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Year 3 OSCE > Case 3- HPB > Flashcards

Case 3- HPB Flashcards

1
Q

Cholecystitis features

A

RUQ pain
Fever
Murphy’s sign
Nausea and vomiting
General malaise
Right shoulder pain

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2
Q

Ascending cholangitis features

A

Charcot’s triad- RUQ pain, fever, jaundice
Reynold’s Pentad- RUQ pain, fever, jaundice, hypotension, altered mental status

NB- cholangitis is jaundice, cholecystitis isn’t

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3
Q

Primary sclerosing cholangitis

A

Damage to the medium and large bile ducts

Associated with IBD

Causes cholestasis- itching/pain/fatigue/weight loss/jaundice

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4
Q

Primary biliary cholangitis

A

Small bile ducts are affected

Associated with women/autoimmunity/sicca syndrome

Causes cholestasis- itching/pain/fatigue/weight loss/jaundice

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5
Q

Stepwise progression of ALD

A

Alcohol related fatty liver
Alcoholic hepatitis
Cirrhosis (irreversible)

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6
Q

Investigations for ALD

A

Bed side- observations, abdominal examination
Bloods- LFT FBC (anaemia- raised MCV) UE alphafetoprotein albumin clotting screen gamma GT viral serology (drinkers may be at more risk)
Imaging and specialist- Liver ultrasound, fibroscan- elastography, Biopsy, endoscopy (varices), CT/MRI (HCC)

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7
Q

Wernickes encepahlopathy triad

A

Confusion
Oculomotor disturbance
Ataxia (co-ordinated movements)

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8
Q

Korsakoff’s syndrome

A

Memory impairment- confabulation
Behavioural changes

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9
Q

Causes of liver failure

A

Acute- paracetamol overdose, alcohol

Chronic- viral hepatitis, yellow fever, alcohol, fatty liver disease, PBS, PSC, hemochromatosis, malignancy

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10
Q

Cirrhosis management

A

Alcohol abstinence
Ultrasound and alpha alphafetoprotein every 6 months
Endoscopy every 3 years (varices)
High protein low sodium diet
UKLED score every 6 months (assess transplant need)
Management of specific complications

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11
Q

Investigations for suspected pancreatic cancer

A

LFT, FBC, UE, calcium (metastatic cancer)
Ca19-9 tumour marker
CT abdomen (double duct sign)- investigation of choice

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12
Q

Pre-hepatic jaundice stool and urine

A

Normal stools
Normal urine

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13
Q

Hepatic jaundice stool and urine

A

Dark urine
Normal (pale) stools

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14
Q

Post-hepatic jaundice stool and urine

A

Dark urine
Pale stools (acholic)

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15
Q

Management of alcoholic liver disease

A

All investigations listed previously

Encourage to stop drinking alcohol- help from a detox regime
Nutritional support (esp. thiamine (B1) and protein)

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16
Q

Features of liver cirrhosis

A

Jaundice – caused by raised bilirubin
Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic cirulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease
Atrophic testes

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17
Q

Cirrhosis investigations

A

Bed side- observations, abdominal examination, ascetic tap (if relevant)
Bloods- LFT FBC UE alphafetoprotein viral serology (viral hepatitis) albumin clotting screen autoantibodies
Imaging and specialist- Liver ultrasound, fibroscan- elastography, Biopsy, endoscopy (varices), CT/MRI (HCC)

NB- Thrombocytopenia (platelet count <150,000 mm^3) is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease

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18
Q

Pancreatitis investigations

A

LFT FBC Lipase (longer half life than amylase) CRP haematocrit Ca (hypercalcaemia can cause it)
CXR exclude others causes
USS abdomen (gallstones?) or CT scan (goldstandard for chornic)(can do X-RAY- pancreatic calcification)
ERCP or MRCP

NB- a diagnosis can be made based on clinical findings and a lipase/amylase 3x normal level, but early USS is important to assess aetiology

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19
Q

Pancreatitis differentials

A

PUD, perforated viscous, oesophageal spasm, intestinal obstruction, AAA, cholangitis, cholecystitis, MI

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20
Q

Pancreatic cancer tumour marker

A

CA 19-9

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21
Q

Cholecystitis vs cholelithiasis/ biliary colic

A

Cholelithiasis causes biliary colic- repeated attacks of abdominal pain (often after a heavy meal- not necessarily fatty)

Cholecystitis- more acute illness. Inflamed gallbladder (usually due to stones) causes nausea, vomiting, pain and fever

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22
Q

Biliary colic/cholecystitis/cholangitis investigations

A

Bedside- observations, abdominal examination, urine dip (exclude UTI)
Bloods- FBC (WCC), UE (loss of appetite), LFT, CRP (inflammation- cholangitis), Calcium (can cause abdo pain), Lipid profile (increases chance of stones), cultures from 2 sites (if concerned about cholangitis) , Lipase/ amylase- rule out pancreatitis
Imaging- Abdominal ultrasound (look for stones), MRCP

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23
Q

Liver failure

A

Development of coagulopathy and encephalopathy (better to monitor PT time as it has a shorter half life than albumin)

In previously healthy person- acute
On background of cirrhosis- chronic

Fulminant- resulting from massive necrosis of liver cells

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24
Q

Liver failure symptoms

A

Jaundice, hepatic encephalopathy, fetor hepaticus, asterixis and apraxia

NB- cirrhosis would have all tell tale signs of liver disease (hepatomegaly, ascites, but difference with liver failure is that you get encephalopathy and deranged clotting)

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25
Q

Liver failure investigations

A

Mini mental state examination (test mental impairment/ encephalopathy)
FBC UE (hepatorenal syndrome) LFT Clotting screen ammonia Viral serology alpha fetoprotein
Abdominal ultrasound
CT scan
OGD- assess for varices

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26
Q

Management of alcoholic hepatitis

A

Glucocorticoids

NB- Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy
it is calculated by a formula using prothrombin time and bilirubin concentration

(Pentoxyphylline is sometimes used)

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27
Q

Management of ascites

A

Reduce dietary sodium- most important
Fluid restriction (sodium below 125)
Aldosterone antagonist eg. Spironolactone
Tense ascites- paracentesis (requires albumin cover eg. IV human albumin solution)
Prophylactic ABX if cirrhosis present and protein below 15 (ciprofloxacin)
Surgery- TIPS

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28
Q

Autoimmune hepatitis features

A

Signs of chronic liver disease or acute hepatitis (fever, jaundice etc.)
Amenorrhea

Investigations- ANA, SMA, LKM1, anti-LC1 antibodies, raised IgG, LFT- raised AST/ALT (hepatic picture), diagnosis can be confirmed via biopsy if in doubt

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29
Q

Management of autoimmune hepatitis

A

Steroids/other immunosuppressants eg. Azathioprine
Liver transplantation

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30
Q

Bile acid malabsorption

A

Causes of chronic diarrhoea

Causes
Primary- excessive bilateral acid production
Secondary- Crohn’s disease, cholecystectomy, coeliac disease

Investigation- SeHCAT scan

Management- bile acid sequestrant eg. Cholestyramine

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31
Q

Causes of budd chiari syndrome (hepatic vein thrombosis)

A

Polycythaemia rubra Vera
Thrombophilia eg. Antitnrombin III deficiency
Pregnancy
Combined OCP

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32
Q

Features of budd chiari syndrome

A

Sudden onset abdominal pain
Ascites
Tender hepatomegaly

USS with Doppler flow studies- gold standard (not venogram initially)

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33
Q

Drugs that cause hepatocellular liver disease

A

Paracetamol
Sodium valproate
MAOI
Anti TB drugs
Statin
Alcohol
Amiodarone

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34
Q

Drugs that cause cholestasis (+/- hepatic) liver disease

A

Combined OCP
Flucloxacillin, co amoxiclav, erythromycin
Anabolic Steroids
Chlorpromazine, prochlorperazine
Sulfonylureas

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35
Q

Drugs that can cause cirrhosis

A

Methotrexate
Methyldopa
Amiodarone

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36
Q

Gilbert’s syndrome

A

Autosomal recessive
Unconjugated hyperbilirubinaemia (not in urine)- jaundice may only be seen during an inter current illness, exercise, or fasting
Investigation- rise in bilirubin following fasting (do other tests to exclude other pathology)
No treatment

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37
Q

Features of haemachromatosis

A

Autosomal recessive

Lethargy and arthralgia (hands)- Pseudogout
Erectile dysfunction
Bronze skin pigmentation
Diabetes Mellitus
Stigmata of liver disease
Cardiac failure (dilated cardiomyopathy)
Hypogonadism (secondary to cirrhosis and pituitary dysfunction)
Cranial diabetes insipidus

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38
Q

Investigations for haemochromatosis

A

Iron studies
High transferrin saturation (men 55, women 50)
Raised ferritin and iron
Low TBIC

Imaging- liver biopsy (Perls stain), joint x ray (chondrocalcinosis (calcium deposits in joint space aka. pseudogout)), MRI whole body (iron deposits)

NB- obviously other tests to rule out other causes including bloods and exam, and HFE genetic testing for family members

NB- ferritin and transferrin % are used in monitoring

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39
Q

Management of haemochromatosis

A

Genetic counselling, avoid alcohol
Regular venesection (keep transferrin and serum ferritin below 50)
Desferrioxamine second line

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40
Q

Management of hepatic encephalopathy

A

Treat underlying cause
As with any delirium- reassure, calm, same staff, re orientate etc.
Lactulose first line, with rifaximin (ABX) for secondary prophylaxis of hepatic encephalopathy
Nutritional support. They may need nasogastric feeding.

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41
Q

Risk factors for HCC

A

Hepatitis B (world), hepatitis C (UK)
Alcohol
Haemachromatosis
NAFLD
Any chronic liver disease
PSC

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42
Q

Features of HCC

A

Late presentation of liver cirrhosis or failure stigmata
Raised AFP for HCC, Ca19-9 for cholangiocarcinoma

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43
Q

Management of HCC

A

Early disease- surgical resection
Liver transplant
Sorafenib

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44
Q

Ischaemic hepatitis

A

Acute hypoperfusion diagnosed in presence of an inciting event eg. Cardiac arrest and marked increase in aminotransferases
Often in conjunction with AKI

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45
Q

NAFLD associations

A

Obesity
T2DM
Hyperlipidaemia
Sudden weight loss or starvation

NB- insulin resistance is thought to be involved

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46
Q

Investigations for NAFLD

A

Bedside- observations, abdominal exam
Bloods- LFT, FBC, UE, Enhanced Liver Fibrosis (ELF) blood test (HA, PIIINP and TIMP-1)
Imaging and specialist- USS, NAFLD fibrosis score, fibroscan

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47
Q

Pancreatic cancer associations

A

Increasing age
Smoking
Diabetes
Chronic pancreatitis
HNPCC
MEN
BRAC2

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48
Q

Features of pancreatic cancer

A

Painless jaundice (pale stools, dark urine, pruritus)
Anorexia, weight loss, epigastric pain
Steatorrhoea (loss of exocrine function)
DM (loss of endocrine function)
Atypical back pain
Migratory thrombophlebitis

Cholestatic liver function tests

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49
Q

Histology of pancreatic cancer

A

80% are adenocarcinoma of the head of the pancreas

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50
Q

Management of a phonemic liver abscess

A

Caused by staph in children and E. coli in adults

Drain with ABX
Amoxicillin, ciprofloxacin, metronidazole

51
Q

What is Wilson’s disease

A

Excess copper deposition in bodily tissues

52
Q

Features of Wilson’s disease

A

Hepatitis, cirrhosis
Basal ganglia degeneration- Parkinsonism, asterixis, chorea
Speech, behavioural, dementia, psychiatric problems
Kayser-fleischer rings (green brown rings in periphery of iris)
Renal tubular acidosis
Haemolysis
Blue nails

53
Q

Investigations for Wilson’s disease

A

Slit lamp evaluation (Kayser-fleischer rings)
Reduced serum caeruloplasmin
Reduced total serum copper
Increased 24 hour urinary copper excretion
Liver biopsy

54
Q

Management of Wilson’s disease

A

Copper chelation using penicillamine (or trientene)

55
Q

Management of cholecystitis

A

Analgesia antiemetics fluids
IV antibiotics
Early laparoscopic cholecystectomy within 1 week of diagnosis

56
Q

Factors suggesting severe pancreatitis

A

55+
Hypocalcaemia
Hyperglycaemia
Hypoxia
Neutrophilia
Elevated LDH and AST

NB- amylase level isn’t of prognostic value

57
Q

Causes of pancreatitis

A

GallStones and alcohol are most common in UK

GET SMASHED

Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyper triglyceridaemia/hypercalcaemia/hypothermia
ERCP
Drugs- azathioprine, mesalazine, furosemide, valproate

58
Q

Complications of acute pancreatitis

A

Peripancreatic fluid collection- no wall of granulation tissue. No treatment

Pseudocysts- wall of fibrosis granulation tissue. 4 weeks after attack. Persistent mild elevation of amylase. Observe for 12 weeks, then radiological drainage

Pancreatic necrosis- necrosectomy has a high mortality rate

Pancreatic abscess

Haemorrhage- may see grey turners sign

ARDS- high mortality rate

59
Q

Management of acute pancreatitis

A

IV fluids
Analgesia (IV opioids)
Not NBM unless vomiting- offer enteral nutrition eg. NG
Don’t offer prophylactic ABX
Treat underlying cause eg. Cholecystectomy for gall stones, ERCP to remove stones in biliary system

60
Q

Management of ascending cholangitis

A

Conservative- pain relief, anti emetics, IV fluids, admit to hospital, bleep seniors/ general surgeons, oxygen, NBM
Medical- IV ABX (local policy)
Surgical- ERCP (remove blockage), cholecystectomy may be necessary

61
Q

Features of chronic pancreatitis

A

Epigastric pain radiating to the back
Pain worse 15-30 minutes after eating a meal
Steatorrhoea (5-25 years later)
DM (20 years later)

62
Q

Investigations for chronic pancreatitis

A

AXR
CT abdomen (investigation of choice- calcification)
Faecal elastase as a functional test (exocrine function)

63
Q

Management of chronic pancreatitis

A

Conservative- Analgesia, Abstinence from alcohol and smoking
Medical- Pancreatic enzyme supplements
Surgery- to treat complications such as cysts

Key complications of chronic pancreatitis include;

Loss of exocrine function, resulting in a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract
Loss of endocrine function, resulting in a lack of insulin, leading to diabetes

64
Q

Management of choledocholithiasis

A

Analgesia antiemetics antispasmodics
Surgical-ERCP to remove the stone

65
Q

Investigations for cholecystitis or cholangitis

A

Bedside- observations, A-E, full abdominal examination, pregnancy test (if appropriate)
Bloods- FBC UE LFT CRP 2x blood cultures ABG amylase and lipase
Imaging- RUQ USS

66
Q

When does delirium tremens occur

A

48-72 hours after termination of drinking

67
Q

Management of delirium tremens

A

Librium (chlordiazepoxide)
IV pabrinex (thiamine (B1) and vitamin C)

no lorazepam

68
Q

Management of liver failure

A

Supportive- NG tube, catheter, Haemodialysis, vitamin deficiencies etc,
Medical- laxatives
Surgical- transplant

69
Q

Features of hepatitis

A

Abdominal pain, fatigue, pruritus, myalgia, nausea and vomiting, jaundice, fever (viral hepatitis)

70
Q

Investigations for hepatitis of unknown cause

A

Observations, full abdominal examination

Bloods- FBC, UE, LFT gamma GT (alcohol), CRP, haemanitics, coagulation screen, viral serology, antibodies (autoimmune hepatitis)

Imaging- abdominal USS

71
Q

Features of acute pancreatitis

A

Constant severe epigastric pain, radiates to back, worse after meals and when supine, improves on leaning forward
Nausea and vomiting
Signs of shock and possible jaundice
Abdominal tenderness
Skin changes eg. Cullens or grey turners

72
Q

Alcoholic ketoacidosis

A

A non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol.

Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration

The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.

NB- Metabolic ketoacidosis with normal or low glucose: think alcohol

NB- this is different to alcoholic hepatitis where steroids are required

73
Q

Features of gallstones ie. biliary colic

A

Severe, colicky epigastric or right upper quadrant pain
Often triggered by meals (particularly high fat meals)
Lasting between 30 minutes and 8 hours
May be associated with nausea and vomiting

74
Q

Complications of biliary colic

A

Acute cholecystitis
Acute cholangitis
Obstructive jaundice (if the stone blocks the ducts)
Pancreatitis

75
Q

LFT in biliary colic/gallstones

A

Normal

If in bile duct- may show cholestatic picture eg. raised bilirubin, raised ALP (more so than ALT/AST)

76
Q

Management of gallstones

A

Asymptomatic- conservative ie. dietary and weight advice

Symptomatic- laparoscopic cholecystectomy

77
Q

Management of cholecystitis

A

Conservative- admission to hospital, NBM, NG tube, IV fluids
Medical- IV ABX
Surgical- ERCP (remove stones), cholecystectomy in 1 week

78
Q

Organisms that cause ascending cholangitis

A

Escherichia coli
Klebsiella species
Enterococcus species

79
Q

Common causes of cirrhosis

A

Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C

80
Q

Rare causes of cirrhosis

A

Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons Disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (e.g. amiodarone, methotrexate, sodium valproate)

81
Q

Scoring systems for cirrhosis

A

Child-Pugh- severity (bilirubin, PT time, ascites, encephalopathy, albumin)

UKMELD- 3 month mortality/ requirement for liver transplant ( bilirubin, creatinine, INR and sodium and whether they are requiring dialysis)

82
Q

Complications of cirrhosis

A

Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma

83
Q

Common locations of varices

A

Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)

84
Q

Predisposing factors for hepatic encephalopathy

A

Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative medications)

85
Q

General Management of ALD

A

Conservative- stop drinking alcohol, detox programme
Medical- nutritional support (thiamine (B1)), high protein diet, steroids (severe alcoholic hepatitis)
Further- Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy), Referral for liver transplant in severe disease (abstain from alcohol for 3 months prior to referral)

86
Q

Alcohol withdrawal timeline

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”

87
Q

Features of delirium tremens

A

Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias

88
Q

Non invasive liver screen (when cause of abnormal LFT’s is unknown)

A

Ultrasound Liver
Hepatitis B and C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)
Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)
Caeruloplasmin (Wilsons disease)
Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency)
Ferritin and Transferrin Saturation (hereditary haemochromatosis)

89
Q

Management of NAFLD

A

Conservative- Weight loss, Exercise, Stop smoking
Control of diabetes, blood pressure and cholesterol, Avoid alcohol

90
Q

Causes of hepatitis

A

Alcoholic hepatitis
Non alcoholic fatty liver disease
Viral hepatitis
Autoimmune hepatitis
Drug induced hepatitis (e.g. paracetamol overdose)

91
Q

Hepatitis A

A

RNA virus
Faeco-oral route
Most common worldwide
Cholestasis
Resolves without treatment
No complications
Vaccine- chronic LD/MSM/haemophilia/ high incidence/ IVDU/ occupational risks

92
Q

Hepatitis B

A

DNA virus
Blood born, sexual, and vertical transmission
Chronic infection, cirrhosis, HCC, polyarteritis nodosa, cryoglobulinemia
10% untreatable
Vaccine available

NB- The appearance of ground-glass hepatocytes on light microscopy can point towards a diagnosis of chronic hepatitis B infection

93
Q

Hepatitis C

A

RNA Virus
Blood borne, sexual, and vertical transmission
Chronic infection (majority), Cirrhosis , Hepatocellular cancer
Treatable with antivirals (ribavirin: no pregnancy for 6 months after)

94
Q

Hepatitis C

A

RNA Virus
Blood borne, sexual, and vertical transmission
Yes (80%)
Chronic infection, Cirrhosis , Hepatocellular cancer
Treatable with antivirals

95
Q

Management of hepatitis C

A

Conservative- screen for other blood borne diseases, refer to hepatology/ID, notify PHE, stop smoking and alcohol, education about transmission (contact tracing)
Medical- test for complications eg. fibro scan, Antiviral treatment with direct acting antivirals (DAAs)
Surgical- Liver transplantation for end-stage liver disease

96
Q

Hepatitis D

A

RNA virus
Can only survive with hepatitis B

97
Q

Hepatitis E

A

RNA virus
Transmitted via faeco-oral route
Disease is worse during pregnancy
Resolves without treatment- no long term complications or chronic infection

98
Q

What is primary biliary cholangitis

A

Immune system attacks small bile ducts in liver

99
Q

Features of PBC

A

Fatigue
Pruritus
GI disturbance and abdominal pain
Jaundice
Pale stools
Xanthoma and xanthelasma
Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)

100
Q

Associations with PBC

A

Middle aged women
Other autoimmune diseases (e.g. thyroid, coeliac)
Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis)

101
Q

Investigations for PBC

A

Bedside- abdominal examination, observations
Bloods- LFT (ALP raised), autoantibodies (AMA, ANA), IgM and ESR raised
Specialist- biopsy

102
Q

Treatment for PBC

A

Conservative- general lifestyle interventions
Medical- Ursodeoxycholic acid reduces the intestinal absorption of cholesterol and is used to prevent disease progression (even when asymptomatic), Colestyramine (prevents bile acid absorption and gives symptomatic relief from pruritus), immunosuppression (steroids)
Surgical- liver transplant (bilirubin >100)

103
Q

Complications of PBC

A

Advanced liver cirrhosis
Portal HTN
Symptomatic pruritus
Fatigue
Steatorrhoea (greasy stools due to lack of bile salts to digest fats)
Distal renal tubular acidosis
Hypothyroidism
Osteoporosis
Hepatocellular carcinoma

104
Q

What is primary sclerosing cholangitis (PSC)

A

A condition where the intrahepatic or extrahepatic ducts become strictured and fibrotic

105
Q

Risk factors for PSC

A

Male
Aged 30-40
Ulcerative Colitis
Family History

106
Q

Presentation of PSC

A

Jaundice
Chronic right upper quadrant pain
Pruritus
Fatigue
Hepatomegaly

107
Q

Investigations for PSC

A

Bedside- observations, abdominal examination
Bloods- LFT (cholestatic picture), UE, FBC etc. (no autoantibodies are highly sensitive or specific, but can try ANA pANCA (show if there is an immune component, may respond to immunosuppression)
Imaging- MRCP (diagnostic)

108
Q

Associations and complications of PSC

A

Acute bacterial cholangitis
Cholangiocarcinoma develops in 10-20% of cases
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble vitamin deficiencies

109
Q

Management of PSC

A

Conservative- general lifestyle measures, monitor for complications
Medical- cholestyramine (reduce bile acid absorption)
Surgical- ERCP (stent any strictures)

110
Q

Complications of haemochromatosis

A

Type 1 Diabetes (iron affects the functioning of the pancreas)
Liver Cirrhosis
Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
Cardiomyopathy (iron deposits in the heart)
Hepatocellular Carcinoma
Hypothyroidism (iron deposits in the thyroid)
Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis

111
Q

What is the only suspected cancers that GP’s can directly refer patients for a CT scan (don’t need to see specialist)

A

Pancreatic cancer

112
Q

Named signs in pancreatic malignancy

A

Courvoisier’s law- a palpable gallbladder along with jaundice is unlikely to be gallstones. The cause is usually cholangiocarcinoma or pancreatic cancer.

Trousseau’s sign of malignancy- migratory thrombophlebitis as a sign of malignancy, particularly pancreatic adenocarcinoma.

113
Q

Antibody associated with PBC

A

Anti mitochondrial (IgM)

114
Q

Constituents of pabrinex

A

Vitamin B1 (thiamine)
Vitamin C

115
Q

Difference in complications of PSC and PBC

A

PSC- cholangiocarcinoma and CRC

PBC- HCC, cirrhosis and subsequent variceal haemorrhage, osteoporosis

NB- cirrhosis more likely in PBC

116
Q

Antibiotic prophylaxis should be given to patients with ascites under what circumstances

A

-patients who have had an episode of SBP
-patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome

NB- oral ciprofloxacin or norfloxacin

117
Q

Scoring systems for acute pancreatitis

A

eg. Glasgow/APACHE

Some common criteria;

age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST

118
Q

Scoring systems for acute pancreatitis

A

eg. Glasgow/APACHE

Some common criteria;

age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST

NB- amylase level is not taken into account

119
Q

Gallstone Ileus

A

In gallstone ileus, a plain abdominal film classically shows small bowel obstruction and air in the biliary tree (symptoms similar to obstruction)

120
Q

Mirizzi’s syndrome

A

where a gallstone within the gallbladder compresses the bile duct to cause an obstructive jaundice

121
Q

Spider naevi vs telangiectasia

A

Spider naevi can be differentiated from telangiectasia by pressing on them and watching them fill. Spider naevi fill from the centre, telangiectasia from the edge

NB- spiders in the centre of their webs

122
Q

Stratification of Acute Pancreatitis

A

Mild No organ failure, no local complications
Moderately severe No or transient organ failure (<48 hours), possible local complications
Severe Persistent organ failure (>48 hours), possible local complications

123
Q

Management of a variceal bleed vs peptic ulcer bleed

A

Same stabilisation techniques
Variceal- terlipressin/IV AVX/ endoscopic intervention eg. band ligation
Peptic ulcer- IV PPI/ endoscopic intervention (adrenaline injection)

Year 3 OSCE (61 decks)

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