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Year 3 > Case Nine - Acute cholecystitis > Flashcards

Case Nine - Acute cholecystitis Flashcards

1
Q

what is acute cholecystitis caused by

A

a blockage in the cystic duct or neck of the gallbladder (95% of the cases are gallstones or sludge)

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2
Q

what can the obstruction cause

A

increase in mucus secretions from the gallbladder which causes gallbladder distension, and may affect the blood supply to the gallbladder

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3
Q

what is often the initial event in cholecystitis

A

often an obstruction to gallbladder emptying

in 95% of the cases, a gallstone is the cause. it is different to biliary colic because it is not a problem in the bile duct, but a problem in the gallbladder or in the cystic duct

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4
Q

what are the two effects of distension of the bile ducts

A

obstruction of blood flow to the gallbladder, as well as initiating an inflammatory response to the bile retained in the gallbladder

this can lead to mucosal damage, which in turn leads to the release of phospholipase,

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5
Q

what does phospholipase do

A

converts lecithin into lysolecithin which is a very potent toxin

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6
Q

what are the symptoms of acute cholecystitis and what are the y similar to

A

similar to biliary colic, and often differentiation is difficult

cholecystitis often results in a more prolonged pain with a fever and leukocytosis

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7
Q

what is Murphys sign

A

there will be RUQ pain

this is usually worse on inspiration. Murphy’s sign is where you would put your hand under the patient’s ribs and ask them to breathe in. As they do so, their gallbladder will be forced down against your hand, and it will cause them a lot of pain

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8
Q

when is Murphy’s sign only a positive result

A

only a positive result if the sign is negative in the LUQ

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9
Q

why does the pain radiate in acute cholecystitis and how does this differentiate

A

the pain is more likely to radiate to the shoulder tip in this than in other biliary conditions because the radiation is caused by irritation of the diaphragm and this is more likely in cholecystitis

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10
Q

what are the investigations carried out for acute cholecytsisis

A

FBC
serum amylase
serum bilirubin
USS

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11
Q

what would an FBC in acute cholecystitis show

A

raised ESR, CRP, WCC

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12
Q

what would a serum amylase show

A

increase as acute pancreatitis may be present as a compliation of gallstones

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13
Q

what would the USS detect

A

gallstones
gallbladder wall thickening
dilated common bile duct >6mm

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14
Q

what are the antibiotics given in acute cholecystitis

A

cefuroxime
metronidazole

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15
Q

what are the pain reliefs given in acute cholecysistis

A

usually diclofenac (NSAID) with pethidine (fast acting opioid) in more severe cases

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16
Q

what are the complications of acute cholecystitis

A

gangrene
bacterial infection and subsequent empyema

perforation

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17
Q

what is empyema

A

this is a collection of pus in the body cavity . it is different from an abcess, which is a colleciton of pus in a newly formed body cavity

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18
Q

what may be seen in patients with chronic cholecystisis

A

vague abdominal symptoms
sometimes associated with GI malignancy

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19
Q

what investigations are used to look for chronic cholecystitis

A

USS - evidence of gallstones and check common bile duct diameter

MRCP - may also be used to check for stones. In this procedure, MRI scanning is used to visualise the biliary tree. It is much less invasive than ERCP - which requires the insertion of dye into the biliary tree via OGD. ERCP has obvious therapeutic advantages that MRCP does not.

M,RCP is used to supplement USS

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20
Q

what is the treatment of chronic cholecystitis

A

ERCP - usually performed to remove any stones from the common bile duct and perform sphincterotomy before cholecystectomy

cholecystectomy - performed in troubling cases

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21
Q

what does the inflammatory response in acute cholecystitis cause

A

wall ischaemia and infection to ensue to cause localised peritonitis

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22
Q

what are the several modalities used to image a stone in the common bile duct

A

transabdominal ultrasound first line
MRCP
EUS

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23
Q

what is the gold standard for visualising stones in the CBD

A

endoscopic ultrasound (EUS)

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24
Q

why must any CBD stones causing obstructive jaundice be removed first prior to a laparoscopic cholecystectomy

A

a high biliary pressure from any obstruction can cause a bile leak from the cystic duct stump where the gallbladder is amputated during the cholecystectomy

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25
Q

what does a thickened wall gallbladder indicate

A

either acute or chronic inflammation of the gallbladder

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26
Q

what kind of finding is pericholecystic fluid

A

an acute finding

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27
Q

what is the intial treatment in AandE of acute cholecystitis

A

Initial treatment would include:
- Analgesia
- Antiemetics
- Antibiotics (according to hospital guidelines)
- Fluid balance (intravenous fluids)
- Venous thromboembolism prophylaxis
- Nil by mouth, in anticipation for surgery

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28
Q

what definitive management would you offer

A

laparoscopic cholecystectomy

surgery should be considered to remove the gallbladder on the same hospital admission (laparoscopic cholecystectomy)

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29
Q

what are the risks of laparoscopic cholecystectomy surgery

A

The general risks of surgery include bleeding, infection, pain, chest and urinary infections, deep vein thrombosis/pulmonary embolism and risks associated with general anaesthesia. Specifically for a laparoscopic cholecystectomy:
- Damage to the common bile duct
- Bile leak
- Damage to surrounding structures (such as the duodenum or stomach)
- Conversion from a laparoscopic procedure to an open procedure

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30
Q

what are the components of Charcot’s triad for diagnosing acute cholangitis

A

right upper quadrant pain
jaundice
pyrexia

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30
Q

what does Reynolds pentad include

A

it has the three components of Charcot’s - RUQ pain, jaundice and temp

but it also includes mental status alterations and sepsis

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31
Q

what does an obstructive pattern of jaundice to the LFT’s suggest

A

common bile duct obstruction

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32
Q

what is the definition of acute cholangitis

A

infection of the biliary tree caused by a downstream obstruction of the common bile duct

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33
Q

what are the causes of acute cholangitis

A

cholelithiasis (most common)
benign biliary structure
sclerosing cholangitis
malignant strictures

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34
Q

what are the risk factors for acute cholangitis

A

age
history of gallstones
previous biliary surgery that may lead to a narrowing of the bile duct

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35
Q

what investigations should be performed to investigate a suspected diagnosis of acute cholangitis

A

an urgent US of the abdomen should be performed to investigate the cause of the biliary obstruction

relieving the biliary obstruction will treat the cute cholangitis

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36
Q

what are the principles of treating a common bile duct obstruction

A

to either remove the cause or relieve the obstruction using a stent (in the case of a stricture)

this can be achieved endoscopically by an ERCP

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37
Q

what is an ERCP

A

endoscopic retrograde cholangiopancreatohraphy

it is an endoscopic procedure where a side viewing endoscope is used to identify and cannulate the ampulla of Vater which opens into the second part of the duodenum

a radio-opaque dye is then injected retrograde and passes up Into the CBD and the pancreatic duct

fluoroscopy are used to visualise the dye to detect any ‘filling defects’ that could indicate either a stone or a stricture

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38
Q

what is the advantage of an ERCP

A

that it can also be used to perform certain therapeutic procedures in the same procedure, such as extracting the stone using a wire basket, a sphincterterotomy of the sphincter of Oddi (to better allow the passage of bile) to to insert a stent across the obstruction to relieve the jaundice

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39
Q

what is ERCP NOT used for

A

a diagnostic procedure

first line is USS and MRCP to diagnose the cause of the biliary obstruction before an ERCP os performed

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40
Q

what are the risks of ERCP

A

acute pancreatitis (5%)
gastric/duodenal perforation
bleeding
risks associated with sedation

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41
Q

what is the initial treatment for acute cholangitis

A

Initial treatment would include:
● Analgesia
● Antiemetics
● Antibiotics (according to hospital guidelines)
● Fluid balance (intravenous fluids and urinary catheter)
● Venous thromboembolism prophylaxis
● Nil by mouth, in anticipation for an ERC

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42
Q

how would you treat acute pancreatitis after ERCP for acute cholangitis

A

analgesia
antiemetics
no antibiotics (still on these for cholangitis)
fluid balance
VTP

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43
Q

what is not a risk factor for developing gallstone disease

A

younger age

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44
Q

what condition is not associated with gallstone disease

A

peptic ulcer disease

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45
Q

what is Mirizzi’s syndrome

A

this is compression of the CBD from a gallstone in Hartmann’s pouch

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46
Q

A 35-year-old woman presents with intermittent right upper quadrant pain which lasts for a few hours each time she eats fatty foods. Bloods show a normal WCC and CRP, as well as normal LFTs and lipase. What is the most likely diagnosis?

A

biliary colic

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47
Q

A 78-year-old female presents with a 1-day history of confusion and ‘generally unwell’. She has a past medical history of hypertension and is known to have gallstones. Her observations are: BP 90/75, HR 120, RR 20 and a temperature of 38.9°C. On examination, she is visibly jaundiced, and she has guarding in her right upper quadrant. An urgent ultrasound scan shows a dilated common bile duct of 10mm with intrahepatic duct dilatation. After initial treatment of ABCDE, what is the definitive management of this patient?

A

ERCP

this is the most appropriate treatment to clear the CBD of obstructing stones to treat the acute cholangitis

48
Q

what is pancreatitis

A

condition involving inflammation of the pancreas. it can be acute or chronic

49
Q

what accounts for the vast majority of pancreatitis episodes

A

gallstones and alcohol

50
Q

what is the pneumonic used to remember the causes of pancreatitis

A

GET SMASHED

51
Q

what does each letter in GET SMASHED stand for

A

G – Gallstones
E – Ethanol (alcohol!)
T – Trauma
S – Steroids
M – Mumps
A – Autoimmune – e.g. SLE
S – Scorpion bites (rare!)
H – Hypercalcaemia, hypothermia, hyperlipiaemia
E – ERCP
D – Drugs – e.g. azathiaprin

52
Q

what are the four steps of pathogenesis of pancreatitis

A

necrosis
autolysis
infection
pseudocyst

53
Q

explain the pathogenesis of pancreatitis

A
  • the final common pathway has marked increase in intracellular calcium which then leads to activation of intracellular proteases
  • there is evidence that alcohol interferes with calcium homeostasis in pancreatic acinar cells
  • in severe inflammation, it becomes swollen and haemorrhaic
  • proteases digest the walls of the blood vessel which leads to blood extravasation
  • amylase is release into the blood
  • released lipase cause fat necrosis within the abdomen and subcutaneous tissue
54
Q

what can the released lipase cause

A

discolouration of the skin - Grey Turner’s sign

55
Q

what can the released fatty acids bind to and what does this lead to

A

bind to Ca2+ and this leads to Hypocalcaemia

56
Q

what can concomitant destruction of adjacent islets do

A

lead to hyperglycaemia and thus can cause type II diabetes

57
Q

what is pulmonary failure in acute pancreatitis believed to be caused by

A

circulating activated digestion enzymes

58
Q

what are these digestion enzymes

A

trypsin, phospholipase A2 etc

59
Q

what does this circulating level of activated digestion enzymes lead to

A

a loss of surfactant, atelectasis and irritation eventually leading to ARDS, and pleural effusion

60
Q

what else can also occur in severe acute pancreatitis

A

cardiac depression and breakdown of the BBB

61
Q

what are the clinical features of acute pancreatitis

A

upper abdominal pain, normally beginning in the epigastrium accompanied by nausea and vomiting

often radiates too the back

62
Q

in severe cases of AP, what other symptoms can people have

A

tachycardia, hypotension and be oliguric

63
Q

what would an abdominal examination show

A

widespread tenderness with guarding; also reduced/absent bowel sounds

64
Q

what is Cullens sign

A

periumbilical bruising

65
Q

what is Grey Turner’s sign

A

flank bruising

66
Q

when are Cullens and turners signs present

A

in severe necrotiising pancratiits

67
Q

what is indicative in poor prognosis

A

left sided pleural effusion

68
Q

what will blood tests show in pancreatitis

A

raised serum amylase, lipase , also with raised urinary amylase

69
Q

is amylase prognostic

A

no, nor is the level related to the degree of tissue damage

70
Q

what is the most specific blood test for pancreatitis

A

lipase levels, and may relate to the level of tissue damage, but levels do not rise up until 8 hours after the onset of symptoms

71
Q

what imaging is used to exclude gaastroduodenal perforation

A

CXR is used which also causes raised serum amylase

72
Q

what is the treatment for pancreatitis

A

replace lost fluids

nasogastric suction to prevent abdominal distension and vomiting

analgesia - pethidine and tramadol

enteral nutrition

73
Q

what are the three key cases of pancreatitis to remember

A

gallstones
alcohol
post-ERCP

74
Q

how does alcohol cause pancreatitis

A

directly toxic to pancreatic cells, resulting in inflammation.

75
Q

how much is amylase raised in pancreatitis

A

raised more than three times the upper limit of normal in acute pancreatitis

in chronic pancreatitis it may not rise because the pancreas has reduced function

76
Q

what is the Glasgow score

A

used to assess the severity of pancreatitis. it gives a numerical score based on how many of the key criteria are present:

0 or 1 – mild pancreatitis
2 – moderate pancreatitis
3 or more – severe pancreatitis

77
Q

how can the criteria for the Glasgow score be remembered

A

using the PANCREAS pneumonic (1 point for each answer)

P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)

78
Q

what may be required in chronic pancreatitis if there is loss of pancreatic enzymes

A

Creon

79
Q

what are the two types of hiatus hernia

A

sliding hiatus hernia and rolling hiatus hernia

80
Q

what is the most common type of hernia

A

sliding hiatus hernia. accounts for 95% of cases

81
Q

what are they associated with

A

an increased incidence of GORD

82
Q

what is a sliding hiatus hernia

A

when part of the stomach at the oesophageal gastric junction is pulled upwards through the diaphragm

this reduces the angle between the oesophagus and the stomach, and thus removes one of the natural anatomic barriers to reflux.

83
Q

how is the sliding hiatus hernia covered

A

only by peritoneum on its lateral and anterior sides

the posterior is not covered due to the bare area on the back of the stomach

84
Q

when does a rolling hiatus hernia occur

A

when part of the fundus of the stomach will extend through the diaphragm at a separate site to the oesophagus
they can sometimes be huge, with almost the whole stomach becoming herniated, leading the gastro-oesophageal function lying right alongside the pylorus

85
Q

what is the rolling hiatus hernia surrounded by

A

completely surrounded by a peritoneal sac

86
Q

what are the three key complications of hernias

A

Incarceration
Obstruction
Strangulation

87
Q

what does Courvoisier’s law state

A

Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

88
Q

what are the features of carcinoid syndrome

A

abdominal pain
diarrhoea
flushing

releases serotonin into systematic circulation when there is metastasis to the liver

89
Q

what is the AST/ALT ratio in alcoholic hepatitis

A

the ratio is 2:1

90
Q

what diagnosis has a positive pANCA test

A

primary sclerosing cholangitis

91
Q

what is upper GI bleeding

A

bleeding from the oesophagus, stomach or duodenu

92
Q

what are the causes of upper GI bleeding

A

peptic ulcers
Mallory-Weiss tear
Oesophogeal Marikes
stomach cancers

93
Q

what is a Mallory Weiss tear

A

a tear of the oesophagus mucosa

94
Q

what is the presentation of upper GI bleeding

A

haematemesis (vomiting blood)
coffee ground vomit
melaena

95
Q

what is the cause of coffee ground vomit

A

caused by vomiting digested blood with the appearance of coffee grounds

96
Q

what does haemodynamic instability occur with

A

significant blood loss, causing low blood pressure, tachycardia, and other signs of shock

97
Q

what are peptic ulcers associated with

A

history of epigastric pain and dyspepsia

they may be taking NSAIDS

98
Q

when do Mallory Weiss tears occur

A

after heavy retching or vomiting, which may be caused by binge drinking, gastroenteritis, or hyperemesis gravidum

99
Q

when does hyperemesis gravidarum occur

A

during early pregnancy

100
Q

what are oesophageal varcices associated with

A

liver cirrhosis and portal hypertension

the patient will have signs of these conditions, such as ascites, jaundice and caput medusae

101
Q

what is stomach cancer associated with

A

history of weight loss, epigastric pain, treatment resistant dyspepsia, low haemoglobin (anaemia) and a raised platelet count

102
Q

what is the bleeding score used in the initial presentation of a suspected upper GI bleed

A

the Glasgow-Blatchford score

103
Q

what does the Glasgow-Blatchford score do

A

estimates the risk of patient having an upper GI bleed

104
Q

what score on the Glasgow Blatchford scale indicates high risk bleed

A

a score above 0 indicates a high risk for an Upper GI bleed

105
Q

what factors does the Glasgow-Blatchford score take into account

A

Haemoglobin (falls in upper GI bleeding)
Urea (rises in upper GI bleeding)
Systolic blood pressure
Heart rate
Presence of melaena (black, tarry stools)
Syncope (loss of consciousness)
Liver disease
Heart failure

106
Q

what is the association between an upper GI bleed and increased blood urea

A

acid and digestive enzymes break down blood in the upper GI tract.

one of the breakdown products is urea, which is then absorbed into the intestines, causing a rise in blood urea

107
Q

what is the management of an upper GI bleed

A

the ABATED pneumonic

108
Q

what does the ABATED pneumonic stand for

A

A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 x large bore cannula)
T – Transfusions are required
E – Endoscopy (within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

109
Q

what do you send bloods for in suspected GI bleed

A

Haemoglobin (FBC)
Urea (U&Es)
Coagulation (INR and FBC for platelets)
Liver disease (LFTs)
Crossmatch 2 units of blood

110
Q

what is group and save

A

when the lab checks the patient’s blood group and saves a blood sample to match blood if needed.

crossmatch is where the lab allocated units of blood, tests that it is compatible and keeps it ready in the fridge

111
Q

when are blood, platelets and clotting factors given

A

to patients with a massive bleed

112
Q

what is given in active bleeding

A

platelets are given in active bleeding plus thrombocytopenia (platelet count less than 50)

113
Q

what is given to patients taking warfarin that are actively bleeding

A

prothrombin complex concentrate

114
Q

what are the additional steps taken if oesophageal varies are suspected

A

terlipresisn
broad spectrum antibiotics

115
Q

what is required to diagnose and treat the source of the bleeding

A

OGD
(endoscopy)

116
Q

what do the NICE guidelines recommended against using until after Endoscopy in patients with non-varicial upper GI bleeding

A

recommend against using a proton pump inhibitor

117
Q
A

Year 3 (63 decks)

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