Hamzah's liver and friends pathology Flashcards
1
Q
What is liver failure?
A
When the liver is losing or has lost all of its function
- LOSS OF LIVER’S ABILITY TO REGENERATE ITSELF
2
Q
What is acute hepatic failure?
A
Liver failure occurring suddenly in a healthy liver
3
Q
What is chronic hepatic failure?
A
liver failure as a result of background cirrhosis
4
Q
What is fulminant hepatic failure?
A
A clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of renal function
5
Q
Aetiology of liver failure
A
- Infections - Viral hepatitis (B, C), yellow fever
- Drugs - paracetamol overdose, halothane
- Toxins - amanita phalloides mushroom, CCl4
- Vascular - Budd-Chiari syndrome, Veno-occlusive disease
- Others - alcohol, haemochromatosis, malignancy
6
Q
Pathophysiology of liver failure
A
Depends on the aetiology
generally = destruction of hepatocytes –> fibrosis in response to chronic inflammation
The destruction of the architecture of the nodules of the liver removes the liver’s ability to adequately perform functions, repair and regenerate.
7
Q
Symptoms of liver failure
A
RUQ pain, nausea and vomiting
8
Q
Signs of liver failure
A
jaundice hepatic encephalopathy fetor hepaticus - pear drop smell asterixis - tremor of hand construction apraxia - cannot copy a 5 pointed side
9
Q
Diagnostic tests for liver failure
A
Blood = FBC, U&Es, LFT, clotting, glucose, paracetamol levels, hepatitis, ferritin, autoantibodies Microbiology = blood culture, urine culture, aseptic tap for MC&S Radiology = CXR, abdominal ultrasound Raised bilirubin Low glucose (no gluconeogenesis)
10
Q
Treatment of liver failure
A
ITU - protect the airway, monitor vitals, insert catheters Treat cause if known IV glucose to avoid hypoglycemia Check FBC, U&Es, LFTs, INR daily optimise nutrition - give thiamine (B1 vit) and folate supplements Lorazepam or Phenytoin for seizures Haemodialysis if renal failure develops Liver transplantation in severe cases
11
Q
Complications of liver failure
A
cerebral oedema –> 20% mannitol IV, hyperventilate
ascites –> salt and fluid restriction, diuretics
bleeding –> vitamin K, blood transfusion
blind antibiotics for infection –> ceftriaxone (NOT GENTAMICIN AS INCREASED RISK OF RENAL FAILURE)
Encephalopathy –> avoid sedatives, correct electrolytes, lactulose
Hypoglycemia –> IV glucose
12
Q
What is used to treat a paracetamol overdose?
A
acetylcysteine
13
Q
What is used to treat a opioid overdose?
A
naloxone = (opioid receptor antagonist)
14
Q
Where is bile produced and concentrated?
A
produced in the liver
stored and concentrated in the gall bladder
15
Q
what does bile contain?
A
water, bile acids, phospholipids, cholesterol
16
Q
Bile functions
A
lipid digestion and absorption
cholesterol homeostasis
antimicrobial
17
Q
What are cholesterol stones?
A
large –> caused by high cholesterol, obesity, FH, Male gender
18
Q
What are pigment stones?
A
small, irregular and friable stones. made of unconjugated bilirubin and calcium
19
Q
What are mixed stones?
A
faceted (calcium salts, pigment and cholesterol)
20
Q
Risk factors for bile stones becoming symptomatic
A
smoking and giving birth
21
Q
What is a biliary colic?
A
Term used for the pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the gallbladder
22
Q
Clinical presentation for biliary colic
A
RUQ pain that radiates to back
Can have jaundice
23
Q
What is acute cholecystitis?
A
A stone lodged at the neck of the gallbladder causes obstruction of gallbladder emptying.
If stone moves to common bile duct –> obstructive jaundice and cholangitis
24
Q
Symptoms of acute cholecystitis
A
Vomiting, fever, local peritonitis, gallbladder mass
Continuous epigastric or RUQ pain –> referred to right shoulder
25
Signs of acute cholecystitis
Murphy's sign = place 2 fingers over RUQ, ask patient to breathe in --> causes pain and arrest of inspiration as gallbladder impinges on finger
26
What is the main difference between a biliary colic and acute cholecystitis?
acute cholecystitis involves an inflammatory component --> local peritonitis, fever, high white cell count
27
Diagnostic tests for acute cholecystitis
High WCC
US - thick walled, shrunken gallbladder, common bile duct dilatation, stones
AXR - only shows 10% of gallstones
HIDA scan
28
Treatment of acute cholecystitis
nil by mouth, pain relief, IV fluids, IV antibiotics, laparoscopic cholecystectomy
29
What is chronic cholecystitis?
repeated attacks of pain (biliary colic) --> the gallbladder is damaged by repeated attacks of acute inflammation
30
Clinical presentation of chronic cholecystitis
```
Flatulent dyspepsia = vague abdominal discomfort
Distension
Nausea
Flatulence
Fat intolerance
```
31
Diagnostic tests for chronic cholecystitis
US - to image stones and assess common bile duct diameter
| MRCP - to find stones
32
Treatment of chronic cholecystitis
cholecystectomy
33
What is cholangitis
a bile duct infection
34
Common bacteria that cause cholangitis
Escherichia coli, Klebsiella
35
Clinical presentation of cholangitis
RUQ pain, jaundice, fever = Charcot's triad
36
Treatmnet of cholangitis
cefuroxime (antibiotic)
37
Complications of gallstones in the gallbladder and cystic duct
biliary colic, acute and chronic cholecystitis, empyema
38
Complications of gallstones in the bile ducts
obstructive jaundice, cholangitis, pancreatitis
39
Complications of gallstones in the gut
Gallstone ileus
40
What is acute pancreatitis?
inflammation of the pancreas and peripancreatic tissues by enzyme-related autodigestion.
Oedema and fluid shift causes hypovolaemia as ECF is trapped in the gut, peritoneum and retroperitoneum
41
Aetiology of acute pancreatitis
GET SMASHED
gallstones and alcohol abuse = main causes
trauma, steroids, autoimmune, hypercalcaemia, drugs, ERCP
Idiopathic
42
RIsk factors for acute pancreatitis
excessive alcohol consumption
FH
obesity
smoking
43
Pathogenesis of acute pancreatitis
- Injury to the pancreas leads to the release and activation of digestive enzymes which cause necrosis of pancreatic and peripancreatic tissue
- Exudation of plasma into the retroperitoneal space leads to hypovolaemia and cardiovascular instability
44
Symptoms of acute pancreatitis
- Epigastric/central abdomianl pain. (pain becomes more intense as inflammation spreds throughout the peritoneal cavity)
- Pain radiates to back
- Sitting may relieve pain
- Vomiting
45
Signs of acute pancreatitis
- Tachycardia, fever, jaundice, shock, ileus
- Cullen's sign (periumbilical bruising) and Turner's sign (flank bruising) - from blood vessel autodigestion and retroperitoneal haemorrhage
- Fox's sign = bruising seen over the inguinal ligament (occurs in patients with retroperitoneal bleeding)
46
Differential diagnosis of acute pancreatitis
IBS, MI, gastroenteritis, DKA, pneumonia, malaria
47
Diagnostic tests for acute pancreatitis
raised serum amylase (above 3x upper limit)
urinary amylase
serum lipase
AXR - no psoas shadow (due to increased retroperitoneal fluid)
48
Treatment of acute pancreatitis
supportive therapy - oxygen, analgesia, nil by mouth, IV saline
antibiotics
49
Early complications of acute pancreatitis
Shock, ARDS, renal failure, DIC, sepsis, hypocalcaemia
50
Late complications of acute pancreatitis
Pancreatic necrosis, bleeding, thrombosis, fistulae
51
What is chronic pancreatitis?
A chronic inflammatory process of the pancreas leading to irreversible loss of pancreatic function
52
Aetiology of chronic pancreatitis
most cases = alcohol abuse
| autoimmune, CF, pancreatic duct obstruction, hyperparathyroidism
53
Pathophysiology of chronic pancreatitis
- The inappropriate activation of enzymes within the pancreas leads to protein plugs developing in the lumen of ducts.
- This leads to ductal hypertension and further pancreatic damage.
- Increased cytokine activation leads to pancreatic inflammation.
Irreversible morphological change --> loss of pancreatic function
54
Clinical presentation of chronic pancreatitis
- Epigastric pain bores through to back - relieved by sitting forward or hot water bottles
- Bloating, steatorrhoea, DM occur late when most of the gland is destroyed
- Weight loss
55
Diagnostic tests for chronic pancreatitis
US/CT - look for pancreatic calcifications
MRCP and ERCP - rises in acute attack
AXR - speckled calcification
56
Treatment of chronic pancreatitis
- Drugs = analgesia, lipase, fat-soluble vitamins, insulin
- Diet = no alcohol, low-fat diet
- surgery = pancreatectomy or pancreatojejunostomy
57
Complications of chronic pancreatitis
Pseudocyst, diabetes, biliary obstruction, pancreatic carcinoma
58
What is alcoholic liver disease?
liver disease due to excessive alcohol consumption
59
3 patterns of alcoholic liver disease
steatosis
alcoholic steatohepatitis (ASH)
cirrhosis
60
In who is alcoholic liver disease most common?
men in their 50s
61
Pathogenesis of alcoholic liver disease
- Alcohol metabolism in the liver generates high levels of NADH which stimulates fatty acid synthesis and production of triglycerides, leading to steatosis
- Oxidative stress from alcohol metabolism leads to hepatocyte injury and necro-inflammatory activity
- Ongoing necro-inflammtory activity causes liver fibrosis --> cirrhosis
62
Stages of alcoholic liver disease
1. steatosis - drinking large volumes of alcohol causes fatty acids to collect in the liver
2. Alcoholic steatohepatitis = continued alcohol intake will lead to ingoing liver inflammation (hepatocytes contain Mallory's hyaline)
3. cirrhosis - fibrosis occurs due to chronic inflammation of the liver
63
Risk factors for alcoholic liver disease
Excessive alcohol consumption
female gender
Genetic factors
64
Clinical features of alcoholic hepatitis
rapid onset jaundice
| Nausea, anorexia, RUQ pain, encephalopathy, fever, ascites, tender hepatomegaly
65
Diagnostic tests in alcoholic hepatits
- FBC - leucocytosis, elevated MCV, thrombocytopenia (bone marrow hyperplasia)
- U&Es - hyponatremia (increased release of ADH)
- LFTs - elevated AST and ALT (disproportionate rise in AST), elevated bilirubin
- MCS of blood, urine and ascitic fluid
- US
66
Treatment/management of alcoholic hepatitis
Supportive therapy
Possible NG feeding
alcohol cessation
corticosteroids - prednisolone (if ver severe)
67
Alcoholic corrhosis
= FInal stage of alcoholic liver disease
Destruction of liver architecture and fibrosis --> regenerating nodules produce micronodular cirrhosis
Treatment = liver transplantation
68
Complications of alcoholic liver disease
If untreated = liver failure
69
What is cirrhosis?
= Irreversible replacement of normal liver architecture by bands of fibrous tissue separating nodules of regenerating hepatocytes
70
Aetiology of cirrhosis
alcohol abuse, HBV, HCV, non-alcoholic fatty liver diseases
rare = haemochromatosis, Wislon's disease
drugs = amiodarone
71
Pathophysiology of cirrhosis
persistent injury leads to Kupffer cells releasing cytokines which activate ito (stellate) cells
stellate cells secrete large amounts of dense collagen --> irreversible liver fibrosis and hepatocyte loss
72
Effects of cirrhosis
- reduced synthesis of coagulation factors
- low glycogen stores
- reduced clearance of organisms by Kupffer cells
- portal hypertension with hypersplenism and oesophageal varices
- splanchnic vasodilation --> decreased renal bloodflow --> secondary hyperaldosteronism --> ascites
73
Symptoms of cirrhosis
upper abdominal pain, nausea, vomiting, weight loss, weakness, easily bruising
74
Signs of cirrhosis
Pruritus and jaundice
rasied LFTs
clubbing
palmar erythema
xanthelasma - yellowish deposits of cholesterol underneath the skin
Terry's nails - white proximally but distal 1/3 reddened
leukonychia - white discolouration appearing on nails
Spider naevi
75
Complications of cirrhosis
- Hepatic failure - coagulopathy, encephalopathy, hypoalbuminemia
- Portal hypertension
- Increased risk of HCC
76
Diagnostic tests for cirrhosis
- Bloods - LFTs raised, raised bilirubin, low albumin, low leukocytes and platelets
- Liver US and doppler - small/enlarged liver, splenomegaly, ascites, reversed flow in portal vein
- MRI - big caudate lobe
- Ascitic tap - send for MCS (blood culture)
- Liver biopsy = confirms clinical diagnosis
77
Treatment of cirrhosis
General = good nutrition, alcohol abstinence, avoid NSAIDs, sedatives and opiates
cholestyramine - pruritus
treat underlying cause
Liver transplant = the only definitive treatment for cirrhosis
78
What is portal hypertension?
= An increase in the blood pressure in the hepatic portal system
79
Aetiology of portal hypertesnion
most common = cirrhosis
| blood clots in portal vein, schistosomiasis, IVC obstruction, right sided HF
80
Complications of portal hypertension
oesophageal varices, ascites, splenomegaly --> anaemia, low leukocyte count, thrombocytopenia
81
Symptoms of portal hypertension
black and bloody stools
| vomiting of blood
82
Signs of portal hypertension
Ascites, splenomegaly, anorectal varices, oesophageal varices, caput medusae (swollen veins on anterior abdominal wall)
83
Diagnostic tests for portal hypertension
Abdominal US - dilated portal vein
| Ascites
84
Treatment of portal hypertension
Beta blockers = reduce pressure in varices
portosystemic shunts
transjugular intrahepatic portosystemic shunting (TIPS)
lactulose --> hepatic encephalopathy
85
What is acute viral hepatitis?
infection of the liver by hepatitis A, B, C, D, E lasting <6 months
86
What is chronic viral hepatitis?
infection of the liver by hepatitis B. C, D lasting >6 months
87
What viral hepatitis types are common worldwide?
HAV and HCV
88
Clinical presentation of viral hepatitis
fever, malaise, anorexia, nausea, arthralgia (joint pain)
| THEN: jaundice, hepatosplenomegaly, lymphadenopathy
89
Hepatitis A
- RNA virus
- faecal-oral transmission
- endemic in africa and south america
- incubation = 2-6 weeks
- AST and ALT rise 22-40 days after exposure
- IgG detectable for life
Treatment = supportive therapy, avoid alcohol
90
Hepatitis B
- DNA virus
- blood/body fluid transmission
- incubation = 1-6 months
- signs = arthralgia and urticaria are more common
- Diagnostic tests = HbsAg (surface antigen) present for 1-6 months after exposure, HbeAg present for 1.5-3 months after acute illness
- vaccination
- treatment = avoid alcohol, immunise sexual contacts, antivirals,
91
Complications of Hep B
Cirrhosis, HCC, fulminant hepatic failure, cholangiocarcinoma
92
What type of virus is HCV?
RNA flavivirus
93
Transmission of HCV
blood/body fluids - transfusion before 1991, IVDU, secual intercourse, acupuncture
94
risk factors for HCV progression
males, older age, higher viral load, alcohol use, HIV, HBV
95
Diagnostic tests for HCV
LFTs, anti-HCV antibodies, HCV-PCR (confirms ongoing infection), liver biopsy, HCV genotype
96
HCV treatment
3 serine protease inhibitors - Telaprevir
Ribavirin
Alcohol abstinence
97
HCV complications
glomerulonephritis, thyroiditis, autoimmune hepatitis, cirrhosis
98
What type of virus is HDV?
incomplete RNA virus - requires the helper function of HBV to replicate
99
HDV complications
cirrhosis, acute liver failure
100
Diagnostic tests for HDV
anti-HDV antibodies
101
Treatment of HDV
Liver transplant may be needed if it progresses to chronic
102
What type of virus is HEV?
RNA virus
103
Transmission of HEV
foecal-oral
104
HEV treatment
supportive therapy
105
What is hereditary haemochromatosis?
an inherited autosomal recessive disorder characterised by increased intestinal absorption of iron, leading to iron overload in multiple organs (= liver, heart, pancreas, joints)
106
What is the mutation in haemochromatosis?
autosomal recessive disorder caused by mutations on the HFE gene on chromosome 6p. HFE codes for the iron regulatory hormone hepcidin
mis-sense mutation
107
Pathogenesis of haemochromatosis
Hepcidin controls plasma iron concentrations by inhibiting iron export by ferroportin from enterocytes in the duodenum.
Deficiency of hepcidin results in raised plasma iron concentrations and accumulation in multiple organs
108
Clinical presentation of haemochromatosis
```
early = asymptomatic, joint pain, erectile dysfunction
later = grey pigmentation, cirrhosis, osteoporosis, hypogonadism, DM (bronze diabetes)
```
109
Diagnostic tests for haemochromatosis
BLOOD = raised LFTs, raised serum ferritin, HFE genotypes
Imaging - Liver MRI = iron overload
Liver biopsy - PERLS stain quantifies iron loading
110
Treatment of haemochromatosis
Venesection - regular removal of blood (1 unit every 1-3 weeks)
Deferoxamine - binds iron and aluminium
Diet
- decrease iron absorption = tea, coffee, red wine
- increase iron absorption = fruit, white wine
111
What is alpha 1 antitrypsin deficiency?
Recessive disorder that may result in lung or liver disease
112
What does A1AT do
glycoprotein and serine protease inhibitor that controls inflammatory cascades
113
What does A1AT do in the lung?
protects against tissue damage from neutrophil elastase - induced by smoking
114
Aetiology of A1AT deficiency
Mutation in A1AT gene on chromosome 14
```
Genetic variants of A1AT are characterised by electrophoretic mobilities:
- M = medium
- S = slow
- Z = very slow
Normal genotype = PiMM
Symptomatic genotype = PiZZ
```
115
Clinical presentation of A1AT deficiency
Dyspnoea from emphysema, cirrhosis, cholestatic jaundice
116
Diagnostic tests for A1AT deficiency
Serum A1AT levels decreased, liver biopsy - PAS=positive, genotyping to confirm diagnosis
117
Treatment of A1AT deficiency
family screening, supportive treatment, quit smoking, lung and liver transplant
118
What is Wilson's disease / hepatolenticular degeneration
A rare inherited disorder of copper metabolism, leading to the accumulation of toxic levels of copper in the liver and brain
119
When do most cases of Wilson's disease present?
childhood or young adulthood
120
Aetiology of Wilson's disease
Autosomal recessive disorder
| Mutations in gene ATP7B on chromosome 13
121
Pathophysiology of Wilson's disease
Mutation in ATP7B gene leads to decreased secretion of copper into the biliary system and reduced incorporation of copper into procaeruloplasmin. (caeruploplasmin is the major copper-carrying protein in blood)
Intestinal copper absorption and transport into the liver are intact but copper incorporation into caeruloplasmin in hepatocytes and excretion into bile are impaired.
122
Clinical presentation of Wislon's disease
children present with liver disease = hepatitis, cirrhosis, fulminant liver failure
Young adults present with CNS signs = tremor, dysarthria (slurred speech). dysphagia, dementia, dyskinesias, clumsiness
Mood = depression, high and low libido, personality change
Cognition = decreased memory function, short temper, low IQ
Kayser-Fleischer rings = copper in iris
123
Diagnostic tests for Wilson's disease
```
Urine - 24hr copper excretion is high
LFTs raised
Serum copper
Decreased serum ceruloplasmin
Molecular genetic testing
Slit lamp exam - KF rings
MRI - degeneration in basal ganglia
```
124
Treatment of Wilson's disease
Diet = avoid liver, chocolate, mushrooms, shellfish, analyse copper content of water
Drugs = lifelong penicillamine - SE=rash,nausea,depleted leukocytes
Liver transplant if severe disease
Screen siblings
125
What percentage of liver tumours are secondary tumours?
90%
126
What are common origins of liver tumours in men?
stomach, lung, colon
127
What are common origins of liver tumours in women?
breast, stomach, colon, uterus
128
Examples of primary liver tumours
```
Malignant = HCC, cholangiocarcinoma, angiosarcoma
Benign = cysts, hemangioma (common in women), fibroma
```
129
Symptoms of malignant liver tumours
weight loss, RUQ pain, jaundice is late (except in cholangiocarcinoma), fever, malaise, anorexia
130
Symptoms of benign liver tumours
Asymptomatic
131
Signs of liver tumours
- Hepatomegaly - smooth or hard and irregular
- signs of chronic liver disease
- decompensation = jaundice and ascites
- abdominal mass
- Bruit over liver - HCC
132
Diagnostic tests for liver tumours
- Blood - FBC, clotting, LFTs, hepatitis serology, alpha-fetoprotein (raised in HCC)
- Imaging - US, CT = identify lesions + guide biopsy, MRI - distinguishes malignant and benign lesions
- Liver biopsy
- Find primary tumour = CT, MRI, CXR, endoscopy
133
Liver metastases
signify advanced disease, most treatment is palliative
134
What are hepatocellular carcinomas?
A malignant epithelial neoplasm of the liver derived from hepatocytes.
HBV and haemochromatosis are carcinogenic.
More common in men
135
Clinical presentation of HCC
RUQ pain, weight loss, fatigue, jaundice, ascites, haemophilia
136
Aetiology of HCC
HBV = main cause
| - HCV, autoimmune hepatitis, cirrhosis, non-alcoholic fatty liver liver
137
Diagnostic tests for HCC
4 phase CT, MRI, biopsy
138
Treatment of HCC
resection of solitary tumours, liver transplant, percutaneous ablation and tumour embolisation
139
What is a cholangiocarcinoma?
Biliary tree cancer
140
Causes of cholangiocarcinoma
HBV, HCV, DM, liver flukes (parasites=Clonorchis Sinesis)
141
Clinical presentation of cholangiocarcinoma
abdominal pain, ascites, fever, elevated bilirubin
142
Are cholangiocarcinomas fast or slow growing?
slow growing
143
Management of cholangiocarcinoma
Most can't have surgery
post op complications = liver failure, bile leak, GI bleeds
Stenting of an obstructed extrahepatic biliary tree
144
What is a hemangioma?
Most common benign tumour of the liver
No treatment required
DON'T BIOPSY
145
Liver adenoma
- Caused by anabolic steroids, oral contraceptives, pregnancy
- Only treat if symptomatic
146
How many deaths arise from pancreatic cancer in the UK?
6500 deaths per year
147
Typical patient suffering from pancreatic cancer
60 year old male
148
Risk factors for pancreatic cancer
smoking, alcohol, carcinogens, DM, chronic pancreatitis, central adiposity, high fat diet, red meat and processed food
149
Pathology of pancrreatic cancer
mostly ductal adenocarcinoma - metastasise early and present late
60%=pancreatic head, 25%=pancreatic body,
Few arise in ampulla of Vater or pancreatic islet cells (insulinoma, gastrinoma, glucagonoma) - these have a better prognosis
95% = mutations in the KRA52 gene
150
Clinical presentation of pancreatic cancer
Tumours in head of pancreas = painless obstructive jaundice
75% of body/tail tumours present with epigastric pain radiating to back and relieved by sitting forward
anorexia, weight loss, DM, acute pancreatitis
Signs =
jaundice, palpable gallbladder, hepatomegaly, ascites
151
Diagnostic tests for pancreatic tumours
Jaundice, US/CT = show pancreatic mass, dilated biliary tree, guides biopsy and helps staging prior to surgery
152
Treatment of pancreatic tumours
- surgery - pancreaticoduodenectomy if patient is fit and has no metastases
- laparoscopic excision
- post-op chemo
- palliation of jaundice - stent insertion
- opiates or radiotherapy for pain
153
Prognosis of pancreatic cancers
dismal
| mean survical = <6 months
154
What is peritonitis?
inflammation of the peritonitis
155
What is primary peritonitis?
infection of the peritoneal cavity not directly related to other intra-abdominal abnormalities
extremely rare
at risk groups = liver disease, females, immunocompromised patients, peritoneal dialysis patients, ascites
156
What is secondary peritonitis?
Bacterial peritonitis secondary to intra abdominal lesions such as perforation of a hollow viscous.
caused by TB, chemical irritation
157
Symptoms of peritonitis
dull abdominal pain that quickly becomes severe
nausea and vomiting
systemic symptoms
inability to move due to pain
158
Signs of peritonitis
tenderness - localised which progresses to generalised
| cloudy dialysis fluid (if patient is receiving peritoneal dialysis)
159
General examination of peritonitis
pyrexia and tachycardia, confusion (encephalopathy)
patients lie still - localized=avoid strain on affected area, generalised=lie very still
Hypotension, hypoxia
160
Abdominal examination of peritonitis
guarding, rebounding, rigidity
| silent abdomen = ominous sign
161
Investigations of peritonitis
Bloods = FBC, U&Es, amylase, LFTs
X-ray = erect chest, abdomen
CT of abdomen
SPB = infection of ascitic fluid - MC&S and neutrophil count
162
Management of peritonitis
ABCDE
Antibiotics - metronidazole
treat cause
- medical = primary peritonitis
- surgical = repair perforated viscus and excise perforated organ
