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YEAR 3 & 5 CORE CONDITIONS > GI 2 (liver, pancreas, gallbladder) > Flashcards

GI 2 (liver, pancreas, gallbladder) Flashcards

1
Q

What are the causes of acute pancreatitis?

A

GET SMASHED

Gallstones
Ethanol (alcohol) 
Trauma
Steroids
Mumps
Autoimmune e.g. polyarteritis nodosa, SLE 
Scorpion venom
Hyperlipidaemia, hypercalcaemia 
ERCP, emboli
Drugs e.g. azathioprine, NSAIDs, diuretics
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2
Q

How does acute pancreatitis present?

A

Severe epigastric/central abdominal pain that radiates to the back and may be relieved by sitting forwards
Nausea and vomiting - often profuse

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3
Q

What signs might you find on examination of acute pancreatitis?

A

Epigastric tenderness +/- guarding
Cullen’s sign - bruising around the umbilicus
Grey Turner’s sign - bruising in the flanks

(Cullen’s and Grey Turner’s are due to blood vessel autodigestion and retroperitoneal haemorrhage)

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4
Q

What is the criteria for predicting the severity of pancreatitis?

A

Glasgow criteria

PaO2 < 8 kPa
Age > 55 years
Neutrophilia > 15
Calcium < 2mmol/L
Renal function (urea) > 16
Enzymes - LDH > 600; AST > 200
Albumin < 32g/L
Sugar (glucose) > 10mmol/L

Patients with 3+ positive factors within first 48 hours should be sent to HDU

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5
Q

What is diagnostic of acute pancreatitis?

A

Serum amylase - diagnostic if 3x upper limit of normal

Levels do not directly correlate with disease severity as they start to fall within 24-48hours

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6
Q

What else can cause high amylase levels?

A

Bowel perforation
Ectopic pregnancy
DKA

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7
Q

What drugs can cause acute pancreatitis?

A 
Thiazides
Azathioprine
Tetracyclines
Sodium valproate
Steroids
Sulphonamides
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8
Q

What signs would be seen on an abdominal Xray in acute pancreatitis?

A

Loss of psoas shadow = increased retroperitoneal fluid

‘Sentinel loop’ sign = dilated loop of small bowel adjacent to pancreas that occurs secondary to localised inflammation

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9
Q

How do you manage acute pancreatitis?

A

FLUIDS FLUIDS FLUIDS FLUIDS !!!

  1. Nil by mouth - NJ feeding to reduce pancreatic stimulation
  2. IV fluid resuscitation - most important!
  3. Catheterise - monitor fluid balance
  4. Analgesia - pethidine (synthetic opioid) or morphine (may cause spasm of sphincter of Oddi)
  5. Only give broad spectrum antibiotics if it is necrotic
  6. Treat the underlying cause e.g. ERCP + gallstone removal if progressive jaundice
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10
Q

What are some causes of chronic pancreatitis? What is the most common cause?

A
  1. Chronic alcohol abuse - 60%
  2. Smoking - inhibits exocrine secretion
  3. Autoimmune

Rare:

  • Cystic fibrosis
  • Haemochromatosis
  • Pancreatic duct obstruction
  • Metabolic - hyperlipidaemia, hypercalcaemia
  • Infection - HIV, mumps, coxsackie
  • Congenital (pancreas divisum)
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11
Q

How does chronic pancreatitis present?

A

Epigastric pain that bores through to the back
Worse after eating fatty food
Relieved by sitting forward or with a hot water bottle
Nausea and vomiting

Endocrine dysfunction

  • Impaired glucose regulation
  • Diabetes mellitus (polyuria, polydipsia)

Exocrine dysfunction

  • Weight loss
  • Diarrhoea
  • Steatorrhoea
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12
Q

What confirms the diagnosis of chronic pancreatitis?

A

Pancreatic calcifications seen on ultrasound + CT

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13
Q

What tests differentiate acute and chronic pancreatitis?

A

Serum amylase and lipase - not raised in chronic pancreatitis but raised in acute

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14
Q

What is a secretin stimulation test?

A

Measures the ability of the pancreas to respond to the hormone secretin
There will be a positive result if over 60% of the pancreatic exocrine function is damaged

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15
Q

What is the management of chronic pancreatitis?

A

Medical

  • Analgesia = mainstay of treatment
  • Fat-soluble vitamin supplementation (A, D, E, K)
  • Management of endocrine dysfunction with insulin
  • Management of exocrine dysfunction with pancreatic enzyme replacement (Creon)

Surgical

  • Coeliac plexus block
  • Pancreatectomy
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16
Q

Who classically gets gallstones?

A

Fair, fat, fertile, female, forty

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17
Q

What are the main components of bile?

A

Cholesterol
Bile pigments from broken down Hb
Phospholipids

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18
Q

What are the different types of gallstones? How are they different?

A

Cholesterol stones

  • 90% stones in UK
  • Large, often solitary
  • Caused by obesity

Pigment stones

  • Small, irregular
  • Friable (easily crumbled)
  • Caused by haemolysis, stasis and infection

Mixed stones
- Calcium salts, pigment, cholesterol

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19
Q

What is Admirand’s triangle?

A

Increased risk of stone if:

  • Low lecithin (essential fat)
  • Low bile salts
  • High cholesterol
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20
Q

How do gallstones present if they are symptomatic?

A

Biliary colic either due to obstruction of cystic duct or if they pass through the common bile duct

  • Colicky RUQ pain that is worse after eating (especially fatty foods)
  • Jaundice (only if obstructing CBD)

Acute cholecystitis due to stone blocking bile duct so bile can’t get out of gallbladder leading to inflammatory response

  • RUQ/epigastric pain
  • Refers to right shoulder tip if diaphragm irritated
  • Local peritonitis - tender on palpation
  • Nausea and vomiting
  • Fever
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21
Q

What sign is classic in cholecystitis?

A

Murphy’s sign

  • Lay 2 fingers over RUG, ask patient to breathe in, causes patient to catch their breath due to impingement of gallbladder on fingers
  • Only positive if same test over LUQ does not cause pain
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22
Q

What investigation is used to diagnose gallstones?

A

Ultrasound - gold standard diagnostic test

  • Thickened wall
  • Shrunken gallbladder
  • Dilated CBD
  • Stones
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23
Q

What is the treatment for biliary colic?

A

Analgesia - morphine 5-10mg QDS

Elective laparoscopic cholecystectomy

Give antibiotics before e.g. co-amoxiclav +/- metronidazole

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24
Q

What is cholangitis?

A

Bacterial infection of the bile duct, often a complication of gallstones

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25
Q

How does cholangitis present?

A

Charcot’s triad:

  • Jaundice
  • Fever
  • RUQ pain

Sepsis

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26
Q

What is the treatment for cholangitis?

A

IV abx for sepsis e.g. piperacillin/tazobactam (tazocin)

Biliary drainage using ERCP

Laparoscopic cholecystectomy if gallstones was the cause

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27
Q

What do LFTs look like in obstructive jaundice?

A

ALP +++
ALT +/normal
Bilirubin +++

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28
Q

What can be used for prophylaxis of gallstones in high risk patients?

A

Ursodeoxycholic acid

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29
Q

What symptoms differentiate between biliary colic, acute cholecystitis and cholangitis?

A

Biliary colic

  • RUQ pain
  • No fever
  • No jaundice

Acute cholecystitis

  • RUQ pain
  • Fever
  • No jaundice

Cholangitis

  • RUQ pain
  • Fever
  • Jaundice
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30
Q

What is the most common cause of acute and of chronic viral hepatitis?

A

Hepatitis A = acute

Hepatitis B = chronic

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31
Q

What kind of viruses are hepatitis A, B, C?

A 
A = RNA virus
B = dsDNA virus
C = RNA flavivirus
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32
Q

What are some other infective causes of hepatitis?

A 
EBV
CMV
Malaria
Syphilis
Yellow fever
Adenovirus
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33
Q

How is hepatitis A spread?

A

Faeco-oral spread - food sources or anal sex

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34
Q

What is the presentation of hepatitis A?

A

Flu-like symptoms e.g. nausea, vomiting, fatigue, anorexia

Icteric phase (jaundice phase)

  • Dark urine and pale stools
  • Jaundice
  • Abdominal phase
  • Can last up to a year
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35
Q

What is the incubation period for hepatitis A?

A

14-28 days

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36
Q

How do you test for hepatitis A?

A

IgM (undetectable after 6 months so do IgG, which is detectable for life)

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37
Q

How is hepatitis B spread?

A

Transmission is via infected blood or body fluids

Sexual route, IVDU - USA/UK

Vertical transmission - endemic countries (Far East, Africa, Mediterranean)

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38
Q

What are some signs of chronic liver disease?

A
  • Leukonychia
  • Palmar erythema
  • Dupytrens contracture
  • Spider naevi
  • Gynaecomastia
  • Loss of axillary hair
  • Parotid swelling
  • Caput medusa
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39
Q

What antigens/antibodies are present in hepatitis B - natural infection and vaccination?

A
  • HbsAg (surface antigen) is present in both natural infection and vaccination 1-6 months after exposure
  • HbeAg (e antigen) is present for 1.5-3 months after acute illness and implies high infectivity
  • Anti-HBc (core antibodies) only present in natural infection - implies past infection
  • IgM (is a type of core antibody) to HbcAg (core antigen) = acute
  • IgG to HbcAg (core antigen) = chronic
  • Anti-HBs (antibodies to surface antigen) only present in vaccination or they are immune in natural infection but it would be negative in chronic disease
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40
Q

What is the treatment for hepatitis B?

A

Pegylated interferon alfa-2a = first-line

Second-line alternatives:

  • Nucleoside analogues (lamivudine, entecavir)
  • Nucleotide analogues (adeofovir, tenofovir)
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41
Q

How is hepatitis C spread?

A

Blood and bodily fluid spread

IVDU
MSM
Contaminated medical equipment

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42
Q

How does hepatitis C present?

A

Often asymptomatic or very mild

85% develop silent chronic infection

43
Q

What are the investigations for hepatitis C?

A

Anti-HCV confirm exposure 3 months after infection
If positive, do reflex testing with PCR
If PCR is positive, it confirms ongoing infection/chronicity so do a liver biopsy to assess damage and need for treatment
Also, test for the HCV genotype

44
Q

What is the treatment for hepatitis C?

A 
Pegylated interferon SC weekly
Nucleoside analogues (now generally preferred) e.g. sofosbuvir
45
Q

How is hepatitis E spread?

A

Consumption of pork/shellfish/molluscs

46
Q

What are the risk factors for pancreatic carcinoma?

A
  • Smoking
  • Alcohol
  • KRAS2 gene mutation (95%)
  • Diabetes mellitus
  • Chronic pancreatitis
  • High fat, processed meat diet
47
Q

Where in the pancreas are carcinomas most common?

A
  1. Head of pancreas - 60%
  2. Body - 25%
  3. Tail - 15%
48
Q

How do tumours in the head of the pancreas present?

A

Painless obstructive jaundice - due to compression of the common bile duct

49
Q

How do tumours in the body and tail of the pancreas present?

A

Epigastric pain that radiates to back and is relieved by sitting forwards - due to invasion of the coeliac plexus or secondary to pancreatitis

50
Q

What are some rarer features of pancreatic carcinoma?

A
  • Thrombophlebitis migrans (e.g. arm vein becomes swollen and red, then leg vein)
  • Hypercalcaemia
  • Marantic endocarditis (due to wasting away)
  • Portal hypertension (splenic vein thrombosis)
  • Nephrosis (renal vein metastases)
51
Q

What is Courvoisier’s law?

A

If there is a palpable gallbladder with painless jaundice, the cause is not gallstones and malignancy of the biliary tree or pancreas should be strongly suspected

52
Q

What tumour marker is associated with pancreatic carcinoma? What is it used for?

A

CA19-9

Used to monitor disease progression and response to treatment, not for diagnosis

53
Q

What is the surgical treatment for pancreatic carcinoma of the head of the pancreas?

A

Whipple’s procedure = pancreatoduodenectomy (only done where vascular invasion is minimal)
95% are not suitable for resection

Radical resection of the head of the pancreas, the antrum of the stomach, 1st and 2nd parts of the duodenum, the common bile duct and the gallbladder (due to their common arterial supply - gastroduodenal artery)

54
Q

What is the definition of liver failure?

A

The development of coagulopathy and encephalopathy

55
Q

What is fulminant liver failure?

A

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

56
Q

What are some infectious causes of liver failure?

A 
Hepatitis B
Hepatitis C
CMV
Yellow fever 
Leptospirosis
57
Q

What drugs can cause chronic liver failure?

A 
Methotrexate
Paracetamol overdose
Amiodarone 
Sodium valproate
Nitrofurantoin 
Isoniazid
58
Q

What autoimmune conditions can cause chronic liver failure

A 
Primary biliary cholangitis
Primary sclerosing cholangitis 
Haemochromatosis 
Alpha1-antitrypsin deficiency 
Wilson's disease (Chr13 - disorder of hepatic copper deposition) 
Autoimmune hepatitis
59
Q

What would blood results show in chronic liver failure?

A

High INR
Thrombocytopenia

LFTs

  • high ALT, AST
  • high ALP
  • high bilirubin

U&Es

  • high lactate
  • high creatinine
  • low glucose
  • high ammonia
60
Q

What is ascites?

A

Excessive accumulation of fluid in abdominal cavity

61
Q

What is the main cause of ascites?

A

Liver cirrhosis (75% of patients with ascites have cirrhosis)

62
Q

What are some other causes of ascites?

A

Malignancies:

  • GI tract
  • Ovarian (Meig’s) - ascites out of proportion to tumour size
  • Lymphoma
Heart failure
Nephrotic syndrome
Pancreatitis
Hypothyroidism
TB
63
Q

What signs might be found on examination of ascites?

A

Distention of abdomen
Umbilical/inguinal hernia
Shifting dullness
Fluid thrills

64
Q

How do you manage ascites?

A

Reduce salt intake
Diuretics - use potassium sparing (spironolactone) in liver disease
Paracentesis
Albumin infusion

65
Q

What is the initial imaging test for pancreatic carcnoma?

A

Abdominal ultrasound - initial imaging

It is good at seeing tumours of the head of the pancreas but not of the body and tail so a normal USS does not rule out carcinoma

66
Q

What is diagnostic of pancreatic carcinoma?

A

CT abdo-pelvis

67
Q

What are the differentials for obstructive jaundice?

A

Gallstone disease
Cholangiocarcinoma
Carcinoma of the head of the pancreas
Benign gallbladder stricture

68
Q

What can cause portal hypertension?

A

Prehepatic
• Portal vein thrombosis
• Splenic vein thrombosis

Intrahepatic
• Cirrhosis 
• Schistosomiasis 
• Hepatic metastases
• Hepatic sinusoidal obstruction syndrome (aka hepatic veno-occlusive disease)

Post-hepatic
• Budd-Chiari syndrome - hepatic vein obstruction
• Right-sided heart failure
• Constrictive pericarditis

69
Q

How can portal hypertension present? What causes these presentations?

A

Increased blood flow via portosystemic anastomoses

  • Via paraumbilical veins + epigastric veins –> caput medusae
  • Via rectal veins –> haemorrhoids
  • Via veins of the gastric fundus and lower 1/3rd of oseophagus: oesophageal varices - haematemesis; gastric varices - malaena

Congestive splenomegaly

Transudative ascites

70
Q

What is the first line treatment of portal hypertension? How does this work?

A

Propanolol (non-cardiac selective beta-blocker) - first-line treatment

Inhibits beta-2-adrenergic receptors in the GI tract, which causes vasoconstriction in the vessels of the GI system, leading to decreases portal and collateral blood flow, which reduces portal hypertension

71
Q

What is an invasive management option for certain patients with portal hypertension?

A

Trans-jugular intrahepatic portosystemic shunt (TIPSS)

An artificial channel within the liver that establishes communication between the inflow portal vein and the outflow hepatic vein

72
Q

What are some common indications for TIPSS?

A

Secondary prophylaxis for oesophageal variceal bleeding

Treatment of refractory ascites

Treating portal hypertension in Budd-Chiari syndrome

73
Q

Go through the hepatitis vaccinations e.g. active/inactive, how long you’re immune for, boosters

A

Hepatitis A

  • Active immunisation with inactivated viral protein
  • 1 IM dose gives immunity for 1 year
  • 20 years immunity if booster given at 6-12 months

Hepatitis B

  • Passive immunisation with anti-HBV immunoglobulin
  • Dose 1 then dose 2 one month after dose 1
74
Q

What 4 inherited conditions cause a defective conjugation of bilirubin?

A

Gilbert syndrome
Rotor syndrome
Dubin-Johnson syndrome
Crigler Najjar syndrome

75
Q

What would the LFTs show in Gilbert’s syndrome?

A

Raised unconjungated bilirubin
Normal ALT and AST
Normal ALP

76
Q

What is the clinical triad of portal vein thrombosis?

A
  1. Abdominal pain
  2. Hepatomegaly
  3. Ascites
77
Q

How do you diagnosis portal vein thrombosis?

A

USS of abdomen

78
Q

What is the most common source of liver abscess?

A

Biliary tract

  • Gallstones in CBD
  • Biliary strictures
  • Cholangitis
79
Q

What is the most common causative organism of pyogenic liver abscess?

A

E. Coli

Klebsiella is second most common but is most commonly found in Taiwan

80
Q

What is the most common causative organism of non-pyogenic liver abscess?

A

Fungal infection with Candida species

81
Q

What is the confirmatory test for a pyogenic liver abscess?

A

Abdominal USS - confirmatory test for pyogenic liver abscess

Solitary/multiple, poorly demarcated, fluid-filled, roung hypoechoic lesions with surrounding oedema and increased blood flow

82
Q

What pattern of inheritance is there in haemochromatosis?

A

Autosomal recessive

83
Q

Who is most commonly affected by haemochromatosis?

A

Younger males

Females are protected due to iron loss through menstruation

84
Q

How does haemochromatosis typically present?

A
  • Fatigue and lethargy
  • Hyperpigmentation (bronzing) of the skin
  • Bronze diabetes (type 2 diabetes secondary to haemochromatosis i.e. pancreatic damage from iron overload)
  • Joint pain
  • Liver cirrhosis
  • Adrenal insufficiency
85
Q

What would iron studies show in haemochromatosis?

A

Raised serum iron
Raised serum ferritin
Raised transferrin saturation
Low total iron-binding capacity

86
Q

What is the first-line treatment for haemochromatosis?

A

Therapeutic phlebotomy

Initially 1-2 /week until target ferritin and Hb levels reached, then every 2-4 months thereafter

87
Q

Give an example of an iron chelating agent?

A

Deferoxamine

88
Q

What organs does Wilson’s mostly affect?

A

Liver
Cornea
CNS
Kidneys

89
Q

What is seen in the corneas in Wilson’s disease?

A

Kaiser Fleisher rings = copper accumulation in the Descemet membrane of the cornea

90
Q

What renal syndrome does Wilson’s disease cause?

A

Fanconi syndrome - polyuria, polydipsia

91
Q

What is the best initial test for ? Wilson’s disease?

A

Slit lamp examination looking for the Kaiser Fleisher rings

92
Q

What test can you do for copper levels in Wilson’s?

A

Serum copper

  • Raised free serum copper
  • Low total serum copper

Urine
- High urine copper excretion over 24 hours

93
Q

What is the medical therapy for Wilson’s disease? What must you be careful of when starting medical therapy?

A

Chelating agents - they facilitate renal excretion of copper by forming water soluble compounds

e.g. penicillamine, trientine

(make sure to start on low dose and titrate gradually as mobilising copper stores too rapidly can exacerbate neurological sx)

94
Q

Who does PSC affect and who does PBC affect?

A

PSC = middle-aged men

PBC = middle-aged women

95
Q

What condition is PSC typically associated with?

A

Ulcerative colitis - 90% of people with PSC also have UC

96
Q

What is the pathophysiology behind PSC and PBC?

A

PSC = progressive chronic inflammation of both intrahepatic and extrahepatic bile ducts

PBC = progressive destruction of intrahepatic small and medium-sized bile ducts only

97
Q

How does PSC and PBC present?

A
  • Pruritis
  • Fatigue
  • Jaundice
  • Hepatomegaly

Then PBC also has xanthomas and xanthelasmas

98
Q

What antibodies are associated with PSC and PBC?

A

PSC = pANCA

PBC = AMA (anti-mitochondrial antibodies)

99
Q

What would LFTs show in PSC and PBC

A
  • Raised ALP
  • Raised GGP
  • Raised bilirubin
100
Q

What test is diagnostic of PSC and PBC?

A

MRCP

PSC - beading of bile ducts

PBC - intrahepatic bile duct occlusion

101
Q

What causes carcinoid syndrome?

A

Carcinoid tumours = neuroendocrine tumours

Occurs when metastases are present in the liver and release serotonin into the systemic circulation

102
Q

What is the presentation of carcinoid syndrome? What is the first symptom?

A
  • Flushing - earliest symptom
  • Diarrhoea
  • Bronchospasm
  • Hypotension
  • Right heart valvular stenosis
103
Q

What is the management of cholecystitis?

A

• Nil by mouth
• Antibiotics
- Cefuroxime 1.5mg TDS IV
- Metronidazole if patient particularly unwell
• Diclofenac + pethidine if severe
• IV fluids
• Laparoscopic cholecystectomy within 1 week

YEAR 3 & 5 CORE CONDITIONS (30 decks)

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