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
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
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)
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
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
6
Q
What else can cause high amylase levels?
A
Bowel perforation
Ectopic pregnancy
DKA
7
Q
What drugs can cause acute pancreatitis?
A
Thiazides Azathioprine Tetracyclines Sodium valproate Steroids Sulphonamides
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
9
Q
How do you manage acute pancreatitis?
A
FLUIDS FLUIDS FLUIDS FLUIDS !!!
- Nil by mouth - NJ feeding to reduce pancreatic stimulation
- IV fluid resuscitation - most important!
- Catheterise - monitor fluid balance
- Analgesia - pethidine (synthetic opioid) or morphine (may cause spasm of sphincter of Oddi)
- Only give broad spectrum antibiotics if it is necrotic
- Treat the underlying cause e.g. ERCP + gallstone removal if progressive jaundice
10
Q
What are some causes of chronic pancreatitis? What is the most common cause?
A
- Chronic alcohol abuse - 60%
- Smoking - inhibits exocrine secretion
- Autoimmune
Rare:
- Cystic fibrosis
- Haemochromatosis
- Pancreatic duct obstruction
- Metabolic - hyperlipidaemia, hypercalcaemia
- Infection - HIV, mumps, coxsackie
- Congenital (pancreas divisum)
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
12
Q
What confirms the diagnosis of chronic pancreatitis?
A
Pancreatic calcifications seen on ultrasound + CT
13
Q
What tests differentiate acute and chronic pancreatitis?
A
Serum amylase and lipase - not raised in chronic pancreatitis but raised in acute
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
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
16
Q
Who classically gets gallstones?
A
Fair, fat, fertile, female, forty
17
Q
What are the main components of bile?
A
Cholesterol
Bile pigments from broken down Hb
Phospholipids
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
19
Q
What is Admirand’s triangle?
A
Increased risk of stone if:
- Low lecithin (essential fat)
- Low bile salts
- High cholesterol
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
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
22
Q
What investigation is used to diagnose gallstones?
A
Ultrasound - gold standard diagnostic test
- Thickened wall
- Shrunken gallbladder
- Dilated CBD
- Stones
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
24
Q
What is cholangitis?
A
Bacterial infection of the bile duct, often a complication of gallstones
25
How does cholangitis present?
Charcot's triad:
- Jaundice
- Fever
- RUQ pain
Sepsis
26
What is the treatment for cholangitis?
IV abx for sepsis e.g. piperacillin/tazobactam (tazocin)
Biliary drainage using ERCP
Laparoscopic cholecystectomy if gallstones was the cause
27
What do LFTs look like in obstructive jaundice?
ALP +++
ALT +/normal
Bilirubin +++
28
What can be used for prophylaxis of gallstones in high risk patients?
Ursodeoxycholic acid
29
What symptoms differentiate between biliary colic, acute cholecystitis and cholangitis?
Biliary colic
- RUQ pain
- No fever
- No jaundice
Acute cholecystitis
- RUQ pain
- Fever
- No jaundice
Cholangitis
- RUQ pain
- Fever
- Jaundice
30
What is the most common cause of acute and of chronic viral hepatitis?
Hepatitis A = acute
| Hepatitis B = chronic
31
What kind of viruses are hepatitis A, B, C?
```
A = RNA virus
B = dsDNA virus
C = RNA flavivirus
```
32
What are some other infective causes of hepatitis?
```
EBV
CMV
Malaria
Syphilis
Yellow fever
Adenovirus
```
33
How is hepatitis A spread?
Faeco-oral spread - food sources or anal sex
34
What is the presentation of hepatitis 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
35
What is the incubation period for hepatitis A?
14-28 days
36
How do you test for hepatitis A?
IgM (undetectable after 6 months so do IgG, which is detectable for life)
37
How is hepatitis B spread?
Transmission is via infected blood or body fluids
Sexual route, IVDU - USA/UK
Vertical transmission - endemic countries (Far East, Africa, Mediterranean)
38
What are some signs of chronic liver disease?
- Leukonychia
- Palmar erythema
- Dupytrens contracture
- Spider naevi
- Gynaecomastia
- Loss of axillary hair
- Parotid swelling
- Caput medusa
39
What antigens/antibodies are present in hepatitis B - natural infection and vaccination?
- 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
40
What is the treatment for hepatitis B?
Pegylated interferon alfa-2a = first-line
Second-line alternatives:
- Nucleoside analogues (lamivudine, entecavir)
- Nucleotide analogues (adeofovir, tenofovir)
41
How is hepatitis C spread?
Blood and bodily fluid spread
IVDU
MSM
Contaminated medical equipment
42
How does hepatitis C present?
Often asymptomatic or very mild
| 85% develop silent chronic infection
43
What are the investigations for hepatitis C?
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
What is the treatment for hepatitis C?
```
Pegylated interferon SC weekly
Nucleoside analogues (now generally preferred) e.g. sofosbuvir
```
45
How is hepatitis E spread?
Consumption of pork/shellfish/molluscs
46
What are the risk factors for pancreatic carcinoma?
- Smoking
- Alcohol
- KRAS2 gene mutation (95%)
- Diabetes mellitus
- Chronic pancreatitis
- High fat, processed meat diet
47
Where in the pancreas are carcinomas most common?
1. Head of pancreas - 60%
2. Body - 25%
3. Tail - 15%
48
How do tumours in the head of the pancreas present?
Painless obstructive jaundice - due to compression of the common bile duct
49
How do tumours in the body and tail of the pancreas present?
Epigastric pain that radiates to back and is relieved by sitting forwards - due to invasion of the coeliac plexus or secondary to pancreatitis
50
What are some rarer features of pancreatic carcinoma?
- 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
What is Courvoisier's law?
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
What tumour marker is associated with pancreatic carcinoma? What is it used for?
CA19-9
Used to monitor disease progression and response to treatment, not for diagnosis
53
What is the surgical treatment for pancreatic carcinoma of the head of the pancreas?
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
What is the definition of liver failure?
The development of coagulopathy and encephalopathy
55
What is fulminant liver failure?
Clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function
56
What are some infectious causes of liver failure?
```
Hepatitis B
Hepatitis C
CMV
Yellow fever
Leptospirosis
```
57
What drugs can cause chronic liver failure?
```
Methotrexate
Paracetamol overdose
Amiodarone
Sodium valproate
Nitrofurantoin
Isoniazid
```
58
What autoimmune conditions can cause chronic liver failure
```
Primary biliary cholangitis
Primary sclerosing cholangitis
Haemochromatosis
Alpha1-antitrypsin deficiency
Wilson's disease (Chr13 - disorder of hepatic copper deposition)
Autoimmune hepatitis
```
59
What would blood results show in chronic liver failure?
High INR
Thrombocytopenia
LFTs
- high ALT, AST
- high ALP
- high bilirubin
U&Es
- high lactate
- high creatinine
- low glucose
- high ammonia
60
What is ascites?
Excessive accumulation of fluid in abdominal cavity
61
What is the main cause of ascites?
Liver cirrhosis (75% of patients with ascites have cirrhosis)
62
What are some other causes of ascites?
Malignancies:
- GI tract
- Ovarian (Meig's) - ascites out of proportion to tumour size
- Lymphoma
```
Heart failure
Nephrotic syndrome
Pancreatitis
Hypothyroidism
TB
```
63
What signs might be found on examination of ascites?
Distention of abdomen
Umbilical/inguinal hernia
Shifting dullness
Fluid thrills
64
How do you manage ascites?
Reduce salt intake
Diuretics - use potassium sparing (spironolactone) in liver disease
Paracentesis
Albumin infusion
65
What is the initial imaging test for pancreatic carcnoma?
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
What is diagnostic of pancreatic carcinoma?
CT abdo-pelvis
67
What are the differentials for obstructive jaundice?
Gallstone disease
Cholangiocarcinoma
Carcinoma of the head of the pancreas
Benign gallbladder stricture
68
What can cause portal hypertension?
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
How can portal hypertension present? What causes these presentations?
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
What is the first line treatment of portal hypertension? How does this work?
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
What is an invasive management option for certain patients with portal hypertension?
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
What are some common indications for TIPSS?
Secondary prophylaxis for oesophageal variceal bleeding
Treatment of refractory ascites
Treating portal hypertension in Budd-Chiari syndrome
73
Go through the hepatitis vaccinations e.g. active/inactive, how long you're immune for, boosters
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
What 4 inherited conditions cause a defective conjugation of bilirubin?
Gilbert syndrome
Rotor syndrome
Dubin-Johnson syndrome
Crigler Najjar syndrome
75
What would the LFTs show in Gilbert's syndrome?
Raised unconjungated bilirubin
Normal ALT and AST
Normal ALP
76
What is the clinical triad of portal vein thrombosis?
1. Abdominal pain
2. Hepatomegaly
3. Ascites
77
How do you diagnosis portal vein thrombosis?
USS of abdomen
78
What is the most common source of liver abscess?
Biliary tract
- Gallstones in CBD
- Biliary strictures
- Cholangitis
79
What is the most common causative organism of pyogenic liver abscess?
E. Coli
Klebsiella is second most common but is most commonly found in Taiwan
80
What is the most common causative organism of non-pyogenic liver abscess?
Fungal infection with Candida species
81
What is the confirmatory test for a pyogenic liver abscess?
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
What pattern of inheritance is there in haemochromatosis?
Autosomal recessive
83
Who is most commonly affected by haemochromatosis?
Younger males
Females are protected due to iron loss through menstruation
84
How does haemochromatosis typically present?
* 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
What would iron studies show in haemochromatosis?
Raised serum iron
Raised serum ferritin
Raised transferrin saturation
Low total iron-binding capacity
86
What is the first-line treatment for haemochromatosis?
Therapeutic phlebotomy
Initially 1-2 /week until target ferritin and Hb levels reached, then every 2-4 months thereafter
87
Give an example of an iron chelating agent?
Deferoxamine
88
What organs does Wilson's mostly affect?
Liver
Cornea
CNS
Kidneys
89
What is seen in the corneas in Wilson's disease?
Kaiser Fleisher rings = copper accumulation in the Descemet membrane of the cornea
90
What renal syndrome does Wilson's disease cause?
Fanconi syndrome - polyuria, polydipsia
91
What is the best initial test for ? Wilson's disease?
Slit lamp examination looking for the Kaiser Fleisher rings
92
What test can you do for copper levels in Wilson's?
Serum copper
- Raised free serum copper
- Low total serum copper
Urine
- High urine copper excretion over 24 hours
93
What is the medical therapy for Wilson's disease? What must you be careful of when starting medical therapy?
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
Who does PSC affect and who does PBC affect?
PSC = middle-aged men
PBC = middle-aged women
95
What condition is PSC typically associated with?
Ulcerative colitis - 90% of people with PSC also have UC
96
What is the pathophysiology behind PSC and PBC?
PSC = progressive chronic inflammation of both intrahepatic and extrahepatic bile ducts
PBC = progressive destruction of intrahepatic small and medium-sized bile ducts only
97
How does PSC and PBC present?
* Pruritis
* Fatigue
* Jaundice
* Hepatomegaly
Then PBC also has xanthomas and xanthelasmas
98
What antibodies are associated with PSC and PBC?
PSC = pANCA
PBC = AMA (anti-mitochondrial antibodies)
99
What would LFTs show in PSC and PBC
* Raised ALP
* Raised GGP
* Raised bilirubin
100
What test is diagnostic of PSC and PBC?
MRCP
PSC - beading of bile ducts
PBC - intrahepatic bile duct occlusion
101
What causes carcinoid syndrome?
Carcinoid tumours = neuroendocrine tumours
Occurs when metastases are present in the liver and release serotonin into the systemic circulation
102
What is the presentation of carcinoid syndrome? What is the first symptom?
* Flushing - earliest symptom
* Diarrhoea
* Bronchospasm
* Hypotension
* Right heart valvular stenosis
103
What is the management of cholecystitis?
• 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
