Liver, pancreas etc Flashcards

1
Q

List the causes of acute pancreatitis

A

“GET SMASHED”

G - GALLSTONES **
E - ETHANOL **
T - trauma

S - steroids
M - mumps
A - autoimmune
S - scorpion bites
H - hypercalcaemia, hyperlipidaemia
E - ERCP, surgery, endoscopic procedures
D - drugs e.g. thiazide diuretics, NSAIDs, azathioprine, HAART

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2
Q

How does acute pancreatitis present?

A

severe epigastric pain - radiating to the back, relieved by sitting forward, worsened on eating

nausea and vomiting

signs of shock

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3
Q

What are the signs on examination of acute pancreatitis?

A

Grey turners sign -> bruising on the flanks
cUllens sign -> bruising on the Umbilicus (due to haemorrhage in pancreas - poor prognosis)
epigastric tenderness and guarding
tachycardia
fever
jaundice ?

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4
Q

What are the possible local complications of acute pancreatitis?

A
abscess
fistula 
pseudocyt
necrosis 
portal vein hypertension or thrombosis
haemorrhage
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5
Q

What are the possible systemic complications of acute pnacreatitis?

A

sepsis
DIC
AKI
ARDS

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6
Q

How is acute pancreatitis diagnosed?

A

HIGH SERUM LIPASE** AND AMYLASE(x3 normal value)

FBC, UandE, LFT, blood cultures, CRP
abdo ultrasound *- look for gallstones
CT - after 48 hrs to assess for necrosis

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7
Q

Which scale is used to assess severity of acute pancreatitis?

A

GLASGOW SCALE

P - PaO2 <8 kPa
A - age >55 y/o
N - neutrophilia >15
C - calcium <2 mmol/L
R - renal urea >16 mmol/L
E - enzymes AST/ ALT >200 units
A - albumin <32 g/L
S - sugar >10 mmol/L
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8
Q

Describe the difference between mild, moderate and severe acute pancreatitis

A

MILD = no local or systemic complications or organ dysfunction

MODERATE = local complications +/- organ dysfunction but symptoms resolve within 48 hrs

SEVERE = persistent organ dysfunction over 48 hrs and leads to complications e.g. necrosis, abscess

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9
Q

How is acute pancreatitis managed?

A
  1. admit to hospital
  2. IV fluids
  3. analgesia - pethidine +/- benzodiazepines
  4. NBM and enteral feeding
  5. prophylactic abx
  6. refer to ITU if severe
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10
Q

What is chronic pancreatitis?

A

chronic inflammation, fibrosis and calcification of the pancreas leading to irreversible damage and endocrine and exocrine dysfunction

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11
Q

What are the main causes of chronic pancreatitis?

A

alcohol **
idiopathic chronic pancreatitis **

others: autoimmune, previous acute pancreatitis, metabolic, trauma, hypercalcaemia, CF

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12
Q

What are the 4 main pathological features of chronic pancreatitis?

A
  1. chronic inflammation
  2. fibrous scarring
  3. loss of pancreatic tissue
  4. duct strictures with formation of calculi
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13
Q

What are the symptoms of chronic pancreatitis?

A

epigastric pain - chronic , raidates to back, worse on eating, relieved when sitting forward
nausea and vomiting

EXOCRINE DYSFUNCTION - failure to produce digestive enzymes (amylase, lipase, protease) -> malabsorption, weight loss, steatorrhoea, diarrhoea

ENDOCRINE DYSFUNCTION - failure to produce insulin and impaired glucose regulation -> Diabetes mellitus

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14
Q

What are the complications of chronic pancreatitis?

A

pancreatic cancer !!
pseudocyst
calcification

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15
Q

How is chronic pancreatitis managed?

A
  1. abdominal ultrasound
  2. manage pain - pethidine, opiates
  3. manage malabsorption - give pancreatic enzymes (amylase, protease, lipase) and fat soluble vitamins (A,D,E,K)
  4. low fat diet, no alcohol
  5. screen for diabetes - insulin needed?
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16
Q

What is the most common type of pancreatic cancer and where?

A

infiltrating ductal adenocarcinoma in the HEAD of the pancreas

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17
Q

List the risk factors for pancreatic cancer?

A
alcohol *
smoking * 
obesity and diet 
diabetes 
chronic pancreatitis 
FH and syndromes e.g. BRCA2**, FAP, LYNCH, MEN2
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18
Q

when would you suspect pancreatic cancer?

A
epigastric pain / discomfort/ back ache
weight loss, nausea and vomiting 
steattorhoea
progressive obstructive jaundice - pale stools, dark urine, pruritus
palpable gallbladder (Courvoisier)
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19
Q

How is pancreatic cancer diagnosed?

A

abdo USS ** - confirms tumour mass
+ CT/ PET scan - to stage and if any mets
tumour marker : CA19-9 **

+ LFT (raised bilirubin, GGT, ALP), hyperglycaemia

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20
Q

How is pancreatic cancer managed?

A
  1. often metastatic and poor prognosis
  2. 10-20% resectable - WHIPPLES procedure and chemo
  3. ERCP with stenting if palliation
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21
Q

What are the 3 metabolic causes of liver disease?

A
  1. hereditary haemochromatosis
  2. Wilsons disease
  3. alpha 1 anti-trypsin disease
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22
Q

What is hereditary haemochromatosis?

A

deficiency of hepcidin causing increased intestinal absorption of iron and deposition of iron in the tissues

N.B. hepcidin is produced by hepatocytes in response to high iron levels and stops absorption of iron in the enterocytes by blocking ferroportin

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23
Q

How is hereditary haemochromatosis inherited?

A

autosomal recessive

HFE gene in chromosome 6

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24
Q

what are the features of hereditary haemochromatosis?

A

early: fatigue, arthralgia, ED, weakness
late: skin bronzing, cirrhosis, diabetes, impotence, cardiomyopathy

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25
How is hereditary haemochromatosis diagnosed?
1. iron studies: high serum ferritin, high transferrin saturation levels 2. HFE genetic testing 3. liver biopsy with Perls stain 4. LFTs
26
How is hereditary haemochromatosis managed?
1. venesection weekly (400-500ml) 2. low iron diet 3. liver transplant 4. monitor ferritin
27
What is wilsons disease?
accumulation of copper in the tissues caused by increased absorption of copper in the small intestine and decreased hepatic copper excretion
28
How is wilsons disease inherited?
autosomal recessive defect in ATP7B gene on chromosome 13
29
what are the features of wilsons disease?
liver disease - cirrhosis, hepatitis neurological disease - basal ganglia degeneration, behavioural changes, depression
30
What could you see on examination of wilsons disease?
kayser fleischer rings - blue ring circles in the iris caused by copper deposits
31
How is wilsons disease investigated?
serum copper REDUCED serum cerulosplasmin REDUCED increased 24hr urinary copper excretion liver biopsy
32
How is wilsons disease managed?
1. PENICILLAMINE ORAL - copper chelator | 2. avoid foods with copper e.g. chocolate, alcohol, mushrooms
33
What is alpha 1 antitrypsin deficiency disorder and how is it inherited?
autosomal recessive disorder A1AT is a glycoprotein produced in the liver that balances the action of neutrophil elastase in lungs deficiecny of A1AT causes break down of elastin in the alveoli causing destruction
34
What are the features of A1AT deficiency?
1. lung disease = COPD e.g. dyspnoea, wheeze, chest tightness -> CXR, spirometry 2. liver disease = cirrhosis, fibrosis, hepatitis -> LFTs, biopsy
35
How is A1AT deficiecny treated?
1. treat as would for COPD | 2. smoking cessation
36
What are the causes of hepatocellular carcinoma?
chronic liver disease and cirrhosis ** alcohol induced liver disease ** Hepatitis B and C ** + obesity, diabetes, metabolic liver disease, smoking, +ve FH
37
How does hepatocellular carcinoma present?
often incidental finding in patients with cirrhosis ``` VAGUE SYMPTOMS: malaise, weight loss jaundice abdo pain - with acute onset of severe pain (intraperitoneal bleeding due to tumour rupture) abdo distension palpable abdo mass ```
38
How is hepatocellular carcinoma diagnosed?
1st line = ultrasound (hypo or hyperechoic nodules) | tumour marker = alpha fetoprotein (60%)
39
How is hepatocellular carcinoma managed?
surgical resection or transplant | only 5% suitable for curative treatment
40
How can alcohol affect the liver?
1. alcohol induced fatty liver - heavy alcohol over months, reversible if abstinence of alcohol 2. alcohol hepatitis - heavy alcohol over LONG time 3. alcoholic cirrhosis - continued alcohol exposure , irreversible damage
41
How does alcohol hepatitis present?
``` acute onset of malaise jaundice anorexia and malnutrition diarrhoea and nausea tender hepatomegaly ```
42
How is alcohol hepatitis investigated and what do the tests show?
FBC -> raised MCV, raised WCC LFT -> raised GGT, raised bilirubin, increased prothrombin time liver biopsy - affects stellate cells USS and fibroscan
43
What would the biopsy of alcohol hepatitis show?
``` necrosis of liver cells mallory bodies inflammation fatty changes hepatocyte ballooning ```
44
How is alcohol hepatitis managed?
1. monitor urine output as at risk of AKI 2. vit K and thiamine 3. protein supplements and nutrition
45
What are the key characteristics of cirrhosis?
IRREVERSIBLE DAMAGE TO THE LIVER: 1. chronic hepatocyte NECROSIS - impaired liver function and decreased synthesis of clotting factors 2. FIBROSIS - normal matrix replaced by collagen and fibronectin 3. NODULES - hepatocyte regeneration converting normal architecture to nodules and distorting hepatic vasculature
46
What are the causes of liver cirrhosis?
alcohol ** hepatitis B and C ** non alcoholic fatty liver disease metabolic liver disease + biliary cirrhosis, budd chiari syndrome, CF, autoimmune liver disease, gallstones
47
What are the symptoms of cirrhosis?
``` jaundice fatigue, malaise weight loss, muscle wasting splenomegaly, hepatomegaly ascites sexual characteristic changes - gynaecomastia, hirsuitism , testicular atrophy pitting oedema ```
48
What are the signs of cirrhosis?
``` F - finger clubbing L - leukonychia A - asterixis P - palmar erythema S - scratching, spider naevi ```
49
How is cirrhosis investigated?
1. Liver biopsy - 3 characteristics (not done as commonly now fibroscan available) 2. fibroscan ** 3. LFTs - raised GGT (if alcohol), AST and ALT raised , low albumin 4. FBC - increased prothrombin, decrease platelets to find cause: viral screen, ultrasound
50
How is cirrhosis scored?
child pugh score or Model for End Stage Liver Diseases (MELD)
51
how is cirrhosis managed?
1. stop cause - alcohol abstinence, anti virals 2. manage complications 3. 6 monthly checks for HCC (USS and alpha fetoprotein)
52
What are the complications of cirrhosis?
1. hepatocellular carcinoma 2. portal hypertension 3. hepatic encephalopathy 4. oesophageal varices 5. ascites 6. liver failure
53
What is ascites?
abnormal collection of fluid within the peritoneal cavity
54
What are the causes of ascites?
serum ascites with albumin <11 g/L - cirrhosis - liver mets - alcoholic hepatitis - acute liver failure - fatty liver of pregnancy - budd chiari syndrome serum ascites albumin >11 g/L - portal HTN - TB peritonitis - pancreatic ascites - bowel obstruction - biliary ascites
55
How does ascites presents?
abdominal distension weight gain abdo discomfort peripheral oedema
56
What do you find on examination of ascites?
shifting dullness | fluid thrill
57
What are the complications of ascites?
spontaneous bacterial peritonitis | hepatorenal syndrome
58
How is ascites managed?
1. fluid restrict 2. salt restriction 3. diuretics - spironolactone 4. paracentesis 5. peritoneovenous shunt - catheter from peritoneal cavity into internal jugular vein
59
What causes hepatic encephalopathy?
cirrhosis chronic liver failure RF: AKI, spontaneous bacterial peritonitis, GI bleed, constipation, drugs (sedatives, diuretics)
60
How is hepatic encephalopathy graded and what are the features?
0 - minimal change in memory/ intelligence 1- mild confusion, euphoria, depression 2- gross deficits in mental ability, inappropriate behaviour, drowsy 3- somnolent but arousable, confusion, fits 4- coma
61
How is hepatic encephalopathy diagnosed?
SERUM AMMONIA RAISED + ECG (triphasic waves), MRI (for causes)
62
How is hepatic encephalopathy managed?
1. avoid sedatives 2. lactulose - promotes ammonia excretion 3. correct electrolyte imbalance 4. flumazenil (benzodiazepine receptor antagonist) short term
63
What are the 4 characteristics of liver failure?
1. hepatic encephalopathy 2. jaundice 3. abnormal bleeding 4. ascites
64
Define acute liver failure?
rapid onset within 8 weeks of initial illness of hepatocellular dysfunction leading to systemic complications
65
What are the main causes of acute liver failure?
1. paracetemol overdose ** 2. viral hepatitis 3. alcohol
66
How is paracetemol overdose treated?
N- acetylcysteine
67
What are the main features of acute liver failure?
jaundice coagulopathy hypoalbuminaemia
68
What are the complications of acute liver failure?
1. hepatic encephalopathy | 2. hepatorenal syndrome
69
What is the criteria for hepatorenal syndrome?
1. cirrhosis 2. ascites 3. creatine >133 mmol 4. no shock, hypokalaemia
70
Define chronic liver failure
>6 months of liver damage where the functional capacity of the liver is unable to maintain normal physiological conditions
71
What are the main causes of chronic liver failure?
1. hepatocellular carcinoma | 2. metabolic liver disease
72
What are the signs of chronic liver failure?
cirrhosis ascites FLAPS (finger clubbing, leukonychia, asterixis, palmar erythema, spider naevi)
73
How is chronic liver failure managed?
1. bloods: raised ALT, AST, bilirubin, low glucose, raised INR 2. find and treat cause 3. liver transplant
74
Describe the function of the gallbladder
bile is secreted in the liver and stored and concentrated in the gallbladder (via the hepatic duct and cystic duct) cholecystokinin is released when eating a meal so the gallbladder contracts and releases bile to digest food
75
What are the main compositions of gallstones and what are each of their risk factors?
CHOLESTEROL STONES** obesity, high fat diet, diabetes, women, CF ``` PIGMENT STONES (calcium bilirubinate) crohns, haemolytic anaemia, ileal resections, drugs (HRT, ceftriaxone, somatostatin analogues) ```
76
when do gallstones cause symptoms?
when gallstone gets stuck in the neck of the cystic duct so bile cannot escape and gallbladder becomes inflamed
77
Describe the features of symptomatic gallstones?
BILIARY COLIC - severe abdominal (RUQ) pain which comes in waves, sudden onset worsened by eating fatty foods pain radiates to scapular region pain relieved by analgesia or spontaneously associated nausea and vomiting
78
What are the complications of gallstones?
acute cholecystitis **(when bile becomes infected) pancreatitis gallstone ileus ileum obstruction
79
How are gallstones diagnosed?
1. abdominal ultrasound *** | 2. LFTs - rise in ALP, GGT and serum bilirubin
80
How are symptomatic gallstones treated?
analgesia - paracetemol/ NSAIDS or diclofenac/ opioids | laparoscopic cholecystectomy
81
What is acute cholecystitis and how is it caused?
inflammation of the gallbladder usually caused by **gallstones ** - gallstones impact neck of cystic duct causing bile to become concentrated and infected and cause an inflammatory reaction in the gallbladder
82
What are the key symptoms/ signs of acute cholecystitis?
1. RUQ pain (sudden, severe, several hrs) 2. fever (+ systemic upset e.g. nausea, vomiting, anorexia) 3. +/- Murphys sign
83
What are the complications of acute cholecystitis if left untreated?
``` necrosis of the gallbladder perforation of the gallbladder fistula biliary peritonitis jaundice (Mirizzi syndrome) ```
84
How should acute cholecystitis be investigated?
LFTs - abnormal FBC - raised WCC ESR/CRP - raised Ultrasound ** - thickened wall of gallbladder and shrunken gallbladder
85
How is acute cholecystitis treated?
1. IV fluids 2. IV antibiotics (cefuroxime) 3. opioids (pethidine) 4. laparoscopic cholecystectomy within 1 week
86
if a patient has acute cholecystitis but no gallstones, what is the diagnosis and their RF?
acalculous cholecystitis - 5% who present with cholecystitis do not have gallstones (high mortality) RF: trauma, burns, diabetes, narcotics, starvation, sepsis , AKI
87
What is ascending cholangitis?
inflammation of the bile duct (if common bile duct obstructed -> flow of bile reduced -> biliary stasis -> infection)
88
How is ascending cholangitis caused?
gallstones * ERCP * tumours (pancreatic cancer, cholangiocarcinoma) primary sclerosis cholangitis organism = E.COLI , klebsiella, enterococci
89
What are the symptoms of ascending cholangitis?
CHARCOTS TRIAD 1. fever 2. jaundice 3. RUQ pain or REYNOLDS PENTAD ( + altered mental state + hypotension / tachycardia)
90
How is ascending cholangitis investigated?
1. abdominal ultrasound - biliary dilatation 2. LFTs - abnormal 3. FBC - raised WCC, raised CRP
91
How is ascending cholangitis managed?
1. ABCDE (medical emergency) and treat septic shock 2. IV fluids 3. IV antibiotics (metronidazole and ceftriaxone) 4. ERCP (emergency biliary drainage within 24-48 hrs)
92
How is primary biliary cirrhosis caused?
AUTOIMMUNE condition where there is slowly progressive chronic granulomatous inflammation in the small interlobular bile ducts in the liver (typically in MIDDLE AGED FEMALES)
93
How does primary biliary cirrhosis present?
" itching in a middle aged women with autoimmune conditions e.g. SICCA) jaundice pruritus fatigue + hepatosplenomegaly, hyperpigmentation, xanthelasma, clubbing, RUQ pain
94
What is primary biliary cirrhosis associated with/ complications?
sjogrens syndrome ** malabsorption of fat soluble vit portal HTN hepatocellular carcinoma
95
How is primary biliary cirrhosis diagnosed?
1. anti mitochondrial antibody ** 2. LFT - raised ALP, GGT, AST, ALT 3. liver biopsy - granulomatous inflammation
96
How is primary biliary cirrhosis managed?
1. anti histamines for itch - cholestyramine 2. ursodeoxycholic acid (slow disease progression) 3. monitor for cancer (fibroscan and AFP)
97
what is a side effect of ursodeoxycholic acid?
weight gain
98
What is primary sclerosing cholangitis?
inflammation and fibrosis of the intra and extra hepatic bile ducts (in the liver and in the common bile duct)
99
What are the risk factors for primary sclerosing cholangitis?
``` ULCERATIVE COLITIS ** crohns HIV hepatitis males ```
100
How does primary sclerosing cholangitis present?
jaundice + pruritus RUQ pain fatigue
101
What are the worrying complications with primary sclerosing cholangitis?
cholangiocarcinoma colorectal cancer (need yearly colonoscopy and ultrasound)
102
How is primary sclerosing cholangitis investigated?
1. MRCP (magnetic resonance cholangio-pancreaticography) ** - diagnostic 2. ERCP - " beading" 3. liver biopsy - "onion skin fibrosis" 4. LFT - elevated ALK phos 5. ANCA antibodies
103
How is primary sclerosing cholangitis managed?
1. ursodeoxycholic acid (SE= weight gain) 2. symptom relief, stop alcohol 3. liver transplant
104
define portal hypertension
high pressure in the hepatic portal vein (>7mmHg)
105
What are the causes of portal hypertension?
PREHEPATIC - thrombosis HEPATIC - cirrhosis, hepatitis, alcohol hepatitis, schistosomiasis, sarcoidosis POST HEPATIC - R sided heart failure, budd chiari syndrome, veno occlusive disease, constrictive pericarditis
106
What is the function of the portal vein and how is it formed?
the SUPERIOR MESENTERIC VEIN and SPLENIC VEIN unite behind the pancreas to form the PORTAL VEIN which carries deoxygenated blood from the spleen and bowel to the liver to be detoxified before travelling to the heart and lungs
107
What are the signs of portal hypertension?
ascites dilated umbilical veins (caput medusea) splenomegaly signs of bleeding varices e.g. haematemesis and malaena
108
How is portal hypertension investigated?
1. portal pressure by "hepatic venous pressure gradient" 2. USS and fibroscan 3. doppler USS + endoscopy if worried about varices
109
How is portal hypertension managed?
1. treat cause 2. beta blockers to reduce pressure 3. liver transplant?
110
How is bilirubin made and excreted in the body?
1. RBCs breakdown to release haem which contains unconjugated bilirubin 2. albumin attaches to unconjugated bilirubin and travels to liver 3. UGT (uridine glucouranyl transferase) conjugates the bilirubin in the liver 4. the conjugated bilirubin is excreted in the bile into urobilinogen 5. it is then excreted in faeces, urine or return to enterohepatic circulation
111
What are the causes for pre hepatic jaundice?
haemolytic anaemia e.g. sickle cell disease, G6PDD, thalassaemia (increased haemolysis causes excess unconjugated bilirubin which cannot be conjugated in the liver)
112
What are the expected blood results for pre hepatic jaundice?
high unconjugated bilirubin normal ALT/AST normal ALP
113
What are the causes of hepatic jaundice?
damage to the hepatocytes directly 1. Gilberts syndrome 2. Crigler najjar Syndrome 3. viral hepatitis 4. cirrhosis 5. wilsons 6. autoimmune
114
What would you expect on LFTs of hepatic jaundice?
high conjugated bilirubin leves high ALT/AST high ALP increased clotting time
115
What are the causes of post hepatic jaundice?
= passage of conjugated bilirubin through the biliary tree is blocked and leaks into circulation instead which is then excreted in the urine pancreatitis primary biliary cirrhosis gallstones pancreatic carcinoma
116
What are the signs of post hepatic jaundice?
dark urine pale stools itching
117
when is non alcoholic fatty liver suspected?
1. <18 units / week of alcohol 2. fatty liver on ultrasound (RF: diabetes, obesity, Wilsons)
118
List inducers of cytochrome P450
"metabolise the drug quicker in the liver" ``` phenytoin carbamazepine chronic alcohol amiodarone st Johns wart ```
119
List inhibitors of cytochrome P450
sodium valproate acute alcohol SSRI ciprofloxacin
120
What is the cause of itch in liver patients and how do you treat?
increase in BILE SALTS Rx: colestyramine