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Hamzah's liver and friends pathology > Hamzah's liver and friends pathology > Flashcards

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

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2
Q

What is acute hepatic failure?

A

Liver failure occurring suddenly in a healthy liver

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3
Q

What is chronic hepatic failure?

A

liver failure as a result of background cirrhosis

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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

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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
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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.

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7
Q

Symptoms of liver failure

A

RUQ pain, nausea and vomiting

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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
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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)
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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
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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

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12
Q

What is used to treat a paracetamol overdose?

A

acetylcysteine

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13
Q

What is used to treat a opioid overdose?

A

naloxone = (opioid receptor antagonist)

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14
Q

Where is bile produced and concentrated?

A

produced in the liver

stored and concentrated in the gall bladder

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15
Q

what does bile contain?

A

water, bile acids, phospholipids, cholesterol

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16
Q

Bile functions

A

lipid digestion and absorption
cholesterol homeostasis
antimicrobial

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17
Q

What are cholesterol stones?

A

large –> caused by high cholesterol, obesity, FH, Male gender

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18
Q

What are pigment stones?

A

small, irregular and friable stones. made of unconjugated bilirubin and calcium

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19
Q

What are mixed stones?

A

faceted (calcium salts, pigment and cholesterol)

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20
Q

Risk factors for bile stones becoming symptomatic

A

smoking and giving birth

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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

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22
Q

Clinical presentation for biliary colic

A

RUQ pain that radiates to back

Can have jaundice

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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

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24
Q

Symptoms of acute cholecystitis

A

Vomiting, fever, local peritonitis, gallbladder mass

Continuous epigastric or RUQ pain –> referred to right shoulder

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25
Q

Signs of acute cholecystitis

A

Murphy’s sign = place 2 fingers over RUQ, ask patient to breathe in –> causes pain and arrest of inspiration as gallbladder impinges on finger

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26
Q

What is the main difference between a biliary colic and acute cholecystitis?

A

acute cholecystitis involves an inflammatory component –> local peritonitis, fever, high white cell count

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27
Q

Diagnostic tests for acute cholecystitis

A

High WCC
US - thick walled, shrunken gallbladder, common bile duct dilatation, stones
AXR - only shows 10% of gallstones
HIDA scan

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28
Q

Treatment of acute cholecystitis

A

nil by mouth, pain relief, IV fluids, IV antibiotics, laparoscopic cholecystectomy

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29
Q

What is chronic cholecystitis?

A

repeated attacks of pain (biliary colic) –> the gallbladder is damaged by repeated attacks of acute inflammation

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30
Q

Clinical presentation of chronic cholecystitis

A 
Flatulent dyspepsia = vague abdominal discomfort
Distension
Nausea
Flatulence
Fat intolerance
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31
Q

Diagnostic tests for chronic cholecystitis

A

US - to image stones and assess common bile duct diameter

MRCP - to find stones

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32
Q

Treatment of chronic cholecystitis

A

cholecystectomy

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33
Q

What is cholangitis

A

a bile duct infection

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34
Q

Common bacteria that cause cholangitis

A

Escherichia coli, Klebsiella

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35
Q

Clinical presentation of cholangitis

A

RUQ pain, jaundice, fever = Charcot’s triad

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36
Q

Treatmnet of cholangitis

A

cefuroxime (antibiotic)

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37
Q

Complications of gallstones in the gallbladder and cystic duct

A

biliary colic, acute and chronic cholecystitis, empyema

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38
Q

Complications of gallstones in the bile ducts

A

obstructive jaundice, cholangitis, pancreatitis

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39
Q

Complications of gallstones in the gut

A

Gallstone ileus

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40
Q

What is acute pancreatitis?

A

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

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41
Q

Aetiology of acute pancreatitis

A

GET SMASHED
gallstones and alcohol abuse = main causes
trauma, steroids, autoimmune, hypercalcaemia, drugs, ERCP
Idiopathic

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42
Q

RIsk factors for acute pancreatitis

A

excessive alcohol consumption
FH
obesity
smoking

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43
Q

Pathogenesis of acute pancreatitis

A
  • 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
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44
Q

Symptoms of acute pancreatitis

A
  • Epigastric/central abdomianl pain. (pain becomes more intense as inflammation spreds throughout the peritoneal cavity)
  • Pain radiates to back
  • Sitting may relieve pain
  • Vomiting
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45
Q

Signs of acute pancreatitis

A
  • 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)
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46
Q

Differential diagnosis of acute pancreatitis

A

IBS, MI, gastroenteritis, DKA, pneumonia, malaria

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47
Q

Diagnostic tests for acute pancreatitis

A

raised serum amylase (above 3x upper limit)
urinary amylase
serum lipase
AXR - no psoas shadow (due to increased retroperitoneal fluid)

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48
Q

Treatment of acute pancreatitis

A

supportive therapy - oxygen, analgesia, nil by mouth, IV saline
antibiotics

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49
Q

Early complications of acute pancreatitis

A

Shock, ARDS, renal failure, DIC, sepsis, hypocalcaemia

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50
Q

Late complications of acute pancreatitis

A

Pancreatic necrosis, bleeding, thrombosis, fistulae

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51
Q

What is chronic pancreatitis?

A

A chronic inflammatory process of the pancreas leading to irreversible loss of pancreatic function

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52
Q

Aetiology of chronic pancreatitis

A

most cases = alcohol abuse

autoimmune, CF, pancreatic duct obstruction, hyperparathyroidism

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53
Q

Pathophysiology of chronic pancreatitis

A
  • 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

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54
Q

Clinical presentation of chronic pancreatitis

A
  • 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
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55
Q

Diagnostic tests for chronic pancreatitis

A

US/CT - look for pancreatic calcifications
MRCP and ERCP - rises in acute attack
AXR - speckled calcification

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56
Q

Treatment of chronic pancreatitis

A
  • Drugs = analgesia, lipase, fat-soluble vitamins, insulin
  • Diet = no alcohol, low-fat diet
  • surgery = pancreatectomy or pancreatojejunostomy
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57
Q

Complications of chronic pancreatitis

A

Pseudocyst, diabetes, biliary obstruction, pancreatic carcinoma

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58
Q

What is alcoholic liver disease?

A

liver disease due to excessive alcohol consumption

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59
Q

3 patterns of alcoholic liver disease

A

steatosis
alcoholic steatohepatitis (ASH)
cirrhosis

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60
Q

In who is alcoholic liver disease most common?

A

men in their 50s

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61
Q

Pathogenesis of alcoholic liver disease

A
  • 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
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62
Q

Stages of alcoholic liver disease

A
  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
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63
Q

Risk factors for alcoholic liver disease

A

Excessive alcohol consumption
female gender
Genetic factors

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64
Q

Clinical features of alcoholic hepatitis

A

rapid onset jaundice

Nausea, anorexia, RUQ pain, encephalopathy, fever, ascites, tender hepatomegaly

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65
Q

Diagnostic tests in alcoholic hepatits

A
  • 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
Q

Treatment/management of alcoholic hepatitis

A

Supportive therapy
Possible NG feeding
alcohol cessation
corticosteroids - prednisolone (if ver severe)

67
Q

Alcoholic corrhosis

A

= FInal stage of alcoholic liver disease
Destruction of liver architecture and fibrosis –> regenerating nodules produce micronodular cirrhosis
Treatment = liver transplantation

68
Q

Complications of alcoholic liver disease

A

If untreated = liver failure

69
Q

What is cirrhosis?

A

= Irreversible replacement of normal liver architecture by bands of fibrous tissue separating nodules of regenerating hepatocytes

70
Q

Aetiology of cirrhosis

A

alcohol abuse, HBV, HCV, non-alcoholic fatty liver diseases
rare = haemochromatosis, Wislon’s disease
drugs = amiodarone

71
Q

Pathophysiology of cirrhosis

A

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
Q

Effects of cirrhosis

A
  • 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
Q

Symptoms of cirrhosis

A

upper abdominal pain, nausea, vomiting, weight loss, weakness, easily bruising

74
Q

Signs of cirrhosis

A

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
Q

Complications of cirrhosis

A
  • Hepatic failure - coagulopathy, encephalopathy, hypoalbuminemia
  • Portal hypertension
  • Increased risk of HCC
76
Q

Diagnostic tests for cirrhosis

A
  • 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
Q

Treatment of cirrhosis

A

General = good nutrition, alcohol abstinence, avoid NSAIDs, sedatives and opiates
cholestyramine - pruritus
treat underlying cause

Liver transplant = the only definitive treatment for cirrhosis

78
Q

What is portal hypertension?

A

= An increase in the blood pressure in the hepatic portal system

79
Q

Aetiology of portal hypertesnion

A

most common = cirrhosis

blood clots in portal vein, schistosomiasis, IVC obstruction, right sided HF

80
Q

Complications of portal hypertension

A

oesophageal varices, ascites, splenomegaly –> anaemia, low leukocyte count, thrombocytopenia

81
Q

Symptoms of portal hypertension

A

black and bloody stools

vomiting of blood

82
Q

Signs of portal hypertension

A

Ascites, splenomegaly, anorectal varices, oesophageal varices, caput medusae (swollen veins on anterior abdominal wall)

83
Q

Diagnostic tests for portal hypertension

A

Abdominal US - dilated portal vein

Ascites

84
Q

Treatment of portal hypertension

A

Beta blockers = reduce pressure in varices
portosystemic shunts
transjugular intrahepatic portosystemic shunting (TIPS)
lactulose –> hepatic encephalopathy

85
Q

What is acute viral hepatitis?

A

infection of the liver by hepatitis A, B, C, D, E lasting <6 months

86
Q

What is chronic viral hepatitis?

A

infection of the liver by hepatitis B. C, D lasting >6 months

87
Q

What viral hepatitis types are common worldwide?

A

HAV and HCV

88
Q

Clinical presentation of viral hepatitis

A

fever, malaise, anorexia, nausea, arthralgia (joint pain)

THEN: jaundice, hepatosplenomegaly, lymphadenopathy

89
Q

Hepatitis A

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
Q

Hepatitis B

A
  • 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
Q

Complications of Hep B

A

Cirrhosis, HCC, fulminant hepatic failure, cholangiocarcinoma

92
Q

What type of virus is HCV?

A

RNA flavivirus

93
Q

Transmission of HCV

A

blood/body fluids - transfusion before 1991, IVDU, secual intercourse, acupuncture

94
Q

risk factors for HCV progression

A

males, older age, higher viral load, alcohol use, HIV, HBV

95
Q

Diagnostic tests for HCV

A

LFTs, anti-HCV antibodies, HCV-PCR (confirms ongoing infection), liver biopsy, HCV genotype

96
Q

HCV treatment

A

3 serine protease inhibitors - Telaprevir
Ribavirin
Alcohol abstinence

97
Q

HCV complications

A

glomerulonephritis, thyroiditis, autoimmune hepatitis, cirrhosis

98
Q

What type of virus is HDV?

A

incomplete RNA virus - requires the helper function of HBV to replicate

99
Q

HDV complications

A

cirrhosis, acute liver failure

100
Q

Diagnostic tests for HDV

A

anti-HDV antibodies

101
Q

Treatment of HDV

A

Liver transplant may be needed if it progresses to chronic

102
Q

What type of virus is HEV?

A

RNA virus

103
Q

Transmission of HEV

A

foecal-oral

104
Q

HEV treatment

A

supportive therapy

105
Q

What is hereditary haemochromatosis?

A

an inherited autosomal recessive disorder characterised by increased intestinal absorption of iron, leading to iron overload in multiple organs (= liver, heart, pancreas, joints)

106
Q

What is the mutation in haemochromatosis?

A

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
Q

Pathogenesis of haemochromatosis

A

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
Q

Clinical presentation of haemochromatosis

A 
early = asymptomatic, joint pain, erectile dysfunction
later = grey pigmentation, cirrhosis, osteoporosis, hypogonadism, DM (bronze diabetes)
109
Q

Diagnostic tests for haemochromatosis

A

BLOOD = raised LFTs, raised serum ferritin, HFE genotypes
Imaging - Liver MRI = iron overload
Liver biopsy - PERLS stain quantifies iron loading

110
Q

Treatment of haemochromatosis

A

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
Q

What is alpha 1 antitrypsin deficiency?

A

Recessive disorder that may result in lung or liver disease

112
Q

What does A1AT do

A

glycoprotein and serine protease inhibitor that controls inflammatory cascades

113
Q

What does A1AT do in the lung?

A

protects against tissue damage from neutrophil elastase - induced by smoking

114
Q

Aetiology of A1AT deficiency

A

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
Q

Clinical presentation of A1AT deficiency

A

Dyspnoea from emphysema, cirrhosis, cholestatic jaundice

116
Q

Diagnostic tests for A1AT deficiency

A

Serum A1AT levels decreased, liver biopsy - PAS=positive, genotyping to confirm diagnosis

117
Q

Treatment of A1AT deficiency

A

family screening, supportive treatment, quit smoking, lung and liver transplant

118
Q

What is Wilson’s disease / hepatolenticular degeneration

A

A rare inherited disorder of copper metabolism, leading to the accumulation of toxic levels of copper in the liver and brain

119
Q

When do most cases of Wilson’s disease present?

A

childhood or young adulthood

120
Q

Aetiology of Wilson’s disease

A

Autosomal recessive disorder

Mutations in gene ATP7B on chromosome 13

121
Q

Pathophysiology of Wilson’s disease

A

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
Q

Clinical presentation of Wislon’s disease

A

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
Q

Diagnostic tests for Wilson’s disease

A 
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
Q

Treatment of Wilson’s disease

A

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
Q

What percentage of liver tumours are secondary tumours?

A

90%

126
Q

What are common origins of liver tumours in men?

A

stomach, lung, colon

127
Q

What are common origins of liver tumours in women?

A

breast, stomach, colon, uterus

128
Q

Examples of primary liver tumours

A 
Malignant = HCC, cholangiocarcinoma, angiosarcoma
Benign = cysts, hemangioma (common in women), fibroma
129
Q

Symptoms of malignant liver tumours

A

weight loss, RUQ pain, jaundice is late (except in cholangiocarcinoma), fever, malaise, anorexia

130
Q

Symptoms of benign liver tumours

A

Asymptomatic

131
Q

Signs of liver tumours

A
  • Hepatomegaly - smooth or hard and irregular
  • signs of chronic liver disease
  • decompensation = jaundice and ascites
  • abdominal mass
  • Bruit over liver - HCC
132
Q

Diagnostic tests for liver tumours

A
  • 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
Q

Liver metastases

A

signify advanced disease, most treatment is palliative

134
Q

What are hepatocellular carcinomas?

A

A malignant epithelial neoplasm of the liver derived from hepatocytes.
HBV and haemochromatosis are carcinogenic.
More common in men

135
Q

Clinical presentation of HCC

A

RUQ pain, weight loss, fatigue, jaundice, ascites, haemophilia

136
Q

Aetiology of HCC

A

HBV = main cause

- HCV, autoimmune hepatitis, cirrhosis, non-alcoholic fatty liver liver

137
Q

Diagnostic tests for HCC

A

4 phase CT, MRI, biopsy

138
Q

Treatment of HCC

A

resection of solitary tumours, liver transplant, percutaneous ablation and tumour embolisation

139
Q

What is a cholangiocarcinoma?

A

Biliary tree cancer

140
Q

Causes of cholangiocarcinoma

A

HBV, HCV, DM, liver flukes (parasites=Clonorchis Sinesis)

141
Q

Clinical presentation of cholangiocarcinoma

A

abdominal pain, ascites, fever, elevated bilirubin

142
Q

Are cholangiocarcinomas fast or slow growing?

A

slow growing

143
Q

Management of cholangiocarcinoma

A

Most can’t have surgery
post op complications = liver failure, bile leak, GI bleeds
Stenting of an obstructed extrahepatic biliary tree

144
Q

What is a hemangioma?

A

Most common benign tumour of the liver
No treatment required
DON’T BIOPSY

145
Q

Liver adenoma

A
  • Caused by anabolic steroids, oral contraceptives, pregnancy
  • Only treat if symptomatic
146
Q

How many deaths arise from pancreatic cancer in the UK?

A

6500 deaths per year

147
Q

Typical patient suffering from pancreatic cancer

A

60 year old male

148
Q

Risk factors for pancreatic cancer

A

smoking, alcohol, carcinogens, DM, chronic pancreatitis, central adiposity, high fat diet, red meat and processed food

149
Q

Pathology of pancrreatic cancer

A

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
Q

Clinical presentation of pancreatic cancer

A

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
Q

Diagnostic tests for pancreatic tumours

A

Jaundice, US/CT = show pancreatic mass, dilated biliary tree, guides biopsy and helps staging prior to surgery

152
Q

Treatment of pancreatic tumours

A
  • 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
Q

Prognosis of pancreatic cancers

A

dismal

mean survical = <6 months

154
Q

What is peritonitis?

A

inflammation of the peritonitis

155
Q

What is primary peritonitis?

A

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
Q

What is secondary peritonitis?

A

Bacterial peritonitis secondary to intra abdominal lesions such as perforation of a hollow viscous.
caused by TB, chemical irritation

157
Q

Symptoms of peritonitis

A

dull abdominal pain that quickly becomes severe
nausea and vomiting
systemic symptoms
inability to move due to pain

158
Q

Signs of peritonitis

A

tenderness - localised which progresses to generalised

cloudy dialysis fluid (if patient is receiving peritoneal dialysis)

159
Q

General examination of peritonitis

A

pyrexia and tachycardia, confusion (encephalopathy)
patients lie still - localized=avoid strain on affected area, generalised=lie very still
Hypotension, hypoxia

160
Q

Abdominal examination of peritonitis

A

guarding, rebounding, rigidity

silent abdomen = ominous sign

161
Q

Investigations of peritonitis

A

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
Q

Management of peritonitis

A

ABCDE
Antibiotics - metronidazole

treat cause

  • medical = primary peritonitis
  • surgical = repair perforated viscus and excise perforated organ

Hamzah's liver and friends pathology (1 decks)

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