Phase 2 - Liver Flashcards

Question

What is Murphy's sign

Answer 1

Pain on deep inspiration when 2 fingers placed in RUQ (push under ribs) - because diaphragm pushing down on gallbladder

Answer 2

LAPROSCOPIC CHOLECYSTECTOMY (GOLD for all SYMPTOMATIC gallstones - avoid in >80s) - try conservative FIRST - NSAIDs/ANALGESIA If FEBRILE/SEPTIC need to treat INFECTION FIRST: - nil by mouth (can't consume anything) - AGGRESSIVE FLUID RESUS (IV fluids) - Opiate analgesia - IV antibiotics (e.g. CEFUROXIME, CEFTRIAXONE) - Cholecystectomy after symptoms subside - ERCP if small stones at bottom of hepatic duct (involves sphinterectomy; use basket or balloon to remove; mechanical or laser to crush) put in stent (pigtail stent)))?? If pure/near-pure cholesterol stones: - STONE DISSOLUTION by increasing bile salt content - ORAL URSODEOXYCHOLIC ACID (UDCA) - can give statins (simvastatin) to lower cholesterol Shock wave lithotripsy - shock wave fragments stones so they can be passed (only works if duct still patent)

Answer 3

Infection of biliary tree - usually secondary to PROLONGED common bile duct obstruction by stones - Bacteria CLIMB up from DUODENUM -> biliary tree infection + consolidation - SURGICAL EMERGANCY (sepsis = high mortality) benign biliary STRICTURES from biliary SURGERY CANCER of pancreas head compressing bile duct PARASITES in Far East/Mediterranean

Answer 4

- IV ANTIBIOTICS (e.g. CEFOTAXIME/METRONIDAZOLE) continued after drainage till SYMPTOM RESOLUTION - IV FLUIDS Biliary drainage - Endoscopic Retrograde Cholangio-Pancreatography with sphincterotomy - basket or balloon to remove - mechanical or laser to crush - pigtail stent - UNSAFE FOR LARGE STONE -> REQUIRE SURGERY

Answer 5

- In the gallbladder & cystic duct: * Biliary colic * Acute cholecystitis * Empyema - gallbladder fills with pus * Carcinoma * Mirizzi’s syndrome - stone in gallbladder presses on bile duct casing jaundice - In bile ducts: * Obstructive jaundice * Cholangitis (inflammation of bile duct) * Pancreatitis

Answer 6

Disrupt intracellular Ca2+ homeostasis Disrupt bile canalicular transport mechanisms Induce apoptosis Inhibit mitochondrial function -> prevents fatty acid metabolism -> acummulation of lactate and reactive oxygen species

Answer 7

within 3 months/12 weeks of starting drug - usually after at least 1 week can occur weeks after stopping drug usually resolves within 3 months of stopping drug but prolonged injury (over 6 months) -> long term damage

Answer 8

Low dose aspirin NSAIDs other than Diclofenac HRT Beta Blockers ACE Inhibitors Thiazides Calcium channel blockers

Answer 9

Hepatocellular: - ALT >2 ULN, ALT/Alk Phos ratio >=5 Cholestatic: - ALT >2, ratio <=2 Alk phos higher in cholestatic

Answer 10

too much paracetamol over-saturates the Phase II reaction (glucoronidation and sulphate conjugation pathway -> Glucoronide + sulfate metabolites) Normally if metabolised via phase 1 reaction (oxidation) makes reactive compund (NAPQI) which is made non-toxic by CONJUGATION with GLUTATHIONE (anti-oxident -> cystein conjugate) - in over dose GLUCTATHIONE DEPLETES so INCREASED NAPQI -> hepatotoxicity + kidney injury

Answer 11

First 24 hours - Usually asymptomatic then: - SUDDEN ONSET SEVERE RUQ pain - N + V - ANOREXIA - Jaundice - Confusion LFTs show liver damage at 18 HOURS AFTER - RAISED ALT 72-96hrs after - PEAK ALT and Prothrombin time Acute liver injury symptoms: - JAUNDICE AND ENCEPHALOPATHY - HYPOglycaemia (overdose inhibits gluconeogenesis) - Coagulation defects, electrolyte imbalances Potential kidney injury from ACUTE TUBULAR NECROSIS: - METABOLIC ACIDOSIS (lactic acid) - Raised creatinine DIAGNOSED on: - History - Raised ALT - Serum Paracetamol conc

Answer 12

ACTIVATED CHARCOAL - to prevent absorption in stomach (only works if given within 1 hour) - **IV N-ACETYLCYSTEINE** (give immediately - non-toxic form is a cystein conjugate so giving a cystine pushes it in that pathway) - replenishes cellular GLUTATHIONE - rash common side effect -> treat with CHLORPHENAMINE - don't stop unless anaphylactoid

Answer 13

Hepatic encephalopathy Presents with CONFUSION, COMA or FLAPPING TREMOR (ASTERIXIS - flapping tremor with wrist extended) Caused by build up of ammonia passing to brain (neurotoxic - halts Krebs cycle - irreparable/irriversible damage) Also, astrocytes try to clear ammonia by converting glutamate to glutamine but EXCESS GLUTAMINE causes OSMOTIC SHIFT INTO CELLS -> CEREBRAL OEDEMA (risk of oedema decreases the more delayed the onset of encephalopathy) - TREAT WITH IV MANNITOL or LACTULOSE - reduces ammonia) Can also get Wernicke-Korsakoff syndrome - memory disorder due to B1 deficiency (thiamine) (damages neural/supporting cells) - ATAXIA, NYSTAGMUS - MEMORY IMPAIRMENT, confusion, behavioural changes - TREAT WITH IV THIAMINE

Answer 14

Local inflammation: - pritonitis, PANCREATITIS - TB - Abdo CANCERS (esp OVARIAN) Low Protein: - NEPHROTIC syndrome (kidney disease), kidney failure Flow stasis: - CIRRHOSIS/chronic liver disease (MAIN) - Budd-chiari (hepatic vein thrombosis), portal thrombosis - HF, constrictive pericarditis

Answer 15

SHIFTING DULLNESS exam (resonant at top when lying on back but dull at sides as bowels/gas floats; site of resonance changes to flank when on side) - fluid wave/thrill (can feel tapping through fluid on other side of abdomen) ASCITIC TAP/aspiration (peritoneocentesis - 10-20ml fluid) - cytology (WCC) + cultures - proteins + amylase * if TRANSUDATE (pushed out - increased hydrostatic pressure) - CLEAR fluid - <30g/L protein (LOW), Serum albumin-ascitic gradient <11g/L(SAAG - serum albumin-albumin in ascitic fluid) * if EXUDATE (leaks out due to inflammations) - CLOUDY - >=30g/L protein (HIGH), SAAG >= 11g/L IMAGING: - XR (worst sensitivity) - US - CT (best sensitivity)

Answer 16

SODIUM/fluid restriction SPIRONALACTONE (aldosterone antagonist) (furosimide works better on oedema - combined is effective but may contribute to kidney failure (electrolyte imbalance)) PARACENTESIS (draining); pleuric/indwelling drain (smaller volumes) TIPS (transjugular intrahepatic portosystemic shunt) Treat underlying cause: Stop alcohol (usually not viable) Liver transplant (esp if getting peritonitis)

Answer 17

- TIPS - transjugular intrahepatic portosystemic shunt stent connects portal veins to adjacent vessels with lower BP -> relives pressure in liver -> help stop fluid back up INCREASED RISK OF ENCEPHALOPATHY (as blood bypasses liver) - give prophylaxis - CONTRAINDICATED if multiple previous episodes of ENCEPHELOPATHY - VARICEAL BANDING - rubber band ligation if at risk of rupture - TERLIPRESSIN (vesopressin analogue -> SPLANCHNIC VASOCONSTRICTION)

Answer 18

- Normal - Steatosis/fatty liver (smooth; fat-filled hepatocytocytes on cytology) - can be reversed - Alcoholic fibrosis with inflammation -> can progress to **alcoholic hepatitis** (talk about this if we get asked about stages of AFLD) - Cirrhosis (nodular - irreversible) - compensated or uncompensated - Hepatocellular carcinoma (HCC)

Answer 19

- **Binge/chronic drinking** - Obesity - Smoking - FEMALE sex

Answer 20

early - almost asymptomatic more severe -> chronic liver failure/alcohol dependancy - jaundice - hepatomegally - ascites - spider naevi - Hepatic encephalopathy (HE) - palmar erythema, dupuytren contracture (painless, finger bent to palm, maybe cord in palm) - easy bruising

Answer 21

FBC: macrocytic, non-megaloblastic anaemia LFTs: - Raised AST/ALT - PARTICULARLY RAISED GGT (gamma-glutamyl transferase) - raised bilirubin - low albumin - raised prothrombin time (CLOTTING PROFILE) Biopsy to confirm cirrhosis or hepatitis: - inflammation, necrosis - MALLORY BODIES (hyaline (from degeneration of connective tissue - looks darker) cytoplasmic inclusions in hepatocytes)

Answer 22

conservative: - STOP ALCOHOL * DiAZEPAM/LORZEPAM for Delireum tremens - lower fat diet, lower BMI - detox regiem pharm: - short term steroids (only if necessary) - B1 (thiamine)/folate supplements - give prophylactically as alcohol prevents thiamine absorption in gut -> deficiency (may give low/slow opiate analgaesia if viable) surgical: - liver transplant if end-stage (only if abstains for 3 months; Lille score) Treat complications e.g. ascites

Answer 23

- Pancreatitis (increased ethanol) - Encephalopathy - Ascites - ALCOHOL withdrawal - DELERIUM TREMENS - HCC - Mallory Weiss tear (lower oesophageal tear - violent coughing/vomiting) - Wernicke-Korsakoff syndrome (B1 deficiecy/alcohol withdrawal) - treat with IV B1 (thiamine)

Answer 24

Normal Hepatosteatosis (fatty liver - deposited in hepatocytes) Non-alcoholisc steatohepatitis (NASH - fatty+fibrotic) Fibrosis Cirrhosis

Answer 25

Usually asymptomatic (picked up incidentally) If severe - chronic liver failure symptoms - N+V - Diarrhoea - Hepatomegaly

Answer 26

Deranged LFTs: - RAISED PT/INR and BILIRUBIN - LOW ALBUMIN **- Enhanced Liver Fibrosis Test (if you suspect fibrosis)** 1ST LINE : ULTRASOUND liver/abdomen (shows fatty liver) CT/MRI 2nd line: Assess risk of fibrosis (non-invasive scoring system - FIB-4) BIOPSY - DIAGNOSTIC - (may find Mallory bodies if biopsy done)

Answer 27

Conservative + control risk factors - lower BMI/weight - EXERCISE - Stop SMOKING - avoid ALCOHOL - control risk factors - diabetes, HTN, cholesterol ( statins, metformin, ACE-I) - consider pioglitazone to *improve insulin sensitivity* vitamin E can reduce fibrotic appearance (improves liver function)

Answer 28

HCC! portal HTN, varices encephalopathy ascites

Answer 29

SAME AS CVD and DM: - hyperlipidaemia/HIGH CHOLESTEROL - OBESITY - Poor diet/low activity - HTN - T2DM - **insulin resistence** - MIDDLE AGE ONWARDS - SMOKING Family history Endocrine disorders Drugs (NSAIDS, amioderone) (- past bypass)

Answer 30

Constipation Drugs GI bleed Infection HYPO: natreamia, kalaemia, glycaemia Alcohol withdrawal Other (cardiac/intercranial) ALWAYS DO ABCDE first

Answer 31

- impaired reticulo-endothelial function - reduced opsonic activity (normally tag pathogens) - leucocyte function - permeable gut wall

Answer 32

Drugs: - Diuretics - NSAIDS - ACE Inhibitors - Aminoglycosides (DON'T GIVE) Infection GI bleeding Myoglobinuria (muscle brakdown -> too much in blood + urine) Renal tract obstruction

Answer 33

Hepatic encephalopathy (ammonia) - infection - GI bleed - constipation - hypokalaemia - drug (sedatives, analgesics) Hyponatraemia / hypoglycaemia Intracranial event

Answer 34

Serial 7’s WORLD backwards Animal counting in 1 minute Draw 5 point star Number connection test

Answer 35

Viral serology - hepatitis B surface antigen, hepatitis C antibody, hep E IgG antibody, (EBV, CMV, hep A (IgM)) Immunology - autoantibodies - AMA, ANA, ASMA (smooth muscle) - coeliac antibodies - immunoglobulins Biochemistry - iron studies - copper studies - caeruloplasmin (serum copper transport protein) - 24 hr urine copper - α1-antitrypsin level - lipids, glucose Radiological investigations - USS / CT / MRI Biopsy if possible/required

Answer 36

- Female - Other autoimmune conditions (e.g. SLE) - Viral hep - HLA DR3/DR4 (also linked to T1DM)

Answer 37

usually asymp other wise - liver failure COMPLICATION = Cirrhosis

Answer 38

Raised IgG Autoantibodies (not diagnostic): - Type ONE - OLDER women * Anti-nuclear (ANA) * Anti smooth muscle (ASMA) * Anti soluble Liver Antigen (Anti-SLA) - Type 2 - YOUNGER females (rarer) * Anti liver cytosol (ALC-1) * Anti liver kidney micrsomal (ALKM-1) BIOPSY - diagnostic! - presence of plasma cells and other lymphocytes - INTERFACE HEPATITIS (affects hepatocytes around portal tracts); inflammation TREAT WITH STEROIDS (prednisolone) + IMMUNOSUPPRESSANTS (AZATHIOPRINE) - or liver transplant

Answer 39

FEMALE 40-50 y/o Other autoimmune/rheumatoid disease Smoking

Answer 40

T cell mediated immune response causes intralobular (small, in lever) bile duct damage leading to: - Outflow obstruction (Cholestasis) - Chronic, **GRANULOMATOUS INFLAMMATION** CHOLESTASIS -> back-pressure: - fibrosis - chirrhosis - portal HTN - infection - jaundice - reduced secretion of cholesterol via bile ducts causes it to build up in skin and blood vessels -> XANTHELASMA Autonomic neuropathy -> correlates to fatigue Autoantibodies are also present.

Answer 41

usually asymp - early - PRURITIS + FATIGUE - GI disturbance/abdo pain - JAUNDICE - xanthelesma (yellow growths around eyelids - cholesterol deposits)/xanthoma - HEPATOMEGALY (+ other signs of CIRRHOSIS/FAILURE) Complications: - cirrhosis -> HCC - MALABSORPTION of fats/ADEK (due to lack of bile) -> steaorrhoea, OSTEOMALACIA or OSTEOPOROSIS - coagulopathy (from vit K def) - Hypothyroid - Distal renal tubular acidosis (build up of acids)

Answer 42

- Deranged LFTs - ALP, GGT, BILIRUBIN RAISED; - ALBUMIN LOW - Rule out viral - check antibodies/antigens - SEROLOGY - **ANTI MITOCHONDRIAL ANTIBODY (AMA)** - most specific to PBC, (high specificity) - raised IgM - ANA present in 35% USS - exclude extrahepatic cholestasis BIOPSY - PORTAL TRACT LYMPHOCYTIC INFILTRATE + fibrosis - granulomatous - determines staging/diagnosis

Answer 43

1ST LINE - URSDEOXYCHOLIC ACID (UDCA) lifelong - dampens immune; decreases cholestasis (it's a bile acid analogue - slows down progression); - reduces portal pressure + varices - doesn't reduce itching or fibrosis - reduces cholesterol absorption in gut -> less risk of xanthoma/CVD **CHOLESTYRAMINE for pruritis** (RIFAMPICIN also, but can DAMAGE LIVER) - it's a bile acid sequestrate that binds to bile acid to prevent absorption in gut (reduces pruritis) Immunosuppressants (e.g. steroids) in some patients ADEK vit supplement Liver transplant

Answer 44

shows BILE DUCT OBSTRUCTION RUQ pain, fever, jaundice

Answer 45

- MALE (atypical) - FHx - 30-40 y/o - **UC** (in 70%)

Answer 46

- auto antibodies attack intra AND/OR extrahepatic bile ducts - Biliary tree becomes STRICTURED/FIBROTIC (lining stiffens) - OBSTRUCTION - chronic obstruction -> HEPATITIS, fibrosis, cirrhosis

Answer 47

usually asymp - PRURITIS + FATIGUE - Chronic RUQ PAIN - Charcot triad (typically - JAUNDICE regardless) - Hepatosplenomegaly - IBD COMPLICATIONS: - acute bacterial cholangitis - cholangiocarcinoma - colorectal cancer - CIRRHOSIS/FAILURE - BILIARY STRICTURES - FAT soluble VIT DEFEICIENCY

Answer 48

Deranged LFTs U&E, FBC SEROLOGY - no viral, - no AMA, - USUALLY pANCA POSITIVE (anti neutrophil cytoplasmic - non-specific but present 94%) - ANA (77%) - aCL (anticardiolipin) Biopsy - ONION SKIN fibrosis around ducts **GOLD STANDARD - MRCP** (may show bile duct lesion/strictures - ERCP too invasive)

Answer 49

Conservative: - **Cholestyramine (pruritis)** - ADEK vit supplement - monitor for complications - **ERCP can dilate/stent strictures** - consider liver TRANSPLANT UDCA can also be used

Answer 50

Acute - less than 6 months chronic - lasting >6 months

Answer 51

liver failure in acute hepatitis

Answer 52

Viral: - Hep A-E (B and D infect together - D can only infect with B, B can infect alone) - Human herpes viruses (either in first case or on reactivation) -Others like flu, covid etc can cause abnormal LFTs Non-viral: - Spirochaetes, e.g. leptospirosis, syphilis - Mycobacteria, e.g. M. tuberculosis - Bacteria, e.g. bartonella - Parasites, e.g. toxoplasma

Answer 53

Hep B+D (D can only infect alongside B, B can infect alone), C, (E)

Answer 54

Can be asymp Non-specific (malaise, lethargy, myalgia) GI upset, Abdo pain Jaundice + pale stools/dark urine Signs: - Tender hepatomegaly, potentially jaundice - signs of fulminant hepatitis (acute liver failure) * bleeding, ascites, encephalopathy Abnormal LFTs - ALT/AST >> GGT/ALP

Answer 55

asymp/non-specific symptoms Potentially signs of chronic liver disease: - CLUBBING, palmar erythem, Dupuytren's contracture, spider naevi etc. LFTs normal if COMPENSATED. DECOMPENSATED: - coagulopathy, jaundice, low albumin, ascites (potentially spontaneous bacterial peritonitis), encephalopathy complications: HCC, portal HTN -> bleeding

Answer 56

- FAECO-ORAL TRANSMISSION (fAEco = A/E) - contaminated food/drink (SHELLFISH) - linked to access to safe resources/socioeconomic indicators - Close contacts - Homelessness - typically in low income countries in high income countries: - Travel - Sex (MSM) - Injecting drug use

Answer 57

SHORT: 15-50 days (usually 14-28) - incubation period normally lasts ~ 1-6m

Answer 58

USUALLY SYMPTOMATIC in adults: - PRODROMAL (no jaundice) - 1-2 weeks: * constituational symptoms e.g. FEVER, fatigue, NAUSEA, MALAISE * RUQ abdo PAIN - ICTERIC phase (jaundice) - few days - 1 week after pre-icteric starts - 3m: - JAUNDICE - dark urine, pale stools - pruritis SELF-LIMITING - no chronic disease

Answer 59

100% immunity

Answer 60

Acute Hep signs/symptoms - LFTs - RAISED ALT - RAISED total BILIRUBIN - SEROLOGY: Presence of anti-HAV antibody - IgM high if acute - IgG present shows Immunity Can't test IgG by itself so know past infection has occured if Total anti-HAV antibody is positive but IgM is negative.

Answer 61

SUPPORTIVE - anti-emetics, rest Monitor liver function FULMINANT HEP VERY RARELY - consider liver transplant Vaccines to close contacts within 1 week (or human normal immunoglobin within 14 days)

Answer 62

vaccines to high risk groups - travels, MSM, injecting drug users 1 dose - immune for 12 months; 2 dose at 6-12 months - immune for at least 20 years

Answer 63

FAECO-ORAL TRANSMISSION (fAEco = A/E) 4 genotypes: - G 1/2: contaminated food/WATER - G 3/4: UNDERCOOCKED meat from mammals (particularly PORK) G3 most common in UK (endemic) - typically only ACUTE - usually SELF-LIMITING (chronic risk in immunocompromised with G3) TRANSPLANT RECIPIENTS

Answer 64

Usually ASYMPTOMATIC Extra-hepatic manifestations esp neurological (meningoencephalitis, Guillian-Barre etc - confusion, coma, muscle weakness/paralysis) - may be main presentation More common but still rare fulminant hep - esp G1/2 in pregnancy (esp 2/3 trimesters) - risk of CHRONIC in IMMUNOCOMPROMISED (G3/4 only) Occassional acute-on-chronic liver failure (ie fulminant in someone who already had chronic) - high mortality

Answer 65

Immunosupressed with G 3/4 -> more risk of chronic Pregnant ppl (esp 2nd/3rd trimester) with G1/2 -> more risk of fulminant hep

Answer 66

SEROLOGY: ACUTE - anti-HEV IgM + HEV RNA Past infection - anti-HEV IgG - unreliable in immunocompromised HEV RNA - measure/monitor in SERUM/STOOL - if it persists for >6 months - chronic

Answer 67

ACUTE: - SUPPORTIVE (usually self limiting) - Monitor for liver failure * consider transplant or RIBAVIRIN (antiviral) CHRONIC: - Reverse immunosuppression if possible - if HEV RNA persists - treat with RIBAVIRIN >= 3 months - (2nd line: pegylated interferon-a)

Answer 68

- Avoid eating undercooked meats (especially if immunocompromised) - Screening of blood donors (Vaccine available in China only (HEV 239 (Hecolin®) against HEV genotype 1)

Answer 69

Most common - BLOOD-BORNE (and bodily fluids) - MOTHER-TO-CHILD (usually during birth, can occasionally get in-utero transmission if mother acquires acute hep B in pregnancy) - VERTICAL Horizontal: - SEXUAL - injecting drug use (SHARING NEEDLES) - iatrogenic/occupational (needles) - also DIALYSIS - household contact (esp siblings) - blood products (medical)

Answer 70

Mostly SYMPTOMATIC with SPONTANEOUS RESOLUTION (tho genome stays in host so may reactivate if later immunocompromised) - PRODROMAL phase (1-2 weeks) - malaise, RUQ pain, N+V, Fever - ICTERIC phase: jaundice phase - usually few weeks; can last up to 6 months (longer than hep A) - JAUNDICE (with stool/urine change) - PRURITIS - ARTHRALGIA - ascites, encephalopathy, coagulopathy, hypoalbuminaemia, varcies/bleeding (typical more severe hepatic symptoms/signs) <5% -> chronic HBV infection -> 25% progress to cirrhosis -> decompensation (might progress from chronic/cirrhosis to HCC) - some also get fulminant Hep

Answer 71

MUCH MORE LIKELY TO BE CHRONIC - HCC, Cirrhosis

Answer 72

SEROLOGY: Total anti- HB core antibody (IgM + IgG - again no specific IgG test) (Anti Hb C Ag) - IgM if acute (at ~ sign as ALT) - IgG - previous exposure/chronic - HB SURFACE ANTIGEN (Hb S Ag) - CURRENT infection (1st to become positive) - Anti Hb S Ag - indicates IMMUNITY/VACCINATION - 1-3 months after exposure Hb E Ag = INFECTIVITY/viral REPLICATION (2nd) Anti Hb E Ag = LOW activity/infectivity HBV DNA - indicates viral load (2nd)

Answer 73

30 - 180 days (mean 75)

Answer 74

SUPPORTIVE monitor liver function Fulminant very rare - treat with ORAL NUCLEOTIDE ANALOGUES (TENOFOVIR, ENTECAVIR) - pegylated interferon alpha 2a - consider liver transplant vaccinate non-immune close contacts (provides surface antibody only)

Answer 75

They got the vaccine but never had Hep B

Answer 76

e-antigen (eAg) if e-antibody (eAb) present suggests immune system is controlling infection determines whether to treat someone with chronic Hep B or not

Answer 77

pegylated interferon-alpha 2a - weekly sub-cutaneous infection for 5 weeks SIDE EFFECTS: - flu like symptoms, tired/weak, gi issues, skin reaction, hair thinning, insomnia - can stimulate autoimmune conditions (thyroid, T1DM) - lower blood count (cytopenia) - mental health issues ORAL NUCLEOTIDE ANALOGUES - TENOFOVIR DISOPROXIL FUMERATE - ENTECAVIR - inhibit HBV DNA polymerase (and thus replication) - 1 tablet a day - high barrier to resistance - may be lifelong - MINIMAL SIDE EFFECTS BUT: * TDF needs RENAL MONITORING * it can cause a fanconi-like syndrome - loss of electrlytes and stuff through urine

Answer 78

Antenatal screening (HBsAg) - HBIG for baby at birth if high risk - post exposure vaccines after birth - tenofovir given to mother in pregnancy if high HBV DNA Childhood immunisation Immuninsation of healthcare workers and other at risk groups Screening/immunisation of sexual/household contacts Barrier contraception; PrEP (Tenofovir/Emtricitabine) Universal screening of blood products Sterile equipment/universal precautions in healthcare

Answer 79

Low blood count Triggers autoimmune conditions Hair thinning, skin/GI problems Flu like symptoms Mental health issues

Answer 80

Tenofovir DIsoproxil Fumerate a Fanconi-like syndrome - loss of eloctrolytes and stuff through urine

Answer 81

Within 24 hr of birth At 4 weeks At 8, 12, 16 weeks (as part of the hexavalent routine childhood immunisation) At 1 year

Answer 82

Mother has high e-antigen and/or high HBV DNA Baby birth weight <1.5 kg

Answer 83

8, 12 and 16 weeks (as part of a hexavalent vaccine)

Answer 84

Tenofovir/Emtricitabine (normally only used for HIV)

Answer 85

Check vaccine response using anti-HB surface antibody and potentially offer a more immunogenic 2nd line vaccine if required

Answer 86

Alpha-Feto Protein test - screens for development of primary liver cancer

Answer 87

BLOOD-BORNE/bodily fluids - same as hep B - Mother-to-child - INJECTING DRUG USE - BLOOD PRODUCTS - IATROGENIC - Sexual - Household contact - Occupational (tattoos, medical etc)

Answer 88

Hep D is a defective RNA virus Can only replicate in presence of/attached to HBsAg (also needs it for protection)

Answer 89

More aggressive (often acute-on-chronic) More likely to become chronic, cirrhotic and decompensated (accelerated progress to liver fibrosis) - more likely to develop HCC than in just Hep B infection

Answer 90

Hep D antibody if pos -> test for Hep D RNA

Answer 91

Pegylated interferon-a - 48 weeks Tenofovir or Entecavir (oral nucleotide analogues) (buleviritide - blocks from entering hepatocytes - NOT YET approved by NICE)

Answer 92

BLOOD-BORNE/bodily fluids - INJECTING DRUG USE!! (main) - Blood products - Iatrogenic - Mother-to-child - Household contact - Sexual - Occupational - Tattoos, piercings, medical etc.

Answer 93

ACUTE oft ASYMP - may have: - MALAISE, FEVER, Myalgia, Arthralgia, N+V, Diarrhoea 70% chance of becoming CHRONIC - Usual CHRONIC LIVER SIGNS 15-30% chance of becoming cirrhotic within 20 years Most people are not good at making Hep C antibodies

Answer 94

FIRST test HCV IgG ANTIBODY to check for HCV EXPOSURE (may take 4-12 weeks to show up; might look -ve in immunocompromised - repeat downstream testing) If positive -> HCV RNA to check for current infection - if positive, start treatment Check HCV genotype to refine treatment (usually 1a, 1b, 3 - could potentially be any number to 6)

Answer 95

Point of care testing is important (available for antibody test and RNA) Dried blood spot test can be used for RNA/genotype Venous (/capillary if bad veins) blood can be used for any of the above

Answer 96

Common in injecting drug users who can often be unwilling to engage with medical appointments

Answer 97

*NOT* pegylated interferon-a - MENTAL HEALTH SIDE EFFECTS NOT WELL TOLERATED DIRECTLY ACTING ANTIVIRAL (DAA) THERAPY - NS3/4A protease inhibitors (-PREVIR) - NS5A inhibitors (-ASVIR) - NS5B inhibitors (-BUVIR) Once daily tablets, 8-16 weeks - may need to add RIBAVIRIN

Answer 98

Elbasvir/Grazoprevir - only on G1 and G4 Glecaprevir/Pibretasvir - ALL (1-6) Ledipasvir/Sofosbuvir - all but G3 Sofosbuvir/Velpatasvir - ALL (1-6) Sofosbuvir/Velpatasvir/Voxilaprevir - ALL (1-6)

Answer 99

NO VACCINE (most people can't make good immune response to it) - PREVIOUS INFECTION DOES NOT CONFER IMMUNITY Screening blood products Universal precautions when handling bodily fluids Sterile equipment/safe disposal - provision of sterile injecting equipment Optiate addiction treatment Treat/cure transmitters (e.g. IV drug users) Safe sex (barrier contraception)

Answer 100

Intestinal microflora - intere with/compete with pathogens (can produce antibacterials) Gastric acid Bile - antibacterial properties

Answer 101

Passage of increased loose or watery stools (at least 3 times in 24 hours) Acute - 14 days or less Persistant - >14 but <30 days Chronic > 30 days Devided into watery vs bloody (Dysentery - often with fever/abdo pain)

Answer 102

In individuals with: - persistant fever - bloody diarrhoea - severe abdominal pain, - symptoms of volume depletion (eg, dark or scant urine, symptoms of postural/orthostatic hypotension), - history of inflammatory bowel disease, - immunosuppression

Answer 103

PYOGENIC - following biliary sepsis or haematogenous spread - usually polymicrobial: enteric gram -ve and anaerobes AMOEBIC: - Entamoeba histolytica

Answer 104

FEVER + RUQ PAIN - nausea/vomiting - malaise - anorexia/weight loss

Answer 105

- Abdo CT or ultrasound - Blood cultures + E. histolytica serology - Aspiration and culture of the abscess material + E. histolytica molecular testing

Answer 106

Drainage (surgical or imaging guided) Antibiotics

Answer 107

I GET SMASHED - Idiopathic - GALLSTONES (>50% of acute cases) - ETHANOL (50% of chronic cases) - Trauma - STEROIDS - Mumps - Autoimmune - Scorpion/spider venom - HyperCALCAEMIA(/LIPIDAEMIA) - ERCP - Drugs (Azathioprine, NSAIDs, ACE-I)

Answer 108

2 main cuases: gall stones + alcohol GALLSTONES OBSTRUCT pancreatic SECRETIONS (blocks ampulla of Vater) - Reflux of bile into pancreas - ACCUMULATION of DIGESTIVE ENZYMES in pancreas - Host defences (A1AT, PANCREATIC SECRETORY TRYPSIN INHIBITOR) OVERWHELMED -> AUTODIGESTION of gland + nearby structures -> INFLAMMATION + ENZYMES leak in BLOOD - Deranged pancreatic function e.g. insulin def Alcohol = DIRECTLY TOXIC -> inflam

Answer 109

- SUDDEN SEVERE EPIGASTRIC PAIN RADIATING TO BACK (need to consider AAA for diff diagnose) - Nausea + vom (- Jaundice) - Pyrexia/chills - Tachycardia - Anorexia - Steatorrhoea (malabsorption) Haemodynamic instability - GREY TURNERS sign (FLANK RETROPERITONEAL BLEEDING) - CULLEN sign (PERIUMBILICAL BLEEDING) - FOX sign (bruising around inguinal ligament)

Answer 110

Characteristic signs/symptoms Bloods: - RAISED SERUM AMYLASE (gold) - RAISED SERUM LIPASE (more specific than amylase) - CRP raised ABDO US (diagnostic for gallstones) - CT/MRI to see extent of damage _Need at least 2 of above to diagnose_ Urinalysis - raised urine amylase Also: - standing CXR to EXCLUDE gastroduodenal PERFORATION (also has raised amylase/lipase)

Answer 111

- APACHE 2 * assesses SEVERITY within 24HR - Glasgow + Rouson score * prediction of SEVERE attack only within 48HR Glasgow can be remembered by PANCREAS: - P = PaO2 < 8KPa (partial Pa of O2 in blood) - A = Age > 55 - N = Neutrophils (WBC > 15) - C = Calcium < 2 - R = uRea > 16 - E = Enzymes (LDH (lactate dehydrogenase) > 600 or AST/ALT > 200) - A = Albumin < 32 - S = Sugar (Glucose > 10) 0-1 = mild 2 = moderate 3 or more = severe

Answer 112

Assess severity with scoring - NIL BY MOUTH (decreased pancreatic stimulation) - IV FLUID - ANALGESIA (e.g. IV morphine) - Catheterise - Antibiotic prophylaxis - treat gall stones if present - treat any complications (e.g. endoscopic/percutaneous drainage of large collections) careful monitoring

Answer 113

SIRS - SYSTEMIC INFLAMMATORY RESPONSE SYNDROME has 2/more of following: - TACHYCARDIA (>90 bpm) -TACHYPNOEA (>20 resp rate) - PYREXIA (>38 C) - RAISED WCC Can escalate to necrotising pancreatitis (autodigestion - v poor outcome) - infections - abscesses - peripancreatic fluid collections - pseudocyts up to 4wks after - can progress to chronic pancreatitis

Answer 114

3 MONTH history of PANCREATIC DETERIORATION - PERSISTANT IRREVERSIBLE pancreatic INFLAMMATION + FIBROSIS - Caused by CHANGES to pancreatic STRUCTURE - OBSTRUCTION of BICARB secretion into pancreatic lumen -> autodigestion -> fibrosis

Answer 115

- CHRONIC ALCOHOL (main) - CKD - CF (mucus gums up excretory ducts) - Trauma - RECURRENT acute pancreatitis - hereditary - autoimmune - idiopathic

Answer 116

similar symps to acute but generally less intense/longer lasting - EPIGASTRIC PAIN boring through BACK * EXACERBATED by ALCOHOL - BETTER on LEANING FORWRDS - Nausea + vom - Exocrine dysfunction (e.g. steathorrhoea) - Steatorrhoea - Weight loss (malabsorp) - Endocrine dysfunction (e.g. DM) - INSULIN DEPENDANT DM Strictures -> collections of bile + pancreatic juice -> abscesses + pseudocytes

Answer 117

Bloods: - Amylase + lipase UNLIKELY TO BE HIGH IN SEVERE (not enough left to leak out/not enough cell remain to make) typically DECREASED FEACAL ELASTASE (exocrine function marker) Abdo US + CT (DIAGNOSTIC) - detects pancreatic CALCIFICATION - DILATED pancreatic DUCT

Answer 118

- ALCOHOL CEASSATION - NASAIDs for Abdo PAIN - pancreatic supplements (enzymes, insulin etc.) - PPI to help digestion - ERCP or surgery as required

Answer 119

Pre-hepatic: - PORTAL VEIN THROMBUS Intrahepatic: - CIRRHOSIS (main in uk) - SCHISTOSOMIASIS Post-hepatic: - BUDD-CHIARI - RIGHT HF - Constrictive pericarditis (heart can fill properly - backs up)

Answer 120

NORMAL: 5-8mmHg in PORTAL VEIN Cirrhosis -> increased resistance -> COMPENSATORY SPLANCHNIC DILATION + INCREASED CARDIAC OUTPUT -> FLUID OVERLOAD in portal vein (>10mmHg = BAD, >12 = V. BAD) -> COLLATERAL SHUNTING to (usually small) GASTROESOPHAGEAL veins -> OESOPHAGEAL VARICES (esp cardia + lower oes)

Answer 121

usually asymp - present with OESOPHAGEAL VARICEAL RUPTURE - (90% with p htn have o.v. - 1/3 rupture)

Answer 122

Primary: - ASCITES - SPONTANEOUS BACTERIAL PERITONITIS (main) - Primary pneumococcal peritonitis (typically as complication of nephrotic syndrome/cirrhosis) - Familial Mediterranean fever (periodic + self-limiting) Secondary - underlying cause e.g. - BILE (chemical), - TB - malignancy Acute or chronic

Answer 123

G -ve: - E. COLI - KLEBSIELLA (remember it as the sugary bacteria most likely to cause peritonitis) G +ve: - STREP + ENTEROCOCCI (most common g +ve) - STAPH AUREUS

Answer 124

- Bile - barium - Old clotted blood - Ruptured ectopic pregnancy - INTESTINAL PERFORATION (ultimately get infected)

Answer 125

SUDDEN ONSET SEVERE ABDO PAIN -> collapse, septic shock, fever - PAIN LESSENS WHEN RIGID - abdo guarding + rebound tenderness (-> can DIFFERENTIATE FROM RENAL COLIC in this way as renal colic patients CAN'T LIE STILL) * POORLY LOCALISED (only visceral) -> WELL LOCALISED (more inflamed -> more press on parietal) - pelvic peritonitis -> tender rectal/vaginal exam Usually ASCITES

Answer 126

Bloods: - RAISED ESR/CRP, WCC - U + E - ASCITIC TAP: -> NEUTROPHILIA -> CULTURES - causative organism EXCLUDE: - PREGNANCY (beta-hCG test) - BOWEL OBS (ABDO XR) - Urine dipstick (UTI) - serum amylase (pancreatitis) If ERECT CXR shows GAS UNDER DIAPHRAGM -> PERFORATED COLON

Answer 127

ABCDE - analgesia - IV FLUIDS + ANTIBIOTICS (e.g. CEFOTAXIME + METRONIDAZOLE) - URINARY CATHETER (to monitor fluid volume) - GI decopression (nasogastric drain) - Paracentesis Surgery: - PERITONEAL LAVAGE (surgical clean out) (treat underlying cause when stable enough to do so)

Answer 128

SEPTICEMIA if not treated early Subphrenic/PELVIC ABSCESSES Paralytic ILEUS

Answer 129

AUTOSOMAL RECESSIVE - mutation of HFE gene (chromosome 6) - codes for HFE protein (it competitively inhibits transferrin from binding to transferrin receptor 1 - this prevents transferrin from stimulating iron to enter the liver) - EXCESS IRON UPTAKE by TRANSFERRIN-1 receptor - INTO LIVER - REDUCED HEPCIDIN SYNTHESIS (regulates Fe homeostasis) Iron accumulation (20-30g in body vs 3-4g normally) - organ FIBROSIS - esp LIVER (pancreas, kidney, heart, skin, ant pit. gland)

Answer 130

Protein that degrades ferroportin (iron exporter) - REDUCES RELEASE OF IRON FROM STORAGE (in cells esp MACROPHAGES and ENTEROCYTES - duodenum)

Answer 131

20-30g 3-4g

Answer 132

- Fatigue - JOINT PAIN (deposits) - HYPOGONADISM (due to pituitary damage) - SLATE GREY skin -> BRONZE - LIVER CIRRHOSIS Sx - OSTEOPOROSIS (increased iron = increased risk of resorption/formation imbalance) - HF - Irregular heartrate - Diabetes (pancreatic deposits)

Answer 133

BRONZE SKIN HEPATOMEGALY T2DM

Answer 134

IRON STUDIES: - Raised seurm Fe - RAISED FERRITIN - RAISED TRANSFERRIN SAT - Low TIBC GENETIC TEST (HFE gene) LIVER BIPOSY (extent of liver damage - Prussian ble stain)

Answer 135

1ST LINE: - VENESECTION (3-4 years, lifelong) If contraindicated: DESFERRIOXAMINE (chelation) + lifestyle: low iron diet; avoid fruits

Answer 136

family history MALE 50s (women less likely to have due to periods)

Answer 137

AUTOSOMAL RECESSIVE - mutation of ATP7B copper binding protein (supposed to remove Cu from liver) -> impaired COPPER BILIARY EXCRETION + normal transport via CAERULOPLASMIN -> INCREASED Cu ACCUM in LIVER + CNS (basal ganglia) + other organs

Answer 138

HEPATIC - liver disease (JAUNDICE) NEURO - PARKINSONISM (memory issues) - dystonia (muscle spasms/contractions) - dysarthria (difficulty speaking due to weakness in muscles involved in speech) OPTHALMOLOGICAL - KEYSER FLEISHER RINGS (greenish brown copper rings in cornea) - pathogomonic

Answer 139

Copper tests: - LOW SERUM COPPER (most deposited in tissue) - LOW CAERULOPLASMIN (gold???) LIVER BIOPSY - if Dx UNCERTAIN (gold): - RAISED COPPER; hepatitis Brain MRI: - cerebellar + basal ganglia degeneration

Answer 140

1ST LINE: - D-PENICILLAMINE (copper chelation - lifelong) + diet - avoid high Cu e.g. SHELLFISH, MUSHROOM last resort -> consider liver transplant

Answer 141

Mutation of PROTEASE INHIBITOR ('SERPINA-1') gene (chromosome 14) A1AT NORMALLY INHIBITS NEUTROPHIL ELASTASE (degrades elastic tissues) In deficiency - high neutrophil elastase: - LUNGS -> ALVEOLAR COLLAPSE, air trapping + PANACINAR EMPHYSEMA (characteristic - lower lobes vs upper, all acinar involved uniformly - looks even more blobby) - LIVER -> FIBROTIC -> CIRRHOSIS + HCC RISK

Answer 142

Liver SYNTHESES A1AT - damage -> even worse A1AT deficiency

Answer 143

COPD LIKE SYMPTOMS - dyspnoea - chronic cough - sputum - barrel chest CHARACTERISTIC: - YOUNG/MID AGE MALE - LITTLE/NO SMOKING Hx - COPD SYMPTOMS Liver symptoms

Answer 144

- LOW SERUM A1AT (<20mmol/L) - BARREL CHEST (on examination) * CXR - hyper inflated lungs - CT - PANACINAR EMPHYSEMA - SPIROMETRY -> OBSTRUCTION (FEV:FVC <0.7) - GENETIC - PI mutation

Answer 145

NO CURATIVE TREATMENT - smoking ceassastion - inhalres etc. for emphysema - Consider LIVER TRANSPLANT if in HEPATIC DECOMPENSATION - symptomatic managment

Answer 146

Accumulation of excess serous fluid within peritoneal cavity

Answer 147

Men - negligible (baso none) Women - up to 20 ML (ascites can be up to 2L or so)

Answer 148

- Stage 1: detectable only after careful examination / Ultrasound scan (Mild) ● Stage 2: easily detectable but of relatively small volume. ● Stage 3: obvious, not tense ascites. (moderate) ● Stage 4: tense ascites. (Large)

Answer 149

Transudates - fluid with protein <25 g/L Exudates - fluid with protein >25 g/L (cloudy)

Answer 150

PORTAL HTN (thrombosis/cirrhosis) HIGH CENTRAL VENOUS Pa - CONGESTIVE HF LOW PLASMA PROTEIN conc: - Malnutrition - Nephrotic syndrome - Protein losing enteropathy

Answer 151

MALIGNANCY TB PACREATIC ASCITES Budd-Chiari syndrome (inflammation or post hepatic congestion)

Answer 152

Abdo DISTENSION Nausea, LOSS of APPETITE CONSTIPATION Cachexia - apparent wasting PAIN/DISCOMFORT -> MALIGNANT symptoms of underlying cause (oedema, jaundice) may get UMBILICAL HERNIA

Answer 153

Visceral lubrication Fluid + particulate absorption

Answer 154

Acute bacterial cholangitis, Cholangiocarcinoma develops in 10-20% of cases, Colorectal cancer, Cirrhosis and liver failure, Biliary strictures, Fat soluble vitamin deficiencies

Answer 155

- Larger in liver failure - cirrhosis can make it look smaller - can see nodules

Answer 156

- Family history - Male - SMOKING - *Typical exam question would have male with copd-like symp but doesn't smoke*

Answer 157

- adenocarcinoma - Typically in HEAD of pancreas - can COMPRESS bile duct THERE IS MORE, FILL THIS IN

Answer 158

- Gallbladder - BONE

Answer 159

GGT (liver enzyme) will be present in liver pathology

Answer 160

- Detoxification - Clotting factor production - Bilirubin regulation - METABOLISES CARBS - ALBUMIN production - IMMUNITY + Kupffer cells - OESTROGEN REGULATION

Answer 161

Oestrogen regulation issues: - Gynaecomastia in men - Spider naevi - Palmar erythema Detoxification issues - Hepatic encephalopathy Carb metabolism: - HYPOGLYCAEMIA Albumin production issues: - OEDEMA - LEUKONYCHIA (white nails) - ASCITES Clotting issues: - Easy bleeding/bruising Bilirubin issues: - Pruritis - Jaundice with stool/urine changes Immunity issues: - Spontaneous bacterial infections Reduced bile production -> reduced bile salts in lumen - DECREASED absorption of bile salts/FAT SOLUBLE VIT

Answer 162

Liver LOSES ability to REPAIR and REGENARTE leading to DECOMPENSATION (if compensated liver can still function and there are no/few noticible clinical symptoms)

Answer 163

Same as acute injury - JAUNDICE - COAGULOPATHY - FETOR HEPATICUS (musty breath/urine due to retention of sulfur compounds) - Hepatic ENCEPHALOPATHY - Altered mood/dyspraxia - Liver flap/asterixis

Answer 164

- Clinical exam - Ultrasound (can see nodules, blockages etc) - Bloods: - RAISED ALT/AST - RAISED PROTHROMBIN TIME - FBC + U&E - If ascites present - PERITONEAL TAP - Microscopy/culture

Answer 165

- Conservative - ANALGESIA + FLUIDS - Treat complications! - Encephalopathy - LACTULOSE - Ascites - DIURETICS - Cerebral oedema - MANNITOL - Bleeding - VIT K - Sepsis - ANTIBIOTICS - Hypoglycaemia - DEXTROSE - Transplant

Answer 166

5 Fs - FAT - FOURTY - FEMALE - FERTILE - Fair

Answer 167

- RUQ pain - Fever - Jaundice (cholestatic)

Answer 168

- Charcot's triad - RUQ pain - Fever - Jaundice - Sepsis/shock - confusion

Answer 169

Result of CHRONIC INFLAM + DAMAGE to liver cells. Damaged liver cells replaced by FIBROSIS. NODULES of scar tissue form within liver. Thought to be IRREVERSIBLE

Answer 170

- AFLD - NAFLD - Hep B - Hep C viral more common in developing, alcohol more common in developed - Haemochromatosis - Wilson's disease - A1AT deficiency

Answer 171

Similar to chronic liver disease/failure Ascites, jaundice, hepatomegaly, splenomegaly, Spider Naevi, Palmar erythema, bruising, asterixis, caput medusae (vessels around umbilicus)

Answer 172

FBC - thrombocytopenia, high INR, low albumin US and CT - hepatomegaly liver BIOPSY - diagnostic

Answer 173

Same as chronic liver failure Ascites Portal Hypertension Varices/bleeding varices hepatic encephalopathy hepatocellular carcinoma malnutrition Jaundice Coagulopathy oedema - hypoalbuminemia

Answer 174

Liver TRANSPLANT Alcohol ABSTINENCE and good NUTRITION Treat the COMPLICATIONS of liver failure SCREEN for hepatocellular carcinoma every 6 months - Marker for HCC is AFP

Answer 175

Typically ADENOCARCINOMA Typically in HEAD OF PANCREAS - can compress bile ducts

Answer 176

Old age (60+), smoking, obesity, T2DM, FHx, Chronic Pancreatitis

Answer 177

- Obstructive/Painless Jaundice, pale stools, dark urine, generalized itching (pruritus), - weight loss, - worsening of T2DM (or new onset) - Courvoisier’s Sign – palpable gallbladder + jaundice - Can get epigastric pain that radiates to back (body and tail cancer)

Answer 178

- Abdominal Ultrasound - CT of pancreas (identifies mass and helps with staging of cancer) – GOLD STANDARD - Tumour marker – Ca19-9 not diagnostic but helps with monitoring progression

Answer 179

- Surgery to remove tumour – Whipple procedure (pancreaticoduodenectomy + others) - Chemo/Radiotherapy

Answer 180

Poor prognosis as identified late, metastasis to liver, lungs etc.

Answer 181

Liver Cirrhosis due to: - Viral Hepatitis (B and C), Alcohol, NAFLD, other chronic liver diseases

Answer 182

Arises from liver parencyma (not connective/supportive tissue i.e hepatocytes) Metastesis to lymph nodes, lungs, (bones)

Answer 183

Liver specific: - Jaundice - Ascites - Pruritis - hepatic encephalopthy Non-specific: - Weight loss - Fatigue - Weakness - N+V

Answer 184

- 1ST LINE: Abdominal ULTRASOUND - CT to confirm (GOLD STANDARD) - Serum Alpha-Fetoprotein (AFP) = tumour MARKER for HCC

Answer 185

Poor Prognosis - Resection of Tumour - Liver Transplant (if isolated to the liver)

Answer 186

A cancer arising from the BILIARY TREE - usually ADENOCARCINOMA

Answer 187

- **Liver Fluke infections** - **PSC** - **Chronic viral Hep B/C** - Liver Chirrhosis - Biliary Cysts RFx: - older age - smoking - diabetes

Answer 188

Signs of cholestasis: - Jaundice, Pale Stools, Dark Urine, Pruritus + Courvoisier’s Sign (palpable/non-painful gallbladder) Non-specific: - Weight Loss, Fatigue, Weakness, N+V

Answer 189

- 1st LINE – Abdominal Ultrasound and CT - ERCP – used to take biopsies/imaging - GOLD Standard - CA19-9 – Tumour marker for Cholangiocarcinoma/pancreatic - LFTs – raised bilirubin and ALP

Answer 190

- Surgical resection - ERCP -> place STENT (relieves symptoms)

Answer 191

- If you get encephalopathy within 7 days of jaundice = hyperacute - paracetamol, Hep A/E, Ischaemia - within 1-4 weeks = acute - Hep B, drugs - within 5-12 = subacute - Non-paracetamol chronic Acute-on-chronic Fulminant is rapid, severe decline

Answer 192

Jaundice Coagulopathy Encephalopathy

Answer 193

Jaundice with anaemia (yellow mixed with pallor) - pre hepatic jaundice - B12 deficiency - Haemolytic anaemia

Answer 194

Metabolic disease

Answer 195

Patient is jaundiced (skin, whites of eyes + mucous membranes)

Answer 196

Compensated cirrhosis - Stage 1 - no ascites, varices, encephalopathy - maybe jaundice - stage 2 - varices, no asvites, mental state should still be fine, maybe jaundice - stage 3 - ascites +/- varices, confusion/disorientation, jaundice - stage 4 - bleeding +/- more severe ascites

Answer 197

reticular endothelial cells - mainly in spleen (small bit in liver + BM)

Answer 198

attached to albumin - goes to liver

Answer 199

Unconjugated bilirubin is not water soluble (while conjugated is) so it can't be excreted in urine

Answer 200

AUTOSOMAL RECESSIVE - affects UDP gene Main cause of hereditary jaundice - esp in MALES - RFx: T1DM, males Deficient/abnormal UGT (UDP-glucoronyltransferase) -> UNCONJUGATED HYPERBILIRUBINAEMIA SYmp: - 30% aSx - Sudden onset Painless jaundice at young age Relatively benign - usually ok without treatment Crigler Najjar = more severe - jaundice w/ n+v - lethargy

Answer 201

Gall stones in the **common bile duct**

Answer 202

KERNICTERUS - can lead to death in childhood - bilirubin accumulation in BASAL GANGLIA of children causing severe neurological deficits

Answer 203

Phototherapy - breaks down unconj bilirubin

Answer 204

- Scarring/necrosis around central veins of liver - Mallory bodies

Answer 205

Alcohol dehydrogenase (ADH) and mitochondrial aldehyde dehydrogenase (ALDH2) (not particularly needed to remember)

Answer 206

- 6-12 hrs after last drink - relatively mild symptoms of early withdrawal may begin, including headache, mild anxiety, insomnia, small tremors, and stomach upset - 12-24 - hallucinations - 24-48 - highest risk of seizures - 48-72 - delerium tremens - Within 24-72 hours, various symptoms may have peaked and begun to level off or resolve

Answer 207

downregulating gaba + upregulating excitatory systems because alcohol down-regulates excitatory pathways In withdrawal -> alcohol down-regulation removed so double excitation -> Delerium tremens, hallucinations etc

Answer 208

IV CHLORDIAZEPOXIDE or DIAZEPAM

Answer 209

Stellate cells

Answer 210

Electroencephalogram (EEG)

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Phase 2 - Liver Flashcards

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