Hep B?

A

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
Q

How to manage Hepatitis B?

A

Supportive

Anti-viral (lamivudine/entecavir/tenofovir)

FOR CHRONIC - Peginterferon alfa 2a weekly

58
Q

What is Hepatitis D? How is it spread?

A

incomplete RNA virus

requires HBV for assembly

Blood-borne transmission

Acquired simultaneously with HBV

59
Q

What are some complications associated with Hep D?

A

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
Q

What is Hep C? How is it spread?

A

RNA flavivirus

transmitted by blood and blood products - common in haemophiliacs before screening of blood products was introduced

61
Q

How would Hep C present?

A

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
Q

How would you investigate Hepatitis C?

A

enzyme immunoassay or hepatitis antibodies

nucleic acid amplification tests

serum aminotransferases

viral genotyping

63
Q

How would you treat Hep C?

A

Anti-viral - elbasvir + grazoprevir

SC PEGylated interferon-alpha2A/B

64
Q

What is cirrhosis?

A

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
Q

What are some causes of cirrhosis?

A

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
Q

What are the two types of cirrhosis? What are their causes?

A

Micronodular - regenerating <3mm in size - alcohol or biliary tract disease

Macronodular - varying size may be seen within larger noules - chronic viral hepatits

67
Q

How would cirrhosis present?

A

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
Q

What is the the Child-Pugh classification of cirrhosis?

A

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
Q

How would you investigate cirrhosis?

A 
Liver Biopsy
LFTs
GGT
Albumin
PT 
platelet count
antibodies to hepatitis C
hepatitis B antigen
70
Q

What are some complications associated with Cirrhosis?

A

Coagulopathy - fall in clotting factors II, VII, IX & X

Encephalopathy - liver flap, confusion/coma

Hypoalbuminaemia - oedema

Portal hypertension - ascites, oesophageal varices

71
Q

How would you manage cirrhosis?

A

treatment of underlying chronic liver disease

monitoring of complications - abdo USS

Sodium restriction and diuretic for ascites

Liver transplantation

72
Q

What are pre-hepatic causes of Portal Hypertension?

A

Portal Vein Thrombosis

Portal Vein occlusion (malignancy)

Primary Biliary Cirrhosis

73
Q

What are some intra-hepatic causes portal hypertension?

A

cirrhosis (80%)

schistosomiasis

sarcoidosis

acute hepatitis

74
Q

What are some post-hepatic causes of portal hypertension?

A

right heart failure

constrictive pericarditis

IVC obstruction

Budd-chiari

75
Q

How would a patient with portal hypertension present?

A

hematemesis and melena from ruptured gastro-oesophageal varice

clubbing

palmar erythema

dupuytrens contracture

spider naevi

76
Q

How would you manage a variceal haemorrhage?

A

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
Q

What is Primary Biliary Cirrhosis? What are some risk factors?

A

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
Q

How would someone with primary biliary cirrhosis present?

A 
asymp normally
pruritus
lethargy and fatigue
jaundice
hepatomegaly
pigmented xanthelasma
79
Q

How would you investigate primary biliary cirrhosis?

A

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
Q

How would you treat primary biliary cirrhosis?

A

ursodeoxycholic acid

prednisolone

antipruritic - colestyramine

81
Q

What would a liver biopsy show in PBC?

A

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
Q

What are the stages of alcoholic liver disease?

A

Fatty Liver disease
Alcoholic hepatitis
Alcoholic cirrhosis

83
Q

How would fatty liver, alcoholic hepatitis and alcoholic cirrhosis present?

A

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
Q

How would you investigate alcoholic liver disease?

A

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
Q

What are some hepatotoxic drugs?

A

Abx - augmentin, flucloxacillin, TB drugs, erythromycin

CNS drugs - chlorpromazine, carbamazepine

immunosuppresants

analgesic - diclofenac

GI drugs - PPIs

86
Q

What is hereditary haemochromatosis?

A

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
Q

What is the cause of hereditary haemochromatosis?

A

HFE gene mutation on chromosome 6 - autosomal recessive

high intake of iron and chelating agents

alcoholics

88
Q

What is the clinical presentation of haemochromatosis?

A

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
Q

What is the classic triad in haemochromatosis?

A

bronze skin pigmentation
hepatomegaly
diabetes mellitus

90
Q

How would you investigate haemochromatosis?

A

serum transferrin saturation - >45%

serum ferritin - raised

91
Q

How would you treat haemochromatosis?

A

avoid iron or iron containing supplements

hep A and B vaccination

phlebotomy

iron chelation - desferrioxamine

92
Q

What is Wilson’s disease?

A

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
Q

What is the presentation of Wilson’s disease?

A

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
Q

How would you investigate Wilson’s disease?

A

LFTs

24 hour urine copper

slit-lamp examination - Kayser-Fleischer rings

95
Q

How would you treat Wilson’s disease?

A

Zinc
Trientine
Penicillamine

96
Q

What are some signs of liver failure?

A

Hepatic Encephalopathy - confusion, coma, liver flap

Abnormal bleeding

Ascites

jaundice

97
Q

What is fulminant hepatic failure?

A

Clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function

98
Q

What are risk factors for hepatocellular carcinoma?

A

HBV and HCV
Cirrhosis
Haemochromatosis

99
Q

How would HCC present?

A

Weight loss

Anorexia

Fever
Fatigue
Jaundice
Ache
Ascites

Rapid development of these in cirrhotic patients = HCC

100
Q

How would you investigate HCC?

A 
alpha fetoprotein - elevated
USS of liver
FBC
U&amp;Es
LFTs - elevated aminotransferases, alk phos and bilirubin
prothrombin time
101
Q

What are the components of the Barcelona clinic liver cancer?

A

Tumor function - number, size , vascular invasion

Liver function - portal htn, bilirubin

Chris-Pugh score

102
Q

How would you manage HCC?

A

chemo

liver transplant

103
Q

What are risk factors for cholangiocarcinomas?

A

Parasitic worms

Biliary cysts

Inflammatory bowel disease

104
Q

Where are the most common liver mets from?

A

GI tract
Breast
Bronchus

105
Q

What kind of cancers are pancreatic? Which part of the pancreas normally affected?

A

adenocarcinoma

exocrine component of pancreas normally affected

106
Q

What are risk factors for pancreatic adenocarcinomas?

A 
smoking
alcohol
aspirin
diabetes
chronic pancreatitis
genetic mutation - PRSS-1
fam hx
107
Q

How would a pancreatic cancer present?

A 
Anorexia
Weight loss
diabetes
Acute pancreatitis
painless obstructive jaundice

epigastric pain that radiates to the back - relieved by sitting forward

Gastro (4 decks)

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