Liver and friends Flashcards

Question

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

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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%

Answer 7

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

Answer 8

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

Answer 9

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,

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

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

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

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)

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

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%

Answer 22

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

Answer 23

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

Answer 24

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

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

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

Answer 33

``` 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&E stain as to cause of cirrhosis Perl's stain= ferric iron stains blue Granules- 0-4 Haemochromatosis ```

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

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

Answer 42

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%

Answer 43

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

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

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

Answer 57

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

Answer 58

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

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

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

Answer 63

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

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

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

Answer 74

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

Answer 75

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

Answer 76

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

Answer 77

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

Answer 78

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

Answer 79

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

Answer 80

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

Answer 81

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

Answer 82

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

Answer 83

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

Answer 84

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

Answer 85

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

Answer 86

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

Answer 87

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

Answer 88

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

Answer 89

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

Answer 90

>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

Answer 91

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

Answer 92

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

Answer 93

<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

Answer 94

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

Answer 95

``` 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 ```

Answer 96

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

Answer 97

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

Answer 98

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

Answer 99

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

Answer 100

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

Answer 101

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

Answer 102

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

Answer 103

``` 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 ```

Answer 104

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)

Answer 105

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

Answer 106

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

Answer 107

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

Answer 108

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

Answer 109

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

Answer 110

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

Answer 111

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

Answer 112

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

Answer 113

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

Answer 114

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

Answer 115

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

Answer 116

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

Liver and friends Flashcards

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