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Phase 2a Flashcards > Liver and friends > Flashcards

Liver and friends Flashcards

1
Q

Types of liver injury? Presentation?

A

Acute–> liver failure/ recovery
Chronic–> cirrhosis–> liver failure: varices, hepatoma or recovery
Acute= malaise, nausea, anorexia, jaundice
Rarer= confusion, bleeding, liver pain, hypoglycaemia
Chronic= ascites, oedema, haematemesis, malaise, anorexia, wasting, bruising, itching, hepatomegaly, abnormal LFTs
rarer= confusion, jaundice

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2
Q

What serum liver function tests are there? Jaundice types and known as?

A

Serum bilirubin, albumin, prothrombin time
Serum liver enzymes= alkaline phosphatase, gamma-GT, hepatocellular: transaminases (AST, ALT)
Unconjugated= ‘pre-hepatic’, Gilberts, haemolysis
Conjugated= ‘cholestatic,’
liver disease- ‘hepatic,’
bile duct obstruction ‘post hepatic’

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3
Q

Urine, stools, itching and LFTs in pre-hepatic/ hepatic and post-hepatic jaundice?

A

Pre-hepatic- urine= normal, stools= normal, no itching, LFTs normal
Hepatic/ post-hepatic- urine= dark, stools= may be pale, itching= maybe, liver tests= abnormal

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4
Q

Features of gallstones? Risk factors? Presentation?

A

Most form in gallbladder, 1/3 women over 60
70% cholesterol, 30% pigment +/- calcium
Risk factors= female, fat, fertile, most= asymptomatic
Cholecystitis= inflame of gall bladder, cholangitis= inflammation of bile duct

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5
Q

Management of gallstones? Bile duct stones? Other stone types, features and causes? Factors for stones being symptomatic?

A

Laporoscopic cholecystectomy- removal of gall bladder
Bile acid dissolution therapy= <1/3 success

ERCP w/ sphincterotomy and removal, crushing, stent placement, surgery for larger stones

Pigment stones- small friable and irregular, causes= haemolysis
Cholesterol stones- large, often solitary, causes= female, age, obesity
Mixed- faceted (calcium salts, pigment and cholesterol)
Smoking, parity

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6
Q

What is unconjugated hyperbilirubinaemia? Causes x4?

A

Pre-hepatic–> haemolytic jaundice–> normal LFT
Overproduction- haemolysis
Impaired hepatic uptake- drugs, right HF
Impaired conjugation: Gilberts syndrome- decreased UDP glucoronyl transferase enzyme, Crigler-Najjar disease- enzyme mutation
Physiological neonatal jaundice- fetal Hb replaced with adult Hb, excrete bilirubin as quickly as an adult

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7
Q

What is conjugated hyperbilirubinaemia? What is cholestatic jaundice? Divided into what?

A

Increased in conjugated bilirubin- water soluble, dark urine, pale stools
Impaired/ obstructed bile flow- associated with itching and abnormal LFT
Intra-hepatic cholestatis- viruses, pregnancy, cirrhosis, alcohol, drugs–> hepatocellular swelling/ abnormalities of bile excretion
Extra-hepatic cholestasis- bile duct stones, Mirrizi’s syndrome, carcinoma of bile duct or pancreas or PSC–> bile outflow obstruction

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8
Q

Symptoms of jaundice?

A

Biliary pain, rigors, abdomen swelling, weight loss, past history of biliary disease/ intervention/ malignancy/ heart failure/ blood products, drug history, social history, look for hepatomegaly, splenomegaly or ascites

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9
Q

Investigations for jaundice?

A

Liver enzymes- very high AST/ ALT suggests liver disease
Biliary obstruction- 90%= dilated intrahepatic bile ducts on US
CT, MRCP, ERCP
Urine- bilirubin is absent in pre-hepatic causes, obstructive= urobilinogen absent
Haematology- FBC, clotting, film, reticulocyte count, Coombs’ test and haptoglobin for haemolysis, malaria parasites
Chem- U&E, LFT, ALT, AST, alk phos, gamma-GT, total protein, albumin, AST>1000 probably viral hepatitis
Micro- blood and other cultures, leptospirosis, hep A, B, C serology
US to see if bile ducts dilated, gallstones, hepatic metastases, pancreatic mass —> treat cause

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10
Q

What is acute cholecystitis? Causes?

A

Inflammation of the gallbladder
Blockage of cystic duct w/ gallstones (cholelithiasis)–> build-up of bile in gallbladder–> right upper abdominal pain
Conc bile, pressure and bacterial infection- irritates gallbladder wall–> inflammation
May cause continuous epigastric or RUQ pain, vomiting, fever, local peritonism
Main difference from biliary colic= inflammatory component- local peritonism, fever, WCC increase
If moves to CBD- obstructive jaundice and cholangitis may occur

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11
Q

Signs of acute cholecystitis? Tests? Tx?

A

Murphy’s sign- 2 fingers over RUQ, pt breathes in, causes pain and arrest of inspiration, only +ve if same test in LUQ does not cause pain
Phlegmon may be palpable- RUQ mass of inflamed adherent momentum and bowel
WCC increase, US- thick walled, shrunken GB, peri cholecystic fluid, stones, CBD dilated, plain AXR
Nil by mouth, pain relief, IVI- cefuroxime IV
Laparoscopic cholecystectomy
Open surgery if GB perforation
Elderly/ high risk= ERCP, cholecystectomy
Acalculous= cholecystostomy, give IV amoxicillin and clavulinic acid and IV fluids

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12
Q

Symptoms of chronic cholecystitis? Tests and Tx? If symptoms persist post-op consider what?

A

Chronic inflammation +/- colic, flatulent dyspepsia, vague abdominal discomfort, distension, nausea, flatulence, fat intolerance
US to image stones and CBD diameter, MRCP to find CBD stones
Cholecystectomy- dilated CBD with stones= ERCP and sphincterotomy before surgery
Hiatus hernia, IBS, peptic ulcer, relapsing pancreatitis, tumour

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13
Q

What is biliary colic used to describe? Gallstones are symptomatic with what? Rx and Tx?

A

A type of pain related to the gallbladder that occurs when a gallstone transiently obstructs the cystic duct and the gallbladder contracts
With cystic duct obstruction/ passed into CBD, RUQ pain +/- jaundice
Rx= analgesia, rehydrate, NBM, elective laparoscopic cholecystectomy

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14
Q

Diff diagnosis of biliary colic? Other presentations?

A

Overlap as part of spectrum of gallstone disease, urinalysis, CXR and ECG help exclude other diseases
Obstructive jaundice with CBD stones- LFT worsening, ERCP with sphincterotomy and biliary trawl, then cholecystectomy may be needed, or open surgery
Ascending cholangitis
Gallstone ileus
Pancreatitis
Mucocoele/ empyema- obstructed GB filled with mucus
Silent stones
Mirizzi’s syndrome- stone in GB presses on bile duct causing jaundice
Gallbladder perforation- rare due to dual blood supply

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15
Q

Causes of drug induced liver injury? 3 types?

A

Acute hepatitis, acute liver failure, paracetamol, idiosynchratic
Hepatocellular= ALT>2 ULN, ALT/ Alk phos> 5
Cholestatic= Alk phos>2 ULN or ratio <2
Mixed= ratio >2, but <5
Direct toxicity and idiosyncratic DILI

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16
Q

Approach to drug induced liver injury?

A

What did you start recently- contact GP, time course= critical- onset usually 1-12 weeks of starting, earlier= unusual, may be several weeks after stopping
Resolution- 90% within 3 months of stopping, 5-10% prolonged
Inadvertent re-challenge, seen in 6%

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17
Q

Drugs known to cause jaundice? Not involved?

A

Antibiotics- augmenting, flucloxacillin, erythromycin, septrin, TB drugs
CNS drugs- chlorpromazine, carbamazepine valproate, paroxetine, immunosuppressants, analgesics/ musculoskeletal, PPIs, dietary supplements

Low dose aspirin, NSAIDs other than diclofenac, Beta blockers, HRT, ACEi, thiazides, CCBs

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18
Q

What is given to counteract paracetamol induced fulminant hepatic failure? Supportive to correct what? Poor prognosis indicators?

A

N acetyl cysteine (NAC)
Coagulation defects, fluid electrolyte and acid base balance, renal failure, hypoglycaemia, encephalopathy

Late presentation, acidosis<7.3 pH, prothrombin time> 70 seconds, serum creatinine> 300micromol/ l, consider liver transplant- 80% mortality otherwise

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19
Q

What does alcoholic liver disease encompass? Chronic consumption results in what? Still functions after what % hepatocytes dead?

A

Liver manifestations of alcohol overcomsumption, including fatty liver, alcoholic hepatitis and chronic hepatitis w/ liver fibrosis or cirrhosis
Secretion of pro-inflammatory cytokines (tif-alpha, IL6 and IL8), oxidative stress, lipid per oxidation and acetylaldehyde toxicity–> inflammation, apoptosis and eventually fibrosis of liver cells
75%

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20
Q

Changes way liver metabolises/ produces what? Acute alcohol injury causes what and is mediated by what? Injured liver cells may accumulate what? Fat accumulation is known as what within hepatocytes? Large/ small droplet known as what? Associated with and mediated by what?

A

Fat
Hepatocyte ballooning, by neutrophils
Cytoskeletal protein which appears irregular and red on an H&E stain- Mallory’s hyalin
Steatosis- macrovesicular/ micro vesicular- acute/ chronic liver injury, by lymphocytes

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21
Q

Alcohol and other drugs have most affect on cells with lowest what? Damage results in what? % heavy alcohol drinkers getting serious ALD, % stop and % reduce drinking?

A

On cells with lowest oxygen and blood supply (zone 3)- fibrosis, with pericellular fibrosis in zone 3 been more common in alcohol-related injury than fibrosis of portal tracts
10-20%, 25% and 25%

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22
Q

Fatty liver can lead to what? S+S of alcoholic hepatitis? Tests?

A

Alcoholic hepatitis/ cirrhosis + infection–> acute decompensation
Malaise, TPR increase, anorexia, D&V, tender hepatomegaly+/- jaundice, bleeding, ascites
Blood–> WCC increase, platelets decreased, INR increase, AST increase, MCV increase, urea increase

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23
Q

Signs of severe hepatitis? Most need what? Screen for what? Stop what? What vitamin given?

A

Jaundice, encephalopathy or coagulopathy
Hospitalising; urinary catheter and CVP monitoring may be needed
Infections +/- ascitic fluid tap, treat for SBP
Alcohol consumption- chlordiazepoxide ORAL for withdrawal symptoms
Vit K IV for 3 days, thiamine PO

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24
Q

In alcoholic hepatitis, optimise what? Don’t use low what diets? Daily what tests? Prednisolone for 5d tapered over 3 weeks if Maddrey score above what with what? CI? What else? Prognosis?

A

Nutrition- use ideal body weight for calculations
Low-protein diets even if encephalopathy
Daily weight, LFT, U&E, INR, Na+ decrease= common, water restriction may make worse
>31 and encephalopathy
Liver transplant
Mild episodes hardly affect mortality, severe= 50% at 30d, 1 yr after admission= 40% dead

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25
Q

What is biliary sepsis/ ascending cholangitis? Gallstone risk factors? Diagnosis based on Charcots triad?

A

Obstruction of the common bile duct–> bile stasis–> invasion of bacteria from the duodenum e.g. e.coli–> obstructive jaundice
Jaundice, RUQ pain, fever

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26
Q

What is cirrhosis? Signs of this?

A

Where liver does not function properly due to long-term damage, comes on slowly over months/ years, early on= often no symptoms
Scar tissue replaces normal parenchyma= irreversible

None (just increase LFT)/ decompensated end-stage liver disease
Chronic liver disease- Leukonychia= white nails, Terrys nails- white proximally but distal 1/3 reddened by telangiectasis, clubbing, palmar erythema, hyperdynamic circulation; Dupuytren’s contracture; spider naevi, Xanthelasma, Gynaecomastia, atrophic testes, loss of body hair, parotid enlargement, hepatomegaly

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27
Q

Complications of cirrhosis?

A

Hepatic failure- coagulopathy (decreased factors 2, 7, 9 and 10 causes increased INR), encephalopathy, hypoalbumineria, sepsis, SBP, hypoglycaemia
Portal hypertension- ascites, splenomegaly, portosystemic shunt including oesophageal varices, caput medusae- enlarged superficial periumbilical veins
HCC- increased risk

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28
Q

Tests for cirrhosis?

A

Blood= LFT- abnormal/ increased AST, ALT, increased alk phos, increased gamma GT, loss of synthetic function, decreased albumin +/- increased PT/ INR, decreased WCC and platelets= hypersplenism
Liver US- small liver/ hepatomegaly, splenomegaly, focal liver lesion(s), hepatic vein thrombus, reversed flow in portal vein or ascites
MRI= caudate lobe size increased, smaller islands of regenerating nodules
Ascitic tap- fluid sent for urgent MC&S, neutrophils> 250/mm3= SBP
Liver biopsy- clinical diagnosis confirmed

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29
Q

Management of liver cirrhosis?

A

Good nutrition= vital, alcohol abstinence, avoid NSAIDs, sedatives and opiates, colestyramine helps pruritus, US+/- alpha-fetoprotein every 3-6 months to screen for HCC
PBC= high-dose ursodeoxycholic acid may normalise LFT, penicillamine for Wilson’s disease
Ascites= bed rest, fluid restriction, low-salt diet, PO spironolactone, chart daily weight for weight loss, add furosemide if needs be, therapeutic paracentesis with concomitant albumin infusion may be tried
SBP= cefotaxime/ tazocin for 5d, prophylaxis for high risk
Renal failure

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30
Q

Prognosis and poor prognostic indicators in cirrhosis? Survival from liver transplantation?

A

5yr survival= 50%, encephalopathy, serum Na+<110mmol/L, serum albumin< 25g/L; increased INR
Only definitive Tx, increases 5yr survival from 20% in end-stage disease–> 70%

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31
Q

Types of liver failure? What is it? What is fulminant liver failure?

A

Acute hepatic failure- occur suddenly in previously healthy liver, often from decompensation of chronic liver disease= acute-on-chronic hepatic failure
Clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function
Hyperacute= encephalopathy within 7d of onset of jaundice, acute= within 8-28 days, subacute= within 5-26 weeks
Decreasing risk of cerebral oedema as onset of encephalopathy is increasingly delayed

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32
Q

What is acute liver failure? Causes of chronic liver failure?

A

Rapid development of hepatocellular dysfunction- coagulopathy and mental state changes specifically in patient without known liver disease
Alcohol, non-alcoholic steatohepatitis (NASH), viral hep- B,C, immune (autoimmune hep, PBC, sclerosing cholangitis), metabolic- haemochromatosis, Wilsons, alpha 1 antitrypsin deficiency, vascular- Budd-Chiari

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33
Q

Investigations for liver failure? Why do these pts ‘go off’? Signs?

A

Viral serology- hep B surface antigen, hep C antibody, immunology- autoantibodies, coeliac antibodies, Its, biochem- iron, copper studies: caeruloplasmin, 24 hr urine copper, USS/CT/MRI
Constipation, drugs, GI bleed, infection, hypo-naetraemia, kalaemia, glycaemia, alcohol withdrawal, other
Jaundice, hepatic encephalopathy- unable to remove toxins, fetter hepaticus- smells like pear drops, asterisks, constructional apraxia- cannot copy 5-pointed stat,

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34
Q

Tests for liver failure?

A

FBC, U&E, LFT, clotting, glucose, paracetamol level, hepatitis, CMV and EBV serology, ferritin, alpha-1-antitrypsin, caeruloplasmin, autoantibodies
Blood culture, urine culture, ascitic tap for MC&S of ascites
CXR, abode US, Doppler studies of portal vein
EEG, evoked potentials have limited role

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35
Q

Management of liver failure?

A

Beware sepsis, hypoglycaemia, GI varices and encephalopathy
20 degrees uptilit in ITU, protect airway with intubation and insert NG tube to avoid aspiration and remove any blood from stomach
Insert urinary and central venous catheters to help assess fluid status
Montior T degree respirations, pulse, BP, pupils, urine output hourly, daily weights
Check FBC, U&E, LFT and INR daily
10% glucose IV, 1L/12h to avoid hypoglycaemia, blood glucose every 1-4h
Treat the cause
Dietary help
Seizures= lorazepam
Haemodialysis, avoid sedatives
PPI

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36
Q

Liver failure Tx complications? Worse prognosis indicators?

A

Cerebral oedema- 20% mannitol IV ITU
Ascites= restrict fluid, diuretics, weigh daily
Bleeding- vitamin IV for 3 days, platelets, FFP
Infection= ceftriaxone 1-2g/24h IV, not gentamicin
50ml of 50% glucose for hypoglycaemia
Avoid sedatives, head-tilt 20 degrees,, lactulose and regular enemas
Grade 3-4 encephalopathy, age> 40 years, albumin<30g/L, increased INR, drug-induced liver failure, late-onset hepatic failure= worse than fulminant

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37
Q

Renal failure in liver disease due to what? Coma in liver disease due to what? End-stage liver disease represented by what? Risk in long-standing cirrhosis?

A

Drugs, infection, GI bleeding, myoglobinuria, renal tract obstruction
Hepatic encephalopathy, infection, GI bleed, constipation, hypokalaemia, drugs, hyponatraemia/ hypoglycaemia, intracranial event
Cirrhosis- residual nodules remaining small due to micro nodular can regenerate–> macronodular cirrhosis- replications errors–> neoplasia
Hepatocellular carcinoma

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38
Q

Other consequences of liver dysfunction? Drugs prescribing in liver disease?

A

Malnutrition, coagulopathy, endocrine changes, vit K deficiency, hypoglycaemia
Analgesia- sensitive to opiaites, sedation- short-acting benzodiazepines, diuretics- excess weight loss, hyponatraemia, hyperkalaemia, renal failure
Antihypertensives- can often stop, avoid ACE inhibitors, aminoglycosides- avoid

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39
Q

Tx of liver disease consequences?

A 
Malnutrition= naso-gastric feeding, variceal bleeding= endoscopic banding, propanolol, terlipressin, encephalopathy= lactulose, ascites/ oedema= salt/ fluid restriction, diuretics, paracentesis
Infections= antibiotics
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40
Q

What is viral hepatitis? Causes and symptoms of acute hepatitis? Of chronic hepatitis? Complications?

A

Acute<6m since onset, chronic>6m since onset
Infectious(viral- Hep A-E, herpes viruses (EBV, CMV, VZV,) non-viral= leptospirosis, toxoplasmosis, coxiella or non infectious- alcohol, drugs, toxins, pregnancy, autoimmune, hereditary metabolic
Can be asymptomatic, malaise, myalgia, GI upset, abdo pain, +/- jaundice, tender hepatomegaly, raised AST, ALT +/- bilirubin

Can be asymptomatic, signs of chronic liver disease, decompensated= jaundice, ascites, low albumin, coagulopathy, encephalopathy
Hepatocellular carcinoma, portal hypertension

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41
Q

What is and transmission of hep A? Incubation period? Management?

A

Most common, RNA, worldwide, faeco-oral transmission via contaminated food/ water (shellfish, travellers, food handlers)
Short incubation period–> fever, malaise, anorexia, nausea, arthralgia then jaundice, splenomegaly and adenopathy appearing (2-3 weeks,) acute hep only, usually self-limiting, 100% immunity post infection

Supportive, monitor liver function, management of close contacts (HBIG given to within 14 days contact,) primary prevention= vaccine (travellers, work exposure, prevention of secondary cases, lifestyle risk, other liver disease)

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42
Q

What is and transmission of hep E? Presents? Tx?

A

Small RNA virus, faeco-oral transmission, also zoonotic- pig reservoir, self limiting acute hep, mortality increased in pregnant women
Often asymptomatic, can cause chronic in immunocompromised, serology similar to hep A, HEV RNA= detect chronic infection, vaccine being developed
Supportive, ribavirin, prevention- food hygiene, animal husbandry, vaccine being developed

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43
Q

What is and transmission of hep B? Incubation period? Natural history?

A

Hepadnavirus-DNA virus, transmission= blood-borne, vertical, highly infectious
>90% clear acute infection, those–> chronic HBV
1-6m, S&S similar to HAV but arthralgia and urticarial (red rash on skin) more common
Immune tolerance phase= high viral replication, highly infective, ALT normal
Immune clearance phase= liver inflammation with high ALT and HBV DNA levels
Inactive HBV carrier phase- HBV DNA levels low, ALT normal and no liver inflammation, HBeAg absent
Reactivation phase- ALT and HBV DNA levels persistently increased–> inflammation on liver biopsy and fibrosis develops

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44
Q

Management of HBV? Tx?

A

Supportive, monitor liver function, management of contacts w/vaccine and HBIG asap, follow-up HbsAg @6m, primary prevention
Pegylated interferon-alpha-2a SC- immune response, SEs= flu-like, thyroid issues, anaemia, mood disturbance
or nucleotide analogues, tenofovir, entecavir ORAL- inhibits viral replication, high barrier to resistance w/ minimal SEs, need renal monitoring

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45
Q

What is and transmission of hep D? Chronic hep B and D–> what? What is seen with chronic HBV? % response to prolonged course of pegylated interferon-alpha?

A

Defective RNA virus- need presence of HBV, blood and bodily fluids transmission
With HBV–> increased severity of acute infection
Increased rate of fibrosis progression, Hep D= usually dominant (HBV DNA low, HDV RNA high)
Super-infection(secondary acute hepatitis, increased fulminant risk, increased progression of liver disease)
30%

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46
Q

What is and transmission of hep C? HCV testing? Risk factors for progression?

A

Flavivirus (RNA), genotypes 1-6, transmission= blood borne
Look for HCV antibody if you have infection exposure, median of 90 days detection, false negatives if acute infection/ immunocompromised
Look for HCV RNA if have current infection or acute/ chronic infection diagnosis
Male, older, higher viral load, alcohol, HIV, HBV

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47
Q

Tx and prevention of hep C?

A

Pegylated interferon and ribavirin (ORAL)- sustained virological response w/ undetectable HCV RNA for 6m post end of tx–> cure
New direct acting antivirals- protease inhibitors- teleprevir, simeprevir, declatasvir, ledipasvir, sofobusvir
No vaccine, previous infection NOT immunity, screening blood products, lifestyle modification, universal precautions handling bodily fluids

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48
Q

What is autoimmune hepatitis? Classification is by what? Presents and epidemiology?

A

Inflammatory liver disease- suppressor T-cell defects with autoantibodies directed against hepatocyte surface antigens
By autoantibodies
Young/ middle-aged women, up to 40%= acute, signs of AI disease- fever, malaise, urticarial rash, poly arthritis, pleurisy, pulm infiltration or glomerulonephritis
Remainder= gradual jaundice or asymptomatic and diagnosed with chronic liver failure, amenorrhea= common, tends to attenuate pregnancy

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49
Q

Complications and tests for AI hepatitis? Diagnosis?

A

Those with cirrhosis/ drug therapy
Serum bilirubin, AST, ALT and alk phos increased, hypergammaglobulinaemia, +ve autoantibodies, anaemia, WCC decreased and platelets decreased indicated hypersplenism
Liver biopsy- mononuclear infiltrate of lymphocytes and plasma cells in portal and periportal areas –> apoptosis, necrosis, chronic disease–> cirrhosis= worst
MRCP- excludes PSC if alk phos disproportionately increased
Based in IgG levels, autoantibodies, histology, some overlap e.g. PSC, PBC and chronic viral hepatitis

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50
Q

Management and prognosis of AI hepatitis?

A

Immunosuppressant therapy- prednisolone PO for 1 month, decreased by 5mg a month, corticosteroids sometimes stopped after 2 years, azathioprine to maintain remission
Liver transplantation- for decompensated cirrhosis or failure to medical therapy, 10 yr survival= 75%
Doesn’t matter if symptomatic/ asymptomatic, cirrhosis reduces, overlap- AIH-PBC is worse than AIH-AIC

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51
Q

What is primary biliary cirrhosis? What is it marked by? What is cholestasis? Can lead to what?

A

Autoimmune disease of the liver
By slow progressive destruction of the small bile ducts of the liver by chronic autoimmune granulomatous inflammation- intralobular ducts and Canals of Herine affected early in disease
Ducts damaged- bile and other toxins build up in the liver, damages liver over time
Scarring, fibrosis, portal HTN and cirrhosis

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52
Q

The disease of PBC is what? Staging is done by what system?What is stage 1? Close up view of bile duct branch shows what?

A

Patchy- all stages may co-exist in same liver, disease may not be detected on initial biopsy
Ludwig system- stage 1= florid duct lesion- dense mixed inflammatory infiltrate, rich in lymphocytes, present within portal tract, centred on bile duct
Epithelium is disrupted and damaged by lymphocytes, destroys bile duct branch eventually- portal tract has hepatic artery and portal branches but no bile duct= ductopaenia

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53
Q

Primary biliary cirrhosis presents as what? Associated diseases? Cause? What are hallmark of PBC? Risk increased by?

A

Often asymptomatic, alkaline phos increased on routine LFT, lethargy, dry eyes, joint pain, vatical bleeding, liver failure, sleepiness, pruritus
Sjogrens, thyroiditis, scleroderma, CRST, rheumatoid arthritis, lung and coeliac disease
Unknown environmental triggers and genetic predisposition–> loss of immune tolerance to self-mitochondrial proteins
Antimitochondrial antibodies- AMA
+ve family history, many UTIs, smoking, past pregnancy, other AI diseases, increased use of nail polish/ hair dye, typical age= 50 years

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54
Q

Signs and complications of PBC? Tests?

A

Jaundice, skin pigmentation, Xanthelasma- yellow plaques in eye, xanthomata; hepatosplenomegaly
Those of cirrhosis, osteoporosis common, malabsorption of fat-soluble vitamins due to cholestasis and decrease bilirubin in gut lumen–> osteomalacia and coagulopathy; HCC

Blood- increased alk phos, increased gamma GT, mildly increased AST and ALT, late= increased bilirubin decreased albumin, increased prothrombin time, AMA M2 subtype +ve, Igs increased, TSH and cholesterol increased or normal
US exclude extra hepatic cholestasis
Biopsy not usually needed- look for granulomas around bile ducts +/- cirrhosis

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55
Q

Tx of primary biliary cirrhosis? Prognosis?

A

Symptomatic- pruritus- colestyramine PO, naltrexone and rifampicin may help, diarrhoea= codeine phosphate e.g. PO, osteoporosis prevention
Fat-soluble vitamin prophylaxis- A D and K, high dose UDCA–> improved enzymes, bilirubin
Regular LFT,US, AFP
Liver trans for end-stage= bili> 100micromol/L

Once jaundice develops, survival< 2 years without transplantation

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56
Q

What is primary sclerosing cholangitis? Can lead to what? Characterised by what histologically?

A

Disease of bile ducts that causes inflammation and obliterative fibrosis of bile ducts and/ or outside of liver
Impedes flow of bile to intestines–> cirrhosis, LF, strictures +/- gallstones
Early stages= peri-ductal oedema, ‘‘onion ring,’’ lymphocytes, lesions in irregular fashion along ducts, secondary cholangitis with neutrophils within bile ducts may be present

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57
Q

PSC eventually causes what? Shows what in biopsy? Amount of iron present is graded by size of what present? High grade usually associated with what?

A 
Ductopaenia- loss of bile duct branch 
Cirrhosis and ductular proliferation at edges of fibrous septa, minimal chronic inflammation, no signs of acute damage, no clues on H&amp;E stain as to cause of cirrhosis 
Perl's stain= ferric iron stains blue 
Granules- 0-4 
Haemochromatosis
58
Q

Signs and symptoms of primary sclerosing cholangitis? Associations and cancers related?

A

Pruritius, fatigue, advanced–> ascending cholangitis, cirrhosis and end-stage liver failure
Male sex, HLA-A1;B8;DR3, autoimmune hepatitis, IBD IN 50%, usually UC of the whole colon, IBD often before PSC, risk of colorectal malignancy is significantly increased
Bile duct, gallbladder, liver and colon= more common, yearly colonoscopy and ultrasound; cholecystectomy for gallbladder polyps

59
Q

Tests for PSC? Tx?

A

Increased alk phos, then increasded bilirubin; hypergammaglobulinaemia; AMA-ve, but ANA, SMA and ANCA may be +ve, ERCP distinguishes large duct from small duct disease , liver biopy shows a fibrous, obliterative cholangitis
Liver transplant for end-stage disease, recurrence in up to 30%, prognosis worse for IBD, 5-10% colorectal cancer post-transplant, ursodeoxychoic acid may protect against colon cancer and improve LFT, high doses may be harmful
Colestyramine PO for pruritus, antibiotics for bacterial

60
Q

Commonest form of liver tumour? Signs and symptoms? Tests?

A

Secondary from breast, bronchus or the GI tract, primary less common- may be benign or metastatic
Fever, malaise, anorexia, weight loss, RUQ pain, jaundice is late, except with cholangiocarcinoma, bengin= often asymptomatic, tumours rupture–> intraperitoneal haemorrhage
Hepatomegaly, signs of chronic liver disease, jaundice, ascites, feel for abdo mass
FBC, clotting, LFT, hepatitis serology, alpha-fetoprotein, US/ CT to identify lesions and guide biopsy, MRI distinguishes benign or malignant lesions, ERCP and biopsy, liver biopsy

61
Q

What do liver metastases signify? What may be effective? What may be amenable, prognosis?

A

Advanced disease, tx and prognosis vary with type and extent of primary tumour, chemo may be effective
Small, solitary metastases may be amenable to resection, <6 months

62
Q

What is a hepatocellular carcinoma? Several what exist? The patient has what? Causes?

A

An adenocarcinoma/ primary hepatocytes neoplasia accounting for 90% of primary liver cancers, cells resemble normal hepatocytes–> large groups, acini or glands
Growth patterns
Fatigue, appetite loss, RUQ pain, weight loss, jaundice, ascites, haemobilia
HBV, HCV, AIH, cirrhosis, NAFL, aflatoxin, clonorchis sinensis, anabolic steroids

63
Q

Diagnosis of HCC? Treatment? Prevention?

A

4-phase CT, MRI, biopsy, bruit over the liver, blood–> alpha-fetoprotein- increased in 50-80% HCC
Resecting solitary tumours<3cm across increased 3 yr survival to 59% from 13%, liver transplant, percutaneous ablation, tumour embolisation, sorafenib= options
HBV vaccination, don’t reuse needles, screen blood, Aflatoxin exposure, AFP and US, consider increased risk

64
Q

What is cholangiocarcinoma? Causes? The patient has what? Management?

A

Biliary tree cancer, 10% liver primaries
Flukes, PSC, biliary cysts, Caroli’s disease, HBV, HCV, DM, biliary-enteric drainage surgery, N-nitroso toxins
Fever, abdo pain, malaise, raised bilirubin, massively increased alk phos
Usually slow-growing, most= distal extrahepatic or perihilar
70% unsuited to surgery, 76% recur
Major hepatectomy+ extrahepatic bile duct excision and caudate lobe excision- post-op complications
Stenting of obstructed extrahepatic biliary tree, liver transplant rarely, prognosis= <5 months

65
Q

Most common benign liver tumour? Often what? Avoid what when treating? Causes?

A

Haemangiomas, often incidental finding on US/ CT, don’t require treatment, avoid biopsy, adenomas= common
Anabolic steroids, oral contraceptive pill, pregnancy, only treat if symptomatic or >5cm

66
Q

What is non-alcoholic fatty liver? Risk factors? Symptoms?

A

Increased fat in hepatocytes +/- inflammation in pt with increased LFT/ fatty liver on US and drink <18U/ week (<9 U/wk in women)
Obesity, diabetes, hyperlipidaemia, parental feeding, jejuno-ileal bypass, Wilsons disease, drugs- amiodarone, tetracycline, methotrexate, tetracyclin
Usually asymptomatic, liver ache in 10%

67
Q

Fat sometimes with what in NAFL? Need biopsy to distinguish what? Tx?

A

Inflammation, fibrosis (NASH–> important cause of cryptogenic cirrhosis)
NAFL from NASH
Control risk factors, bariatric surgery to treat obesity

68
Q

Causes of hepatic vein occlusion? May present as what? Tx? What is needed?

A

Thrombosis, membrane obstruction, veno-occlusive disease
Congestion–> acute/ chronic liver injury
Abnormal liver tests, ascites, acute liver failure
Anticoagulation, transjugular portosystemic shunt, liver transplantation

69
Q

What is veno-occlusive disease? Appear as what in biopsy? Back pressure leads to what? Causes? Stained with Masson’s trichrome, collagen is stained what?

A

Rare disease, terminal/ central veins become occluded by fibrous tissue, can be seen to be increased in this plate
May be patchy/ absent in a liver biopsy
Back pressure–> portal hypertension
Dilated sinusoids around this vein and the haemorrhage hint at a rise in pressure
Alkaloid ingestion, chemotherapy, following organ transplantation
May mimic Budd-Chiari syndrome
Green

70
Q

Metabolic causes of liver disease? What is A1AT? Deficiency is called what? Leads to what in children and adults?

A

Alpha 1 antitrypsin deficiency, haemochromatosis, Wilsons disease
Conformational disease that can be fatal, present in homozygous/ heterozygous forms
A glycoprotein and one of family of serine protease inhibitors made in the liver that control inflam cascades
Serpinopathy
Inability to export it out of the liver–> deposition of excessive abnormal A1AT in liver cells
Kids–> liver disease due to protein retention–> cirrhosis and HCC
Adults–> emphysema- protein deficiency in blood

71
Q

Gene for A1AT deficiency found on what chromosome? Genetic variants typed by what as what? What 2 types due to single amino acid substitutions at positions 264 and 342? Normal, heterozygote and homozygote?

A

14
Electrophoretic mobility as medium, slow(S) or very slow(Z)
S and Z
PiMM, Pi MZ and Pi SZ, PiZZ

72
Q

Patient with A1AT deficiency present with what? Tests?

A

Pi ZZ genotype, dyspnoea from emphysema; cirrhosis, cholestatic jaundice, cholestasis often remits in adolescence
Serum A1AT levels decreased, liver biopsy= chronic inflammation w/ eosinophilic A1AT globules on H&E, PAS= bright pink, phenotyping, prenatal diagnosis at 11-13 weeks gestation, lung density with CT

73
Q

Management and prognosis of haemochromatosis patients?

A

Joined up thinking with GP, lung and liver specialists and geneticists, supportive Tx for emphysema and liver disease, quit smoking, IV A1AT, pooled from human plasma- expensive, liver transplant in decompensated cirrhosis
Some= life-threatening symptoms in childhood, others= asymptomatic and healthy into old age, worse prognosis if male, smoker or obese, empysema cause of death in most

74
Q

Iron overload most importantly caused by what things? 90% mutations in what gene? Type of inheritance? Diagnosis suggested by what? Iron removal may lead to what?

A

Hereditary haemochromatosis and transfusional iron overload which can result from repeated blood transfusions
HFE gene, C282Y, H63D
Autosomal recessive, incomplete penetrance
Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas
Raised ferritin and transferrin saturation, HFE genotyping and liver biopsy
Cirrhosis= increased HCC risk
Regression of fibrosis

75
Q

What gender affected most by haemochromatosis? HFE gene found on what chromosome? Early on patient has what? Later on?

A

Middle-aged men, women= 10 years later
Short arm of chromosome 6
Nil or tiredness, arthralgia, erections decrease
Slate-grey skin pigmentation, signs of chronic liver disease, hepatomegaly, cirrhosis, dilated cardiomyopathy, osteoporosis
‘Bronze diabetes’ from iron in pancreas, hypgonadism from pituitary dysfunction decreased, hyporeninaemic hypoaldosteronism

76
Q

Tests for haemochromatosis? Management and prognosis? When secondary haemochromatosis? Reduce need for transfusions, find out if respond to what or what?

A

Blood- increased LFT, serum ferritin, transferrin saturation> 45%, liver MRI= Fe overload, liver biopsy- Perl’s stain for iron loading and disease severity, ECG/ ECHO if cardiomyopathy suspected

Venesect- remove RBC/ ferritin in blood until ferritin less than 50 microgram/L, iron continue to accumulate. maintenance venesection needed for life, desferrioxamine if intolerant of this
Monitor LFT and glucose/ diabetes, ensure vitamin= no iron, diet= low-iron diet, screening 1st degree relatives by genetic testing
Venesection returns life expectancy to normal if non-diabetic and noncirrhotic, arthropathy may improve/ worsen
If many transfusions given
Erythropoietin or marrow transplantation- before irreversible effects of iron overload become too great

77
Q

What is Wilson’s disease? Results in what? Copper absorption and transport is intact where, but copper incorporation is impaired where? Mutation in this protein leads to what?

A

Rare autosomal recessive genetic disorder of a gene on chromsome 13 that codes for a copper transporting ATPase–> mutation of protein that is mainly expressed in the liver, kidney and placenta who’s function is to transport copper into bile and incorporate it into caeruloplasmin
Into the liver= intact, into caeruloplasmin in hepatocytes and excretion into bile= impaired
Disorder of biliary copper excretion–> copper accumulates in liver cells which causes oxidative damage, free copper precipitates through body particularly, eyes and basal ganglia–> neurological/ psychiatric symptoms and liver disease

78
Q

Signs of Wilsons disease in children and young adults? Mood in Wilsons disease? Cognition? Also what things?

A

Children= liver disease, spider angiomata- small distended vessels usually on chest, young adults= CNS signs- tremor, dysarthria, dysphagia, dyskinesias, dystonias, purposeless stereotyped movements, dementia, parkinsonism, micrographia, ataxia/ clumsiness, confusion
Mood= depression/ mania, labile emotions, libido increasing/ decreasing, personality change
Memory decrease, quick to anger, slow to solve problems, IQ decrease, delusions, mutism
KF rings- copper in iris, not invariable, haemolysis, blue lunulae, arthritis, hypermobile joints, grey skin

79
Q

Tests for Wilsons disease?

A

Copper studies and expert interpretation, urine- 24h copper excretion is high, LFT increase- non-specific, serum copper<11micromol/L, serum caeruloplasmin decrease< 200mg/L, falsely low caeruloplasmin, falsely high caeruloplasmin, molecular genetic testing, slit lamp exam, liver biopsy- increase hepatic copper, MRI- degeneration in basal ganglia, front-temporal, cerebellar and brainstem

80
Q

Management and prognosis of Wilsons disease?

A

Avoid foods with high copper- liver, chocolate, nuts, mushrooms, legumes and shellfish, lifelong penicillamine- monitor FBC, urinary Cu and protein excretion
Liver transplantation- if severe liver disease, screen siblings, pre-cirrhotic disease= reversible, CNS damage= less so, no clear clinical prognostic indicators, fatal events= liver failure, bleeding, infection

81
Q

4 types of liver abscesses? (cavity w/pus)

A

1) Pyogenic(bacterial)- biliary, haematogenous, direct extension from empyema of gall bladder, traum, infection of tumour/ cyst
2) Hydatid cysts (hepatic)- parasitic by tapeworm
3) Amoebic liver abscesses- entamoeba histolytica
4) Diverticular abscess- complications of diverculosis

82
Q

Commonest sites of pyogenic liver abscess? Clinical features? Investigations and Tx?

A

Biliary tract, dental source, renal/ intestinal= e.coli, k.pneumoniae, strepto milleri, bacterioides
Fever, weight loss, RUQ abdo pain, pleuritic/ R shoulder pain, tender hepatomegaly +/- obstructive jaundice
Blood cultures, CT abdo, US guided aspiration, colonoscopy and others
Amoxicillin, piperacillin, gentamicin, metronidiazole, US guided catheter drainge if large/ definitive surgery of source

83
Q

Symptoms of hydatid cysts? Diagnosis and Tx?

A

Pain associated w infection/ rupture
Via serology ELISA, Xray, US, CT/MRI
Albendazole, precut aspiration, injection of hypertonic solution and re-aspiration

84
Q

Symptoms of amoebic liver abscess? Diagnosis and Tx?

A

Fever, sweats, RUQ pain/ tenderness +/- chest pain, increased WCC
Aspiration of cysts= choc brown material, serology EIA
Metronidazole and luminal agent, aspiration if large

85
Q

Features, complications and Tx of diverticular abscess?

A

From e.coli, gram -ve bacteria
Fever, colicky abdo pain, acute abdomen +/- diarrhoea, constipation, increased WBCC, CT paracolic abscess, rectal mass, pus
Perforation, peritonitis, obstruction
Amoxicillin-clavulinic acid and perc drainage of large abscess

86
Q

What is ascites? Causes?

A

Effusion and accumulation of serous fluid in abdominal cavity or chronic accumulation of fluid within peritoneal cavity
Malignancy(ovary, uterus, pancreas,) infections- TB, decreased albumin, CCF, pericarditis, pancreatitis, mycoedema, ascites w/ poral HTN–> cirrhosis, portal nodes, Budd-Chiari- excessive RBC conc–> clotting in large liver veins, IVC/ portal vein thrombosis, chronic liver disease–> portal HTN–> reduced albumin, nephrotic syndrome–> kidney damage, proteins leak into urine and decreases oncotic pressure

87
Q

Classification of ascites?

A

Stage 1- detectable only after careful US (mild,) stage 2- easily detectable but of small volume, stage 3- obvious (moderate), stage 4- tense ascites (large)
Refractory ascites- not mobilised, early recurrence< 4weeks, cannot be prevented by medical therapy, diuretic intractable

88
Q

Pathogenesis of ascites? Clinically most useful measure? Up to what amount is possible?

A

Transudate- increased pressure in hepatic portal vein e.g. due to cirrhosis, low protein, low LDH, high pH, normal glucose
Exudate- actively secreted fluid due to inflammation/ malignancy, high in protein, high in lactate dehydrogenase, low pH, low glucose and more WBC
Difference between ascitic and serum albumin concs, difference of less than 1g/dl= exudate
35 litres

89
Q

What does portal HTN play important role in with ascites? Complications of ascites?

A

Raises capillary hydrostatic pressure within splanchnic bed due to Na/ water imbalance–> additional fluid retention by kidneys due to stimulatory effects on hormones- aldosterone, renin increased, reduced kidney perfusion

SBP due to decreased antibacterial factors in the ascitic fluid such as complement

90
Q

Signs and symptoms of ascites? History taken?

A

Abdo heaviness, nausea, loss of appetite, constipation, cachexia, weight los, pain/ discomfort- malignant, SOB
Jaundice, other stigmata of liver disease–> abdo distension, flank bulging in reclined position, puddle sign, shifting dullness, fluid thrill
Long term heavy alcohol, infection, jaundice, IV drug use, blood transfusioon, tattoos, birth in hep area, non-alc steatohepatitis, cancer, malnutrition

91
Q

Diagnosis and Tx of ascites?

A

FBC, LFT coagulation tests, paracentesis, analysis of fluid, US, XRAY, CT scan
Paracentasis, liver transplant, treat cause, salt restriction, diuretics which counter aldosterone e.g. oral spironolactone or loop diuretic

92
Q

What is a Mallory-Weiss tear? Symptoms? Exam and tests?

A

Persistent forceful vomiting/ retching causes haematemesis via oesophageal mucosal tear
Bloody stools, vomiting blood
CBC- low haematocrit, oesophagogastroduodenoscopy(EGD,) more likely when active bleeding

93
Q

Tx, prognosis and prevention of Mallory-Weiss tear?

A

Usually resolves itself, fixed by clips during EGD, surgery rare, PPI/H, inhibitors to suppress stomach acid secretion, blood transfusions if severe blood loss
Usually good prognosis, cirrhosis and coag issues may increase likelihood of recurrence
Relieve vomiting and coughing, avoid alcohol excess

94
Q

Causes of portal hypertension? Pathology and consequences?

A

Pre-hep= portal/ splenic vein thrombosis, intra-hep= cirrhosis, schistomasomiasis, sarcoid, myeloproliferative diseases, congenital hepatic fibrosis, post-hep= Budd-Chiari syndrome, right HF; constrictive pericarditis, veno-occlusive
Increased hepatic resistance and increased splanchnic blood flow
Varices, splenomegaly

95
Q

What is peritonitis? Primary and secondary causes? Primary risk groups?

A

Inflammation of the peritoneum
Primary- no reason= rare, causes haematogenous or lymph nodes, RGs= liver disease- SBP, female, immunocompromised, peritoneal dialysis, ascites
Secondary: perforation of hollow viscus, inflammation of abdo organs, peritoneal dialysis pt, TB, ischaemia hollow viscus, chemical

96
Q

Presentation of peritonitis (acute- most)? Diagnosis and investigations?

A

Pain, tenderness(localised progression to generalised,) systemic= nausea, chills, rigor, dizziness, weakness and inability to move due to pain
General examination- pyrexia, tachycardia, confusion, patient lie still, hypotension and hypoxia, abdo examiination- guarding, rebound, rigidity, silent abdomen
Blood tests- FBC, U&E, amylase, LFT, plain Xray, CT-abdomen, primary- culture (blood, ascetic, dialsystate fluid,) ascites lactate> 25mg/dL= 100% sensitive

97
Q

What is SBP? Bacterascites? Management?

A

Complications of ascites in cirrhosis, E.coli etc assessing ascetic fluid, culture -ve neurocytic ascites (CNNA,) defined as ANC> 250 w/ no culture growth
Positive ascetic fluid culture and ANC<250 cells w/ no evidence of systemic /local infectin, due to ascites/ cirrhosis

Resuscitate–> ABC and antibiotics, treat cause- medical only for primary(SBP, pelvic inflam disease, PD related peritonitis,) surgery Tx repair of perforate viscus, excision of perforate organ +/- drainage

98
Q

Pathogenesis of acute appendicitis?

A

Gut organisms invade appendix wall after lumen obstruction by lymphoid hyperplasia, faceolith or filarial worms–> oedema, ischaemic necrosis and perforation, may be impaired ability to prevent invasion, brought about by improved hygiene and less exposure to pathogens

99
Q

Symptoms of acute appendicitis?

A

Classically periumbilical pain that moves to the R iliac fossa, anorexia= important, vomiting= rarely prominent- pain normally precedes vomiting in surgical abdomen, constipation= usual, diarrhoea may occur

100
Q

Special tests and investigations for acute appendicitis?

A

Rovsings sign- pain> in RIF than LIF when LIF is pressed, psoas pain- pain on extending hip if retrocaecal appendix, cope sign- pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus
Blood tests- may reveal neutrophil leucocytosis and elevated CRP, USS may help, appendix not always visualised, CT= high diagnostic accuracy and useful if diagnosis is unclear

101
Q

Variations in clinical picture of acute appendicitis?

A

Inflammation in retrocaecal/ retroperitoneal appendix may cause flank/ RUQ pain, only sign may be tenderness on right on PR
Child with vague abdo pain who won’t eat favourite food
Shocked, confused octogenarian who is not in pain
Mortality higher in pregnancy, perforation commoner and increased fetal mortality, pain often less well localised

102
Q

Hints for acute appendicitis?

A

If child is anxious- use their hand to press tummy, check for recent viral illnesses and lymphadenopathy, don’t palpate in RIF, expect diagnosis to be wrong half of time, re-examine often, normal= removed in 20% patients

103
Q

Tx for acute appendicitis?

A

Prompt appendictectomy, antibiotics= metronidazole and cefuroxime IV starting 1 hr pre-op- reduces wound infections, longer course if perforated
Laparoscopy- diagnostic and therapeutic advantages- esp in women and obese, not in cases of suspected gangrenous perforation

104
Q

Complications of acute appendicitis?

A

Perforation- commoner if faecolith present and in young children- diagnosis more delayed
Appendix mass- when inflamed appendix becomes covered with omentum, US/CT for diagnosis, some advocate early surgery
Initial conservative management- NBM and antibiotics
If mass resolves= interval appendicectomy
Appendix abscess- if appendix mass fails to resolve but enlarges, Tx= drainage, antibiotics

105
Q

What is pancreatitis? What about acute pancreatitis? What may be rapid within this?

A

Inflammatory process w/ cascade release of cytokines and pancreatic enzymes (trypsin/ lipase)
Self perpetuation pancreatic inflammation by enzyme mediated autodigestion, oedema and fluid shifts causing hypovolaemia- EC fluid trapped in gut, peritoneum and retroperitoneum(worsened by vomiting)
Progression from mild oedema to necrotising pancreatitis- complicated by infection

106
Q

Causes of acute pancreatitis? Clinical features?

A

Gallstones, alcohol, hyperlipidaemia, direct damage- trauma/ ERCP, idiopathic, toxic (drugs- azathioprine, diuretics, steroids, NSAIDs,) viral infection, venom= GET SMASHED
Severe epigastric pain radiating into the back, associated anorexia, nausea and vomiting, fever, dehydration, hypotension, tachycardia, abdo guarding on examination
1-3% haemorrhagic pancreatitis; Grey turners signs- left flank ecchymosis- discoloration of skin/ Cullen’s skin- periumbilical ecchymosis- discolouration of skin

107
Q

2 classifications of acute pancreatitis? Diagnosis?

A

1) Oedematous- freq associated w/ phlegmon formation and multiple transient fluid collections
2) Severe/ necrotising- may be sterile/ infections, often associated w/ pseudocyst formation
2/3 of: severe epigastric pain into back, serum amylase> 1000U, abdo CT scan pathology
AXR- no psoas shadow w/ retroperitoneal fluid increase, USS may show gallstones, serum lipase remains elevated for longer than amylase

108
Q

Scoring systems for acute pancreatitis?

A

1) Abbreviated Glasgow scoring system- 3/more of PANCREAS
2) Ranson criteria- point system, >8= organ failure/ necrosis, <3= severe unlikely
3) Balthazar score- CT severity index, Grade A= normal CT= 0 points
4) APACHE II- ICU environment, less common on wards but used w/ CRP measurement, >8= severe disease and 11-18% mortality

109
Q

Management of acute pancreatitis? Complications?

A

Analgesia, catheterise, drain fluid, antibiotics, bowel rest, nutrition- NG tube+ supplements
Systemic inflammatory response syndrome- 2+ of: tachycardia, tachypnoea, pyrexia, raised WCC, multiple organ dysfunction syndrome

110
Q

What is chronic pancreatitis? Causes? How does alcohol cause it?

A

Result of chronic inflammation resulting in irreversible damage
Increased PTH, pancreatic duct obstruction, mechanical- trauma
Reduction in bicarbonate- can be familial–> enzyme activation–> pancreatic tissue necrosis w/ eventual fibrosis
Proteins precipitate in ductal structure–> local dilatation and fibrosis
Direct= free radial formation–> pancreatic damage–> years later= fibrosis

111
Q

Presentation of chronic pancreatitis? Tests?

A

Episodes of exacerbation w/ intervening remissions/ continuous pain in pt. abdo pain, nausea, vomiting, decreased appetite, endocrine/ exocrine dysfunction, malabsorption w/ weight loss, diarrhoea, steatorrhoea, protein deficiency, DM
US and CT–> calcifications confirm, MRCP and ERCP, AXR–> speckled calcification, increased glucose, breath tests complication, pancreatic duct obstruction

112
Q

Tx and complications of chronic pancreatitis?

A

Analgesia–> pain relief, fat soluble vitamins, insulin needs may be high, diet= no alcohol, low fat may help, medium chain triglycerides
Surgery for unremitting pain, narcotic abuse, weight loss (pancreatectomy- all/ part of pancreas or pancreaicojejunostomy- duct drainage procedure)

Pseudocyst, diabetes, biliary obstruction, local arterial aneurysm, splenic vein thrombosis, gastric varices, pancreatic carcinoma

113
Q

How do autoimmune chronic pancreatitis present?

A

Similar to chronic, with elevated serum gamaglobulins, IgG, autoantibodies (AN antibody and rheumatoid factor), steroid responsive and reversible

114
Q

Typical pt for pancreatic cancer? Risk factors? Pathology? 95% mutations in what gene? % in head, body and tail?

A

> 60 y/o, smoking, alcohol, carcinogens, DM, chronic pancreatitis, waist circumference and high fat/ red and processed meat diet
Mostly ductal adenocarcinoma- metastasise early; present late
60%, 25%, 15%, few in ampulla of Vater or pancreatic islet cells
KRAS2 gene

115
Q

Symptoms of tumours in head of pancreas, and body and tail? Rarer features? Signs?

A

Painless obstructive jaundice, 75% in body and tail= epigastric pain radiates to back and relieved by sitting forward, either may cause anorexia, weight loss, diabetes/ acute pancreatitis
Thrombophlebitis migrans- arm vein swollen and red, then leg vein, nephrosis
Jaundice and palpable gallbladder (Courvoisier’s law), epigastric mass, hepatomegaly; splenomegaly; lymphadenopathy; ascites

116
Q

Tests and tx for pancreatic cancer?

A

Blood- cholestatic jaundice, CA 19-9 increase= non-specific, imaging= US/CT, can guide biopsy and help staging prior to surgery/ stent insertion
EUS= most accurate for diagnosis and staging
ERCP shows biliary tree anatomy and may localise site of obstruction

Most ductal cancers= metastatic disease, <20%= radical surgery, surgery= pancreato-duodenectomy- if fit and no metastases, post-op chemo delays progression, palliation of jaundice- stent may help jaundice and anorexia, opiates or radiotherapy for pain, palliative care

117
Q

Prognosis for pancreatic cancer? What does Whipple’s procedure involve?

A

<6 months, 5 yr survival= 3%, after Whipple’s procedure= 5-14%, better if tumour <3cm, no nodes, -ve resection margins at surgery; ampullary or islet cell tumours
Removing head of pancreas, gallbladder, duodenum and pylorus, modified= leaves pylorus

118
Q

What is substance misuse? Categories of drugs?

A

Relates to the harmful use of any substance for non-medical purposes/ effect
Psychoactive substances–> CNS effects; poly drug common
Illicit and legal substances, cannabis= most common worldwide
Opiates= euphoria, analgesia e.g. heroin, tramadol, codeine
Depressants- sedation, anxiolytic e.g. alcohol, benzodiazepines
Stimulants- increases alertness, alter mood e.g. crack, ecstasy, amphetamines
Cannabinoids- relaxation, mild euphoria e.g. cannabis
Hallucinogens- altered sensory perceptions e.g. LSD, mushrooms
Anaesthetic- sedative e.g. ketamine, GHB, NO

119
Q

What are legal highs also known as? Mimic depressants? Stimulants? Cannabinoids? Hallucinogens? Although much lower prevalence, rising worries about increasing use of what?

A 
New psychoactive substances
Mimic other substances, less predictable effects 
Etizolam pyrazolam, mephadrone, BZP, 
spice, clockwork orange, black mamba,
Bromo-Dragonfly 
Prescription meds- licit drug use
120
Q

Effects of drug misuse?

A

Mortality, morbidity- QOL, social- criminal involvement, crime, violence, acceptability, economic- productivity, tax, personal- identity, stigma, relationships
Drug misuse= increased death risk, varies by drug type

121
Q

Main theoretical models related to drug misuse?

A

Disease model- chronic recurrent illness, genetic?, gene therapies, substitution meds
Behavioural- bad habit? law/ justice to deter
Moral- failure of morality? Parenting classes, R.E.
Volitional- failure of will? raise self-efficacy
Socio-cultural- social issues?, target inequality

122
Q

What is addiction? What is dependency?

A

Popular term by law and professional groups, severe substance use disorder (DSM-V)
Compulsive use despite harmful consequences, structural and biochemical changes–> brain= reward, stress and self-control

1) Physical- need more for same effect over time= tolerance, stop–> withdrawals
2) Psychological- life impossible without, emotional if not on drug= fear, pain, shame, guilt, loneliness

123
Q

Risk factors for drug misuse?

A

Family- history, management issues, conflict, being in care
School and community- low academics, availability, disorganisation, transitions, low attainment
Individual and peer- sensation/ risk taking, alienation, friends, attitudes, trauma
Protective- reverse of risk, opportunities/ recognition, opportunities to develop confidence

124
Q

What is a UK unit? Calculation for a unit? When does it become too much? What group of people have highest proportion over 14 units?

A

8g/10 ml pure alcohol
% ABV x amount liquid ml/1000
When it causes/ elevates risk for alcohol related issues/ complicates management of other health issues
Men and women aged 55-64

125
Q

What is the alcohol paradox? Get what with alcohol withdrawal? What is activation syndrome? What is delirium tremens?

A

Low socioeconomic group consume less, experience more harm-related issues
Tremulousness
Agitation, increased HB and BP, seizures, hallucinations
Severe/ fatal, sensitivity to light and sound, disorientation

126
Q

What happens with foetal alcohol syndrome?

A

Pre and post-natal growth retardation, CNS- mental retardation, irritability, incoordination, hyperactivity, craniofacial abnormalities, congenital defects- birthmarks, hernias

127
Q

Psychosocial issues with alcohol? Primary prevention with alcohol?

A 
Interpersonal relationships, work issues, criminality, social disintegration, driving incidents/ offences 
Avoid onset (lifestyle changes, Tx, vaccines,) health promotion- know limits, Drinkaware- labelling, THINK!, drink driving, advertising restriction
Increase minimum pricing- Scotland= 50p/ unit, Wales= March 2020, no plans for England yet
128
Q

Secondary prevention related to alcohol? Tertiary prevention?

A

Screening and intervention= avoid early disease, ask pts routinely using Qs/ tools- interview, CAGE Qs, AVDIT tool- written self report, FAST, severity of dependence questionnaire- 20 Qs
Relating presenting symptom–> lifestyle change, detect problem drinking- lab tests, liver enzymes, feedback

Decrease complications/ progression (stroke/ cardiac rehab)

129
Q

What is ‘at risk drinking’ (hazardous)? What is alcohol abuse (harmful)? What is alcoholic dependence?

A

At risk of phy/ psych harm- screening tools
Likely to cause physical/ psych harm

Set of behavioural, cognitive and physiological responses developed after repeated use - showing tolerance/ withdrawal signs, not sticking to limits, drinking a lot, less time on other stuff, keep drink despite issues

130
Q

Relapse prevention/ dependence Tx? What is assisted withdrawal?

A

Disulfiram- acute sensitivity, acetylaldehyde builds up, not–> acetic acid
Nalmefene- C-antagonist for opioid receptors, less pleasure/ reward feelings, effects still present
Acamprosate- stabilises chemical imbalance, 10%= GI symptoms
Social support- AA
Detoxification, increases GABA and reduces glutamate

131
Q

Acute effects of alcohol? Chronic effects?

A

Accidents, injury, coma, death from resp depression, aspiration pneumonia, oesophagitis, Mallory-Weiss syndrome (gastric tears,) pancreatitis, arrhythmias, CV accidents, myopathy, hypoglycaemia

Pancreatitis, CNS toxicity, dementia, Wernicke-Korsakoff syndrome- thiamine deficiency, co-enzyme for alcohol metabolism
Tx= Pabrinex, and ongoing vit B/ thiamine
Ongoing cerebellar dysfunction, central pontine myelinosis, liver damage

132
Q

Themes of models of care for alcohol misusers? The 4 tiers?

A

Screening and assessment, the Four-Tiered framework, care planning and coordination
1) Non substance misuse specific services 2) Open access drug/ alcohol services 3) Specialist community based clinics 4) Specialist in-patient services

133
Q

The Govt’s alcohol strategy? Prevention at national and local levels? Evidence based clinical tool for screening? Brief intervention from AUDIT score?

A 
Minimum pricing, licensing, the law 
Price, marketing, availability 
School partnerships and licensing 
Alcohol use disorders identification test (AUDIT)
AUDIT score> 8
134
Q

Extended brief interventions for alcohol misuse?

A

Behavioural change, motivational-enhancement therapy, motivational interviewing, structured 20-30 minute session with a follow up, by GP or by specialist service

135
Q

Score higher than what on SADQ indicates severe alcohol dependence? What is usually indicated for someone who scores 16 or over? Interventions for patients who are dependent upon alcohol?

A

> 31
Chlordiazepoxide detoxification regime
Community based assisted withdrawal, in-patient based assisted withdrawal, tx with benzodiazepines, preferred choice= chlordiazepoxide

136
Q

Therapeutic indications for what? What does chlordiazepoxide do?

A

Symptomatic relief of anxiety, muscle spasm, symptomatic relief of acute alcohol withdrawal, not recommended for long term use- 4 weeks max
Inhibits presynaptic Ca2+ entry and transmitter release, potentiates GABA mediated inhibition

137
Q

Absorption of chlordiazepoxide? Distribution and metabolism? Elimination?

A

Well absorbed at small intestine, highly lipophilic, age related, can be delayed in elderly, half life= 6-30 hours, highly protein bound

Metabolised by the liver, active in CNS grey matter

In urine mainly in the form of it’s metabolites, excreted as conjugates (glucuronide or sulphate)

Proposed= enhancing GABA, augmented by BZOs

138
Q

Containdications of chlordiazepoxide? Dependence over time? Withdrawal effects?

A

Hypersensitivity to benzodiazepines, pula insufficiency, phobic and obsessional states, chronic psychosis, hepatic insufficiency, pregnancy, myasthenia gravis - never standalone tx in dep/ anxiety

Increases with increased dose and in alcohol dependency

When tx stops abruptly, headache, muscular pain, anxiety, hallucinations, epileptic seizures

139
Q

Drug interactions of chlordiazepoxide?

A

Alcohol- enhanced sedative effect, central acting drugs= enhanced central depressive effects, anti-epileptic drugs- side effects and toxicity more evidence when used concurrently, compounds affecting hepatic enzymes- reduced clearance rate EG Disulfiram

140
Q

Elevated ALT and AST indicated what? Present where and leak out when damaged? What is more specific to liver as other is present elsewhere? Wernicke’s encephalopathy caused by what? Thiamine used as what?

A 
Inflammation 
Hepatocytes
ALT
Deficiency of thiamine, common in severely dependent drinkers, poor diet, intake of vitamins, gastritis
Co-enzyme for alcohol metabolism

Phase 2a Flashcards (14 decks)

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