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nicks phase 2a flaschards > liver and pancreas > Flashcards

liver and pancreas Flashcards

1
Q

what is acute pancreatitis?

A

self-perpetuating pancreatic inflammation by enzyme-mediated autodigestion

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2
Q

what is the aetiology of acute pancreatitis?

A 
GET SMASHED
•Gallstones
•Ethanol (alcohol)
•Trauma
•Steroids
Mumps
•Autoimmune
•Scorpion venom
•Hyperlipidaemia, hypothermia, hypercalcaemia
•ERCP and emboli
•Drugs
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3
Q

What are the signs and symptoms of acute pancreatitis?

A
  • signs- tachycardia, fever, jaundice, shock

- symptoms- gradual sudden epigastric abdominal pain that radiates to the back, sitting forward relieves pain

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4
Q

what are some differential diagnoses of acute pancreatitis?

A
  • IBS
  • MI
  • Gastroenteritis
  • Diabetic ketoacidosis
  • Peritonitis
  • Pneumonia
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5
Q

how can acute pancreatitis be diagnosed?

A
  • raised serum amylase
  • serum lipase
  • AXR- no psoas shadow
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6
Q

what are the treatment options for a patient with acute pancreatitis?

A
  • IV saline
  • analgesia
  • oxygen
  • ABX If severe
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7
Q

what is chronic pancreatitis?

A

inappropriate activation of enzymes within the pancreas resulting in the precipitation of protein plugs. this leads to fibrosis, atrophy and calcification of the pancreas resulting in an impairment in pancreatic function.

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8
Q

what is the aetiology of chronic pancreatitis?

A
  • Alcohol
  • Tropical chronic pancreatitis
  • Hereditary
  • Autoimmune
  • Cystic fibrosis
  • Haemachromatosis
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9
Q

what is the pathophysiology of chronic pancreatitis?

A

precipitation of protein plugs within the duct lumen forms a point for calcification
•duct blockage leads to ductal hypertension and further pancreatic damage.
This (+cytokine activation) leads to pancreatic inflammation, irreversible morphological change ± impaired pancreatic function

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10
Q

how does chronic pancreatitis present clinically?

A
  • epigastric pain radiating to back
  • relieved by sitting forward
  • bloating
  • steatorrhoea
  • weight loss
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11
Q

how can chronic pancreatitis be diagnosed?

A

ultrasound and CT show pancreatic calcifications

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12
Q

how can chronic pancreatitis be treated?

A
  • drugs- analgesia, lipase, insulin
  • no alcohol, low fat diet
  • pancreatectomy
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13
Q

describe pigment stones and what can cause them

A

small stones formed of unconjugated bilirubin- occur due to haemolytic

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14
Q

describe cholesterol stones and name 3 risk factors for them

A

large, often solitary – age, obesity, female sex, OCP

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15
Q

what can cause acute cholecystitis?

A

lodging of a stone in the gallbladder or impaction at the neck of the gallbladder resulting in inflammation and an increased pressure- this results in bacterial growth

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16
Q

what are the symptoms of acute cholecystitis?

A

vomiting, fever, local peritonism, GB mass

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17
Q

what is Murphy’s sign and what condition is it seen in?

A

2 fingers over the RUQ, ask patient to breath in- causes pain as inflamed GB is impacted on by diaphragm
- acute cholecystitis

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18
Q

how can acute cholecystitis be tested for?

A
  • high WCC
  • US- shrunken GB, common bile duct dilation
  • Murphy’s sign
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19
Q

how is acute cholecystitis treated?

A
  • pain relief
  • IV fluids
  • laparoscopic cholecystectomy
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20
Q

what are the symptoms fo chronic cholecystitis?

A

flatulent dyspepsia
distension
nausea
RUQ pain

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21
Q

what triad of symptoms of seen in ascending cholangitis?

A

Charcot’s triad- RUQ pain, jaundice, rigors

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22
Q

what can cause unconjugated bilirubin to rise?

A
  • overproduction- haemolysis
  • impaired hepatic uptake- drugs, RHF
  • impaired conjugation
  • physical neonatal jaundice
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23
Q

what can cause conjugated bilirubin to rise?

A
  • hepatocellular dysfunction- viruses, drugs, alcohol, cirrhosis
  • impaired hepatic excretion- primary biliary cirrhosis, primary sclerosing cholangitis
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24
Q

what is hepatitis A?

A

RNA virus

faecal-oral spread

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25
Q

what are the symptoms of hepatitis A?

A

fever, malaise, anorexia, nausea, jaundice

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26
Q

what is HBV?

A

DNA virus

spread- blood products, IVDU, sexual and direct contact

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27
Q

who are some at risk groups of HBV?

A 
IVDUs
Their sexual partners/carer
Health workers
Haemophiliacs
Job exposure to blood e.g. morticians
Haemodialysis + chronic renal failure
Sexual promiscuity
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28
Q

How can HBV be tested for?

A
  • HBsAg (surface antigen) presents 1-6 months after exposure- Persisting for >6 months = carrier status
  • HBcAG- core antigen
  • HBeAg (e antigen) – present for 1.5-3 months after acute illness – implies high infectivity- marker of active infection
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29
Q

what is HCV?

A

RNA flavivirus

blood-transfusion, IVDU

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30
Q

how can you diagnose HCV?

A

anti-HCV antibodies

HCV-PCR confirms on-going infection

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31
Q

how can you treat HCV?

A

3-serine protease inhibitors- telaprevir

quit alcohol

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32
Q

what is HDV?

A

incomplete RNA virus that requires HBV for assembly

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33
Q

what is HEV?

A

RNA virus

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34
Q

what is cirrhosis?

A

irreversible liver damaging caused by loss of normal hepatic architecture with. bridging fibrosis

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35
Q

what is the aetiology of cirrhosis (liver failure)?

A
  • chronic alcohol abuse
  • HBV/ HCV
  • haemochromatosis
  • alpha1-antitrypsin deficiency
  • Budd-Chiari
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36
Q

how does cirrhosis (liver failure) present clinically?

A
  • leuconychia
  • clubbing
  • palmar eryhtema
  • spider naevi
  • xanthelasma
  • gynaecomastia
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37
Q

what are the 2 main complications of cirrhosis (liver failure)?

A
  • hepatic failure- coagulopathy, encephalopathy, sepsis

- portal hypertension- ascites, splenomegaly

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38
Q

how is cirrhosis (liver failure) diagnosed?

A
  • raised bilirubin
  • hypoabluminaemia
  • bloods- raised aspartate aminotransferase and alanine aminotransferase
  • MRI- large caudate lobe
  • ascitic tap
  • liver biopsy
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39
Q

how can you treat a patient with cirrhosis (liver failure)?

A
  • quit alcohol
  • treat viral disease
  • bed rest
  • spironolactone
  • liver transplant
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40
Q

what is primary biliary cirrhosis?

A

Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis

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41
Q

how does primary biliary cirrhosis present clinically?

A
  • pruritis
  • jaundice
  • hepatosplenomegaly
  • xanthelasma
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42
Q

what are some differential diagnoses of primary biliary cirrhosis?

A

sarcoidosis
TB
schistosomiasis
drug reactions

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43
Q

how can primary biliary cirrhosis be diagnosed?

A
  • high alkaline phosphatase

- raised Ig’s

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44
Q

what are the treatment options for a patient with primary biliary cirrhosis?

A

if symptomatic- oral rifampicin and codeine phosphate

- can also offer ursodeoxycholic acid, vitamins A,D,K

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45
Q

what is fatty liver?

A
  • First change in the alcoholic liver
  • Regular alcohol use results in fatty liver (steatosis)

this is reversible but can progress

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46
Q

what is alcoholic hepatitis?

A

fibrosis and foamy degeneration of hepatocytes

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47
Q

what are the clinical features of alcoholic hepatitis?

A

rapid onset jaundice

nausea, anorexia, RUQ pain, encephalopathy, fever, ascites

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48
Q

how can alcoholic hepatitis be diagnosed?

A
  • FBC- elevated MCV, leucocytosis

- hyponatraemia on U&E

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49
Q

what is hereditary haemochromatosis?

A

autosomal recessive disorder of iron metabolism- increased intestinal iron absorption leads to iron deposits in joints, liver, heart, pancreas, pituitary, adrenals and skin

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50
Q

what is the clinical presentation of hereditary haemochromatosis?

A
  • erectile dysfunction
  • slate-grey skin
  • hepatomegaly
  • cirrhosis
  • dilated cardiomyopathy
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51
Q

how can hereditary haemochormatosis be diagnosed?

A
  • bloods- raised ferritin and transferrin saturation
  • liver MRI shows iron overload
  • liver biopsy- Perls stain
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52
Q

how would you treat a patient who presents with hereditary haemochromatosis?

A

phlebotomy

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53
Q

what is alpha1 antitrypsin deficiency?

A

autosomal recessive disorder which results in a deficiency in A1AT.

54
Q

what is the clinical presentation of A1AT deficiency?

A
  • dyspnoea
  • SOB
  • wheezing
  • chronic cough
  • mucus production
  • cirrhosis
  • cholestatic jaundice
55
Q

how can A1AT be managed?

A

family screening, quit smoking, liver transplant

56
Q

what is Wilsons disease?

A

Rare inherited disorder of biliary copper excretion with too much copper in liver and CNS

57
Q

in Wilsons disease, where does the copper accumulate and what are the consequences of this?

A

Liver= fulminant hepatic failure and cirrhosis

Basal ganglia= parkinsonism

cerebral cortex= dementia

Cornea = greenish-brown rings (Kayser-Fleischer rings)

Renal tubules

58
Q

how do patients with Wilson’s disease present throughout their life?

A

children- liver disease- hepatitis, cirrhosis

young adults- CNS signs- tremor, dysarthria, dystonia, dementia

progressive mood changes and loss of cognitive function

59
Q

how is Wilson’s disease diagnosed?

A
  • 24h copper excretion high
  • LFT’s raised
  • raised serum copper
  • serum caeruloplasmin decreased
60
Q

what is the pharmacological treatment of Wilson’s disease?

A

lifelong penicillamine

liver transplant if severe

61
Q

what is fulminant hepatic failure?

A

clinical syndrome resulting from massive necrosis of liver cells which cause a severe impairment of liver function

62
Q

what can cause liver failure?

A

infections- viral hepatitis, leptospirosis

drugs- paracetamol overdose

vascular- budd-chiari syndrome

other- alcohol, haemcohromatosis, A1AT deficiency, Wilson’s disease

63
Q

what is hepatic encephalopathy?

A
  • As liver fails ammonia builds up in circulation and passes to brain
  • Astrocytes clear it- conversion of glutamate to glutamine
  • Excess glutamine causes an osmotic imbalance and a shift of fluid into these cells – cerebral oedema
64
Q

how is liver failure treated?

A
  • ITU
  • IV glucose
  • lorazepam
  • treat complications
65
Q

what is ascites and what is the commonest cause of it?

A

presence of fluid in the peritoneal cavity

cirrhosis

66
Q

what can cause ascites?

A

due to cirrhosis- peripheral arterial vasodilation leads to a reduction in effective blood volume.
this leads to activation of SNS and RAAS- promoting salt and water retention.
oedema is encouraged by hypoalbuminemia

67
Q

what are some transudate causes of ascites?

A
  • Portal hypertension e.g. cirrhosis
  • Hepatic outflow obstruction
  • Budd-Chiari syndrome
  • Cardiac failure
68
Q

what are some exudate causes of ascites?

A
  • Peritoneal carcinomatosis
  • Peritoneal TB
  • Pancreatitis
  • Nephrotic syndrome
  • Lymphatic obstruction (chylous ascites)
69
Q

how does ascites present clinically?

A
  • fullness in flanks
  • shifting dullness
  • tense ascites= uncomfortable, respiratory distress
  • pleural effusion
70
Q

how is ascites treated?

A

hypertension- diuretics

paracentesis

71
Q

where do secondary tumours of the liver most commonly arise from in men and women?

A
  • men= stomach, lung, colon

- women= breast, colon, stomach, uterus

72
Q

what are some examples of malignant primary liver tumours?

A
  • HCC
  • Cholangiocarcinoma
  • Angiosarcoma
  • Hepatoblastoma
  • Fibrosarcoma and hepatic gastrointestinal stromal tumours (GIST)
73
Q

what are some examples of benign primary liver tumours?

A
  • Cysts
  • Haemangioma – common, F:M = 5:1
  • Focal nodular hyperplasia
  • Fibroma
  • Benign GIST
74
Q

what are the symptoms of liver tumours?

A
  • Fever
  • Malaise
  • Anorexia
  • Weight loss
  • RUQ pain
  • Jaundice is late – except with cholangiocarcinoma
  • Benign tumours are asymptomatic
75
Q

what is the aetiology of HCC?

A 
o	HBV – main cause
o	HCV
o	Autoimmune hepatitis
o	Cirrhosis – alcohol, haemachromatosis, PBC
o	Non-alcoholic fatty liver
76
Q

where do pancreatic cancers most commonly arise?

A

60% = pancreatic head, 25% = body, 15% = tail

77
Q

what clinical signs does pancreatic cancer present with?

A
  • Jaundice + palpable gallbladder
  • Epigastric mass
  • Hepatomegaly
  • Splenomegaly
  • Lymphadenopathy
  • Ascites
78
Q

how is pancreatic cancer treated?

A
  • pancreaticoduodenectomy

- laparoscopic excision

79
Q

what is the aetiology of liver abscesses?

A
  • biliry sepsis
  • trauma
  • bacteraemia
  • pyogenic abscess- E.coli, strep milleri
  • amoebic obsess- spread of entamoeba histolytic from bowel
80
Q

how do liver abscesses present clinically?

A
  • non-specific- fever, lethargy, weight loss, abdominal pain

- enlarged liver

81
Q

how are liver abscesses treated?

A
  • pyogenic- percutaneous aspiration

- amoebic- metronidazole

82
Q

what bacteria can cause acute cholecystitis?

A

E.coli, clostridium, enterococci

83
Q

what is chronic cholecystitis?

A

chronic inflammation of the GB due to continuous presence of gall stones in either the cystic duct or the GB- epithelial damage results in inflammation

84
Q

what causes cholesterol stones to occur?

A
  • supersaturation of cholesterol in bile

- not enough bile salts, acids or phospholipids- so less solution

85
Q

what are some complications of gall stones in the GB or the cystic duct?

A
  • biliary colic
  • acute and chronic cholecystitis
  • empyema
  • carcinoma
86
Q

what are some complications of gall stones in the GB or the cystic duct?

A
  • obstructive jaundice
  • cholangitis
  • pancreatitis
87
Q

what is biliary colic?

A

The term used for the pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder

88
Q

how is biliary colic treated?

A
  • analgesia
  • rehydrate
  • laparoscopic cholecystectomy
89
Q

what is ascending cholangitis?

A

Inflammation of the biliary tract caused by an obstruction of the common bile duct which allows bacteria from the intestine to work their way up into the bile duct

90
Q

how is ascending cholangitis diagnosed?

A
  • USS
  • ERCP- endoscopic retrograde cholangiopancreatography
  • positive anti-mitochondrial antibody present
91
Q

how is ascending cholangitis treated?

A
  • cefuroxime and metronidazole

- cholecystectomy

92
Q

what is the pathophysiology of acute pancreatitis?

A
  • Aetiological basis (e.g. alcohol) causes increased trypsinogen release from acinar cells- pancreatic juices become viscous
  • This forms plugs that block the pancreatic ducts
  • Trypsinogen broken down into trypsin by lysosomal enzymes- results in autodigestion of pancreas
93
Q

What can be found inside hepatocytes in a patient with alcoholic hepatitis?

A
  • Mallory bodies

- neutrophils

94
Q

what is portal hypertension?

A

liver is unable to filter blood as well so pressure backs up, resulting in portal vein hypertension.

95
Q

why does portal hypertension cause varices?

A

blood always takes the path of least resistance- so due to portal hypertension causing a back up of pressure there is increased flow in the systemic circulation

96
Q

what can cause portal hypertension?

A
  • Cirrhosis
  • Fibrosis
  • hepatitis
  • Portal vein thrombosis
  • Increased hepatic resistance, increased splanchnic blood flow
97
Q

what are 2 consequences of portal hypertension?

A

varices

splenomegaly

98
Q

what are varices?

A

Local dilations of the veins

99
Q

how are varices managed?

A
  • correct clotting abnormalities with vitamin k and platelet transfusions
  • endoscopic banding
100
Q

how can HAV be diagnosed?

A
  • HAV-IgM rises from day 25= active infection

- HAV-IgG detectible forever= previous infection/ vaccination

101
Q

how is HAV treated?

A
  • alcohol cessation

- alpha interferon used if patient develops fulminant hepatitis

102
Q

how can HEV be diagnosed?

A
  • HEV IgM antibody present= active infection

- HEV IgG antibody present= previous infection

103
Q

which types of hepatitis virus can cause acute hepatitis?

A

all can!

104
Q

which types of hepatitis virus can cause chronic hepatitis?

A

HBV

HCV

105
Q

what is a cause of secondary haemochromatosis?

A

frequent blood transfusions

106
Q

what are some complications of haemochromatosis?

A
  • cirrhosis leading to hepatocellular carcinoma
  • type 1 DM
  • malabsorption
  • cardiomyopathy
  • amenorrhoea
  • degenerative joint diseases
107
Q

what is the function of A1AT and why does deficiency of this affect the lungs and liver?

A

Alpha1- antritrypsin is responsible for inactivating elastase- a protease. In the absence of A1AT, elastin is broken down- particularly damages the lungs and liver.
In the lungs, the structural integrity of the alveoli is lost- emphysema

108
Q

how can A1AT be diagnosed?

A
  • Serum alpha1-antitrypsin levels decreased
  • Liver biopsy and liver US
  • Pulmonary function tests
109
Q

what is the key difference between cholangitis and cholecystitis?

A

there is NO JAUNDICE with cholecystitis

110
Q

what clinical features does a patient with HCC Present with?

A

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

111
Q

how is a HCC diagnosed?

A

CT, MRI, biopsy

112
Q

how is a HCC treated?

A

resection of tumour

liver transplant

113
Q

what is a cholangiocarcinoma?

A

adenocarcinoma of the bile duct epithelium

114
Q

what is the aetiology of cholangiocarcinoma?

A

primary sclerosis cholangitis
HBV
HCV
diabetes mellitus

115
Q

how does a patient present with a cholangiocarcinoma?

A

fever
abdo pain
malaise
elevated bilirubin

116
Q

how can ascites be diagnosed?

A
  • diagnostic aspiration of 10-20ml of ascetic fluid
  • gram stain and culture for bacteria
  • cytology for malignancy
117
Q

what are the symptoms of peritonitis?

A

pain, tenderness, dizziness, weakness, nausea, rigor, chills

118
Q

how is peritonitis diagnosed?

A

general examination

abdo exam- guarding, rebound, rigidity, silent abdomen

investigations- CXR, CT abdo

119
Q

how is peritonitis treated?

A

antibiotic prophylaxis

excise perforated organ

120
Q

what are the 2 types of hiatus hernia?

A

sliding, rolling

121
Q

what is a sliding hiatus hernia?

A

Where the gastro-oesophageal junction slides up into the chest

122
Q

what is a rolling hiatus hernia?

A

Where the gastro-oesophageal junction remains in the abdomen but a bulge of stomach herniates up into the chest alongside the oesophagus

123
Q

how are hiatus hernias treated?

A

weight loss

surgery if intractable symptoms

124
Q

what are the 2 types of inguinal hernia?

A
  • Indirect hernias pas through the internal inguinal ring and (if large) out through the external inguinal ring
  • Direct hernias push their way directly forward through the posterior wall of the inguinal canal, into a defect in the abdominal wall
125
Q

what is a femoral hernia?

A

Bowel enters femoral canal, presenting as mass in upper medial thigh or above the inguinal ligament (points down leg, not into groin – this distinguishes it from inguinal)

126
Q

what is an incisional hernia?

A

follows the breakdown of muscle closure after surgery

127
Q

what can cause raised aspartate aminotransferase (AST) levels?

A
  • hepatic necrosis
  • myocardial infarction
  • muscle injury
  • congestive cardiac failure
128
Q

what is the function of aspartate aminotransferase?

A

mitochondrial enzyme

129
Q

what can cause raised alanine aminotransferase levels?

A
  • viral hepatitis

- alcoholic liver disease

130
Q

what is the function of alanine aminotransferase?

A

cytosol enzyme specific to the liver

nicks phase 2a flaschards (15 decks)

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