Liver Flashcards

Question

How are complications of cirrhosis managed?

Answer 1

Malnutrition Varices due to portal HTN - do not cause sx unless they start bleeding Propanolol Elastic band ligation TIPS (stent) If bleeding resus + urgent banding, terlipressin Ascites Diruretics (spironolactone) Low sodium diet Ascitic tap Hepatic encephalopathy Bleeding Oesophageal Varices Resuscitation Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors) Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell Urgent endoscopy Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel Elastic band ligation of varices

Answer 2

As the liver fails, nitrogenous waste e.g. ammonia builds up in the circulation + passes to the brain which can result in permanent brain damage (ammonia is neurotoxic to the brain since it halts the Krebs cycle → IRREPARABLE CELL DAMAGE + neural cell DEATH) As astrocytes try to clear ammonia (using a process involving the conversion of glutamate to glutamine), the excess glutamine causes an osmotic imbalance and a shift of fluid into these cells - hence cerebral oedema - resulting in damage Confusion, coma, liver flap (asterixes - flapping tremor with wrist extended) + drowsiness Treat cerebral edema with MANNITOL LACTULOSE - to convert soluble ammonia to insoluble ammonium. Four stages of hepatic encephalopathy Altered mood and behaviour, disturbance of sleep pattern and dyspraxia Drowsiness, confusion, slurring of speech and personality change Incoherency, restlessness, asterixis Coma

Answer 3

Hepatic failure occurs when the liver loses the ability to regenerate or repair, so that decompensation occurs ACUTE HEPATIC FAILURE = acute liver injury w encephalopathy + deranged coagulation (INR \> 1.5) in a patient with a previously normal liver ACUTE-ON-CHRONIC HEPATIC FAILURE = liver failure as a result of decompensation of chronic liver disease Paracetamol overdose is responsible for 50% of the cases in UK Following ingestion of an overdose (12g in adults can be fatal) patients usually remain asymptomatic for the first 24 hrs and at most develop anorexia, nausea and vomiting with/without right upper quadrant pain Liver damage is not usually detectable on liver biochemistry until at least 18 hours after ingestion Liver damage reaches its peak with raised ALT + prothrombin time at 72-96 hrs after ingestion Then will get jaundice + encephalopathy due to liver damage With no treatment some patients will develop fulminant hepatic failure Acute kidney injury due to acute tubular necrosis occurs in 25% of patients who have severe hepatic damage Would see: Metabolic acidosis HYPOglycaemia (since overdose will inhibit glucose production (gluconeogenesis)) Prolonged prothrombin time Raised creatinine Treat Gastric decontamination - ACTIVATED CHARCOAL Give IV N-ACETYLCYSTEINE which acts by replenishing cellular glutathione stores • Rash is common side effect and treat with CHLORPHENAMINE • Do not stop unless anaphylactoid reaction with shock, vomiting + wheeze

Answer 4

PRIMARY BILIARY CHOLANGITIS / CIRRHOSIS PRIMARY SCLEROSING CHOLANGITIS AUTOIMMUNE HEPATITIS

Answer 5

A chronic disorder with progressive destruction of small bile ducts (interlobar) -\> obstruction of the outflow of bile = cholestasis -\> back-pressure of this -\> fibrosis, cirrhosis + liver failure WOMEN 40-50YRS , may have other autoimmune diseases Serum anti-mitochondrial antibodies (AMA) found in the majority. Presentation Jaundice - due to bilirubin Hepatomegaly Xanthelasma - due to raised cholesterol Pruritus (usually earliest symptom) - caused by leakage of bile acids Lethargy + fatigue Joint pains GI disturbance Bile acids, bilirubin and cholesterol are usually excreted through the bile ducts into the intestines Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation → cholestasis (flow of bile from liver is reduced/blocked so can leak out into blood + other liver cells) which may lead to fibrosis, cirrhosis + portal hypertension. Advanced stage can lead to cirrhosis due to autoimmune attack + infiltration of bile. Serum anti-mitochondrial antibodies (AMA) found in majority. Likely there is an environmental factor that acts of genetically predisposed hosts to trigger disease Bile acids are normally responsible for helping the gut digest fats. Having a lack bile acids in the stool cause gastrointestinal disturbance, malabsorption of fats and greasy stools. Bilirubin normally causes the dark colour of stools, so a lack of bilirubin can cause pale stools.

Answer 6

Increased ALP (first to be raised as has the most obstructive pathology) + cholesterol AMA in 90% - most specific to PBC Anti-nuclear antibodies (ANA) in 35% ESR + IgM raised Liver biopsy to dx + stage

Answer 7

Ursodeoxycholic acid reduces the intestinal absorption of cholesterol Colestyramine - binds to bile acids to prevent absorption in the gut, can help with pruritus Liver transplant in end stage liver disease Immunosuppression (e.g. with steroids) is considered in some patients Disease course and symptoms vary significantly. Some people live decades without symptoms. The most important end results of the disease are advanced liver cirrhosis and portal hypertension. Some other issues / complications: Symptomatic pruritus Fatigue Steatorrhoea (greasy stools due to lack of bile salts to digest fats) Distal renal tubular acidosis Hypothyroidism Osteoporosis Hepatocellular carcinoma

Answer 8

Condition where intra/extrahepatic ducts become strictured + fibrotic -\> obstruction to the flow of bile out of the liver + into the intestines. Sclerosis refers to the stiffening + hardening of the bile ducts, + cholangitis is inflammation of the bile ducts. Chronic bile obstruction eventually leads to liver inflammation (hepatitis), fibrosis + cirrhosis. Male, 30-40, UC Jaundice Chronic right upper quadrant pain Pruritus Fatigue Hepatomegaly GS IX = MRCP - may show bile duct lesions or strictures LFTs show an obstructive picture ERCP to dilate strictures This means alkaline phosphatase is the most deranged LFT + may be the only abnormality at first. There may be a rise in bilirubin as the strictures become more severe + prevent bilirubin from being excreted through the bile duct. Other LFTs (i.e. transaminases: ALT + AST) can also be deranged, particularly as the disease progresses to hepatitis. Liver transplant can be curative but is associated with its own problems (around 80% survival at 5 years). ERCP ((Endoscopic Retrograde Cholangio-Pancreatography) can be used to dilate + stent any strictures Ursodeoxycholic acid - may slow disease progression Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut + can help with pruritus due to raised bile acids Monitoring for complications (such as cholangiocarcinoma, cirrhosis + oesophageal varices) No antibodies are highly sensitive or specific to PSC. They aren’t very helpful in diagnosis but they can indicate where there is an autoimmune element to the disease that may respond to immunosuppression. Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94% Antinuclear antibodies (ANA) in up to 77% Anticardiolipin antibodies (aCL) in up to 63%

Answer 9

Exocrine cells: Acinar (cells that produce digestive enzymes to transport to duodenum) + their draining ductules Endocrine: Islets of Langerhans Alpha cells = glucAgon production Beta cells = insulin production D cells = somatosttin production (inhibits acinar enzyme secretion) PP cells = pancreatic polypeptide (same) Enterochrommaffin cells = serotonin production Exocrine (no ducts, secreted directly to site of action, secrete enzyme, short term activity) Functional unit of the exocrine pancreas comprises of an acinus + its draining ductule A ductule from the acinus drains into interlobar (intercalated) ducts, which in turn drain into the main pancreatic ductal system The main pancreatic duct itself joins the common bile duct to enter the duodenum as a short single duct at the ampulla of Vater Acinar cells are responsible for the production of digestive enzymes e.g. amylase, lipase, colipase, phospholipase + the proteases (trypsinogen + chymotrypsinogen) These enzymes are released by acinar cells + are then transported into the duodenum via pancreatic secretions Stimulus for pancreatic secretion is gastric distension Endocrine (ductless, released directly into the blood, secrete hormones, long term activity) The endocrine component is scattered through the gland in the form of pancreatic islets of Langerhans Alpha cell - glucagon production Beta cells - insulin production D cells - somatostatin (inhibits acinar enzyme secretion) production PP cells - pancreatic polypeptide (inhibits acinar enzyme secretion) Enterochrommaffin cells - serotonin production

Answer 10

Inflammation of the pancreas -\> leakage of enzymes + autodigestion Causes - think any acute injury I - idiopathic G - gallstones E - ethanol T - trauma S - steroids M - mumps A - autoimmune S - scorpion venom H - hyperlipidaemia E - ERCP D - drugs - NSAIDs, ACEis

Answer 11

Signs Bruising around periumbilical region = CULLEN’S SIGN Bruising on flanks = GREY TURNER’S SIGN Tachycardia Abdo guardian + tenderness Distension Fever Jaundice Dehydration Hyperglycaemia from decreased insulin production Symptoms EPIGASTRIC PAIN RADIATING TO THE BACK - RELIEVED BY SITTING FORWARDS N&V Anorexia Don’t confuse the pain from pericarditis - which usually presents in younger patients Clinical dx

Answer 12

INCREASED AMYLASE in serum + urine (but in serum it may be decreased 3/4 days after acute event, other things can also cause this e.g. upper GI perforation. Urinary may be diagnostic as levels remain elevated for a long time) - 3 fold upper limit of normal. Increased lipase (this is more sensitive + specific) Increased CRP - helps assess severity + prognosis LFTs - Raised ALT + AST - but can normalise as the stone leaves. Elevated ALT \>150 suggests gallstones Need erect CXR to exclude gastroduodenal rupture Abdo USS for gallstones Contrast enhanced CT to find extent of necrosis MRI - identify fluid + solid inflam masses APACHE 2, Glasgow + Ranson scoring

Answer 13

Nil by mouth - to drop pancreatic stimulation. NG tube? - for dietary supplements - less pancreatic enzymes are released so need to support nutrition Analgesics Prophylactic abx (not if you think gallstones as can make worse) Drainage of collections? Assess severity!!

Answer 14

Complications (if left untreated/side effects of management) Acute Respiratory Distress Syndrome – leading cause of death Systemic inflammatory response syndrome (SIRS): Pro-inflammatory state Any two of: • Tachycardia greater than 90 bpm • Tachypnoea (fast breathing) greater than 20 breaths per min • Pyrexia with temperature greater than 38 degrees • High white cell count Sepsis Pancreatic pseudocyst Hypovolaemic shock from ruptured vessels DIC

Answer 15

Obstruction of bicarbonate secretion in the pancreatic lumen causes early activation of trypsinogen + autodigestion which is replaced by fibrosis. (i.e. continual inflam process -\> loss of pancreatic tissue -\> fibrosis) Causes: Alcohol excess - commonest cause in dev world (60-70%) CKD Hereditary Autoimmune Presentation Epigastric pain boring through back (worse after fatty food + alcohol, better on leaning forward) 50 year old male N&V, DM due to damaged B cells due to exocrine dysfunction Malabsorption due to endocrine dysfunc - weight loss, steatorrhea, vitamin/protein def, diarrhoea Steatorrhea (excess fat in faeces - pale, loose, foul smelling stools that float) Key complications are: Chronic epigastric pain Loss of exocrine function, resulting in a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract Loss of endocrine function, resulting in a lack of insulin, leading to diabetes Damage and strictures to the duct system, resulting in obstruction in the excretion of pancreatic juice and bile Formation of pseudocysts or abscesses

Answer 16

Serum amylase + lipase (may be increased if there is enough cells to make them - in v advanced disease there is not sufficient residual acinar cells) Abnormal faecal elastase Abdo USS + contrast enhanced CT - detects pancreatic calcification + dilated pancreatic duct to CONFIRM DX AXR - speckled calcification

Answer 17

Alcohol cessation Abdo pain control Duct drainage Pancreatic enzyme supplements PPI to help digestion (-razole) Insulin for DM Surgery? Pancreatectomy

Answer 18

Ascites is fluid in the peritoneal cavity. Hypoalbuminaemia - reduced plasma oncotic pressure. Portal hypertension - increased hydrostatic pressure. There is portal hypertension because there is increased intrahepatic resistance. Renal water retention (peripheral arterial vasodilation mediated by NO etc.)

Answer 19

Fluid in the peritoneal cavity Cirrhosis commonest cause, 50% cirrhosis pts develop ascites in 10yrs. 4 basic mechanisms Peritonitis - more leaky Raised capillary hydrostatic pressure Reduced colloid oncotic pressure Peritoneal lymphatic draining Transudate (protein \<25g/L) - portal HTN (due to cirrhosis), Budd Chiari, low plasma protein, heart failure. Exudate (protein \>25g/L) - peritonitis, peritoneal malignancy SHIFTING DULLNESS, gained weight, abdo distension. Signs of liver disease. Respiratory distress (pleural effusion). Diagnostic aspiration (albumin, neutrophil count) 1st line - salt restriction. Diuretics - furosemide/spironolactone. SBP (8%) - an infection of ascitic fluid. Most common causes are E.coli then K.pneumoniae Healthy men should have no fluid while in women up to 20ml is considered normal. Peritoneal carcinomatosis

Answer 20

High blood pressure in the portal vein. Causes: prehepatic - portal vein thrombosis Intrahepatic - schistosomiasis, cirrhosis. Posthepatic - right sided heart failure Asymptomatic, or Sx of complications: Ascites Bleeding varices

Answer 21

GI bleeds on a background of chronic liver disease Most patients with cirrhosis develop varices, but only ⅓ bleed from them. Bleeding often massive. Portal vein is formed by union of superior mesenteric (from the gut) and splenic vein (from the spleen) and transports blood into the liver through the porta hepatis 1st line/gold std Ix? Upper GI endoscopy Portal vein is formed by union of superior mesenteric (from the gut) and splenic vein (from the spleen) and transports blood into the liver through the porta hepatis Melaena Haematemesis (coffee ground vomit)

Answer 22

Urgent gastroscopy/endoscopy Fluid resuscitation, remember can be massive Terlipressin (ADH analogue) or Octreotide Balloon tamponade Gold std - endoscopic therapy: bang ligation or sclerotherapy. 60-80% of recurrence within 2yrs, so we give secondary prophylaxis: Propranolol / Isosorbide Repeat variceal banding TIPSS ADH analogue for hypovolaemia, also constricts splanchnic arteries to reduce bleeding)May give somatostatin/Octreotide which lowers portal pressure by same mechanisms.

Answer 23

A is Acquired by mouth from Anus, is Always cleared Acutely and only ever Appears once B is Blood-Borne and if not Beaten can be Bad B and D is DastarDly C is usually Chronic but Can be Cured - at a Cost. Caused by Crack (IVDU). E is Even in England and can be Eaten (found in pigs), if not alway beaten

Answer 24

Virus type RNA Transmission Faecal-oral: contaminated food, fly vectors Epidemiology Rarer, high prevalence in Africa, Asia, South America, Middle east. Pathophysiology Acute infection usually cleared by host immune system. Presentation Non-specific symptoms - nausea, anorexia, malaise, After 1-2weeks liver symptoms - jaundiced, hepatomegaly, skin rash. Investigations LFTs - raised ALT, raised bilirubin, serology Treatment Vaccine is available Treatment often not required, generally supportive. Complications Rare, acute liver failure.

Answer 25

Virus type DNA virus (only DNA one). Transmission Blood products (IVDU), sexually (particularly MSM). Vertical transmission is most common transmission worldwide. Epidemiology Present worldwide, prevalent in Africa, Middle and Far East. Pathophysiology Acute infection infects hepatocyte. Cellular response usually clears it. Chronic HBV (5%) if HBsAg \>6 months. Depends on age/ immunocompetence. Inflammation can last 10 yrs -\> cirrhosis. Presentation Similar acute infection. If chronic, then signs of cirrhosis - jaundice, pruritus etc. Investigations LFTs, serology. If Ag after 6 months then can confirm chronic HBV. Treatment Vaccine available - given to those at risk (probs got it in 1st yr). Antiviral treatment - Tenofovir, pegylated interferon alpha 2a Complications If chronic, increased risk of liver cirrhosis, hepatocellular carcinoma

Answer 26

Virus type RNA Transmission Blood borne - sexually, IVDU Pathophysiology Unable to replicate on its own, requires concurrent HBV infection. It makes Hep B infection more likely to progress to cirrhosis/HCC Presentation Clinically indistinguishable from acute HBV infection Treatment Same as HBV Complications Cirrhosis and HCC

Answer 27

Virus type RNA Transmission Blood/blood products - IVDU more than sexually. Epidemiology More common in UK. Again common in Africa. Pathophysiology Acute infection often asymptomatic, allowing it to become chronic. Chronic HCV infection causes a slowly progressive fibrosis over years. Presentation Acute = asymptomatic. Later on signs of chronic liver disease. Investigations LFTs, serology. If Ag after 6 months then can confirm chronic HCV. Treatment Treatment is revolutionising from interferon based regimens to directly acting antiviral agents (Ribavirin) - expensive. Complications Chronic liver disease, hepatocellular carcinoma

Answer 28

Virus type RNA virus Transmission Faeco-oral transmission (undercooked meat) Epidemiology Common in UK Presentation 95% of cases are asymptomatic, as usually self-limiting Investigations Serology Treatment Often not required, but supportive. Complications Rare. Can progressive to cirrhosis in immunocompromised.

Answer 29

Definition Multi-system disorder of dysregulated dietary iron absorption and increased Iron release from macrophages Aetiology Autosomal recessive, can get secondary Iron overload caused by multiple transfusions. Epidemiology Rare. Pathophysiology Iron accumulates in liver, joints, pancreas, heart, skin and gonads. Presentation SLATE GREY SKIN Hypogonadism (ED), or other Sx of complications (e.g. arrhythmias) Investigations Bloods - Iron, LFTs. Diagnostic is liver biopsy. Treatment Venesection 1st line. Iron chelation 2nd line. Definitive = liver transplant Complications Cirrhosis, HCC, diabetes, heart disease.

Answer 30

Definition Too much copper, that builds up in the liver and CNS Aetiology Autosomal recessive, defective enzyme involved in biliary excretion of excess copper. Epidemiology Rare. Pathophysiology Cu2+ accumulates in the liver (liver symptoms), basal ganglia (Parkinson’s symptoms) and cornea (kayser-Fleischer rings). Presentation Liver problems with psychiatric/neurological presentation - Parkinsonian, depression, neurotic behavioural patterns. Kayser-Fleischer ring Investigations 1st line - 24hr urine copper and blood caeruloplasmin. Definitive is liver biopsy. Treatment Pencillamine (copper chelation). Liver transplant Complications Liver failure, neurological problems.

Answer 31

Hepatocellular carcinoma - 80% of cases Presentation → chronic liver failure +- abdo mass Risk Factors → HCV and HBV(80%), EtOH, Aflatoxin Investigations → LFTs, Clotting studies, CT, MRI, Ultrasound guided Biopsy Treatment - depends on staging Partial Hepatectomy or Transplant - curative intention Chemotherapy to downstage and possibly resect or as palliative chemo to prolong life Prognosis → 3-6 months if unresectable - 90%

Answer 32

Pancreatic adenocarcinoma accounts for 90% Who? Men \> women, above 65, smokers, obese, chronic pancreatitis, family history Clinical Presentation: Unrelenting epigastric pain worse at night - 46% Obstructive Jaundice +- pain Weight loss and anorexia Palpable gallbladder (courvoisier's sign) Recent diagnosis of DM Trousseau's sign - Migratory thrombophlebitis Investigations Bloods - Carbohydrate antigen 19-9 + LFTs CT +- Endoscopic USG Biopsy with histological confirmation Management Surgery - Whipple's procedure Chemo - Neoadjuvant, adjuvant or palliative Prognosis 6% overall 5 year survival

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Liver Flashcards

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