GI 2 - liver + co. Flashcards
(137 cards)
1
Q
list 4 causes of acute pancreatitis
A
GET SMASHED Gallstones Ethanol (alcohol) Trauma Steroids Mumps/Malignancy Autoimmune Scorpion venom Hyperlipidaemia, hypothermia, hypercalcaemia ERCP and emboli Drugs
2
Q
describe the pain of acute pancreatitis
A
gradual or sudden severe epigastric/central abdominal pain, radiates to back, may be relieved by sitting forward.
3
Q
give 3 symptoms and signs of acute pancreatitis
A
pain, vomiting. tachycardia, fever, jaundice, shock, ileus, rigid abdomen ± local tenderness. Cullen’s and Grey Turner’s signs.
4
Q
what are Cullen’s and Grey Turner’s signs? what causes them?
A
Cullen’s = periumbilical bruising Grey Turner’s = bruising of flanks. due to blood vessel autodigestion and retroperitoneal haemorrhage.
5
Q
what 2 enzymes would you test for in acute pancreatitis? what would the results be?
A
serum amylase - raised. serum lipase - raised (more sensitive/specific).
6
Q
what investigations would you carry out in acute pancreatitis?
A
serum amylase and lipase. ABG. CT. AXR.
7
Q
give 3 criteria in the Modified Glasgow criteria for predicting severity of pancreatitis
A
PANCREAS: PaO2 low Age >55yrs Neutrophilia Calcium - low Renal function Enzymes Albumin Sugar (blood glucose)
8
Q
how would you medically manage an acute pancreatitis patient?
A
Nil by mouth / NG tube. pethidine (antispasmodic), tramadol (pain relief). prophylactic abx, treat underlying cause.
9
Q
give 2 early and 2 late possible complications of acute pancreatitis
A
early: shock, ARDS, renal failure, DIC, sepsis, hypocalcaemia. late: pancreatic necrosis, abscesses, bleeding, thrombosis, fistulae.
10
Q
explain the pathology of chronic pancreatitis
A
inappropriate activation of enzymes within the pancreas - leads to precipitation of protein plugs within duct lumen - forms a point for calcification - duct blockage - ductal hypertension + pancreatic damage - pancreatic inflammation + impaired function
11
Q
give 3 causes of chronic pancreatitis
A
alcohol, tropical chronic pancreatitis, hereditary, autoimmune, cystic fibrosis, haemachromatosis, pancreatic duct obstruction (stones/tumour), hyperparathyroidism, congenital.
12
Q
give 3 clinical features of chronic pancreatitis
A
epigastric pain boring through to back - relieved by sitting forward or hot water bottles on epigastrium/back. bloating, steatorrhoea, weight loss, brittle diabetes,
13
Q
what would you expect serum pancreatic enzymes levels to be in chronic pancreatitis?
A
amylase and lipase are normal
14
Q
what investigations would you run in chronic pancreatitis?
A
ultrasound + CT.
15
Q
how would you treat a patient with chronic pancreatitis?
A
NSAIDs and tramdol for abdo pain (amitriptyline for more chronic episodes). lipase + fat-soluble vit supplements. no alcohol, low fat diet. surgery if pain can’t be controlled, or there’s weight loss.
16
Q
give 2 possible complications of pancreatitis?
A
pseudocyst, diabetes, biliary obstruction, local arterial aneurysm, splenic vein thrombosis, gastric varices, pancreatic carcinoma
17
Q
describe the 3 different types of gallstones and their causes
A
pigment stones - small, friable, irregular - haemolysis. cholesterol stones - large, often solitary - age, obesity, female sex. mixed stones - faceted (calcium salts, pigment and cholesterol).
18
Q
what are the 2 risk factors for gallstones become symptomatic?
A
smoking and parity (having given birth).
19
Q
how does acute cholecystitis develop from an obstruction?
A
obstruction to gall bladder emptying - increased glandular secretion in gall bladder - distension and inflammatory response to retained bile, leads to infection
20
Q
what special test would you do on examination to confirm cholecystitis?
A
Murphy’s sign - 2 fingers over RUQ + ask patient to breathe in - causes pain and arrest of inspiration as inflamed gallbladder hits your fingers
21
Q
how would you differentiate the pain of biliary colic from cholecystitis?
A
cholecystitis features an inflammatory component - local peritonism, fever, high WCC
22
Q
what are the clinical features of acute cholecystitis?
A
epigastric/RUQ pain, referred to R shoulder. vomiting, fever, local peritonism, possibly a gallbladder mass.
23
Q
what investigations would you perform in cholecystitis?
A
ultrasound - thick walled, shrunken gallbladder, pericholecystic fluid, stones, common bile duct dilation. FBC (high WCC).
24
Q
how would you treat cholecystitis?
A
nil by mouth, analgesia, IV fluids. cefuroxime. laparoscopic cholecystectomy.
25
describe the clinical features of chronic cholecystitis
chronic inflammation ± colic. flatulent dyspepsia - vague abdo discomfort, distension, nausea, flatulence and fat intolerance.
26
describe the pain of biliary colic
severe, constant, increasing pain in RUQ, can radiate to right shoulder/scapula.
27
how would you tell that a gallstone had moved to obstruct the common bile duct?
obstructive jaundice and cholangitis
28
what is the triad of symptoms for acute cholangitis?
Charcot's triad - jaundice, fever, biliary colic.
29
what structure is being obstructed by gallstones if a patient has developed acute cholangitis?
common bile duct
30
what is the gold standard investigation in cholangitis?
transabdominal ultrasound - measure CBD dilatation.
31
how would you treat acute cholangitis?
laparoscopic cholecystectomy with IV abx - cefuroxime and metronidazole
32
list 3 complications of gallstones
in gallbladder and cystic duct: biliary colic, acute and chronic cholecystitis, mucocoele, empyema, carcinoma, Mirizzi's syndrome. in bile ducts: obstructive jaundice, cholangitis, pancreatitis. in gut: gallstone ileus.
33
what is jaundice?
yellowing of the skin, sclerae and mucosae due to increased plasma bilirubin
34
give 3 causes of unconjugated hyperbilirubinaemia (pre-hepatic jaundice)
haemolysis - malaria, DIC. ineffective erythropoiesis. impaired hepatic uptake - drugs (contrast agents, rifampicin), RHF. impaired conjugation - Gilbert's syndrome, Crigler-Najjar.
35
what will the urine and faeces look like in conjugated hyperbilirubinaemia (hepatic/post-hepatic jaundice)? why?
urine = dark - conjugated bilirubin is soluble, so excreted in urine. Faeces = pale - less conjugated bilirubin enters gut.
36
give 3 causes of conjugated hyperbilirubinaemia due to hepatocellular dysfunction
viruses - hep, CMV, EBC. drugs - paracetamol od, isoniazid, rifampicin, pyrazinamide, statins, sodium valproate. alcohol. cirrhosis. liver metastases/abscesses. haemachromatosis. autoimmune hepatitis. septicaemia. syphilis. alpha1-antitrypsin deficiency. Budd-Chiari. Wilson's disease. Right heart failure.
37
give 3 causes of conjugated hyperbilirubinaemia due to impaired hepatic excretion (cholestatic / obstructive jaundice)
primary biliary cirrhosis, primary sclerosing cholangitis, drugs, common bile duct gallstones, pancreatic cancer, compression of the bile duct, choledochal cyst
38
how is hepatitis A spread? what are the risk factors?
faecal-oral route. poor sanitation, overcrowding, contaminated food/water. (fish in sewagey water)
39
what would you find when looking at viral markers for hepatitis A? what other blood test would you perform?
Anti-HAV IgM (acute) and IgG (raised for life - carrier). LFTs - AST/ALT are raised
40
how would you treat hepatitis A?
supportive treatment - self-limiting.
41
how would you prevent hepatitis A?
passive and active immunisation (inactivated protein) and good hygiene
42
what type of virus is hep A?
RNA
43
give 3 symptoms of hep A as well as 2 later signs
symptoms: fever, malaise, anorexia, nausea, arthralgia. later signs - jaundice, hepatosplenomegaly, lymphadenopathy.
44
what type of virus is hep B?
DNA
45
how is hep B spread?
blood products - vertical transmission, IVDU, found in semen and saliva - sexual/direct contact.
46
name 3 of the at-risk groups for hep B
IVDUs, their sexual partners/carers, health workers, haemophiliacs, job exposure to blood (morticians), haemodialysis patients, sexual promiscuity, foster carers, staff/residents of institutions/prisons, babies of +ve mothers
47
what are the clinical features of hep B?
resembles hep A - fever, malaise etc - plus arthralgia and urticaria (hives).
48
what antiviral agents would you give to treat a chronic HBV infection? what would you monitor?
interferon alpha, lamivudine, adefovir. monitor HBV levels and platelets.
49
describe how vaccination is used in hep B
passive immunisation is given to non-immune contacts after high-risk exposure. Hep B vaccine given (UK) to children born to +ve mothers, chronic liver patients, haemophilia patients, offered as a travel vaccine, and to healthworkers.
50
list 2 possible complications of hepatitis B
cirrhosis, HCC, fulminant hepatic failure, cholangiocarcinoma, cryoglobulinaemia
51
what type of virus is hep C?
RNA flavivirus
52
how is hep C transmitted and can the spread be prevented?
blood products, mainly IVDU (also transfusions, sexual etc) Can't prevent spread - vaccination impossible due to rapid change of proteins.
53
what haematological disorder is associated with hep C?
Non-Hodgkin's lymphoma
54
give 3 risk factors for progression of hepatitis C to cirrhosis
male, older, higher viral load, alcohol use, HIV, HBV
55
what viral markers would you look for in hepatitis C at 8 weeks?
HCV RNA at 8weeks.
56
if you took a liver biopsy of a hepatitis C patient, what might you see?
lymphoid follicles in portal tracts and fatty change
57
how would you treat a chronic infection with hepatitis C? what major problem should be noted about one of the drugs?
serine protease inhibitors (boceprevir, telaprevir) - directly acting antivirals against genotype 1 HCV. combine with: interferon alpha. ribavirin - very teratogenic.
58
give 3 possible complications of hepatitis C
glomerulonephritis, cryoglobulinaemia, thyroiditis, autoimmune hepatitis, PAN, polymyositis, porphyria cutanea tarda
59
what other virus is needed for hep D to infect someone? why?
hep B. hep D is an incomplete RNA that needs hep B for assembly.
60
how can hepatitis D be prevented?
hep B vaccine
61
how can you test for hepatitis D?
test for anti-HDV antibody
62
what can hep D cause?
acute liver failure/cirrhosis
63
how can you treat a hep D infection?
may need liver transplant as interferon alpha has limited success.
64
what type of virus is hep E? what infection is it similar to?
RNA. hep A.
65
how is hep E transmitted?
enterally - contaminated water.
66
what can you detect in blood and stools to confirm a diagnosis of hep E?
hep E RNA
67
what collagen type is deposited in the liver in cirrhosis?
type 1 and 3
68
what is the difference between macro and micronodular cirrhosis?
macronodular - variable nodule size, normal acini within, tends to follow hepatitis. micronodular - uniform involvement of liver and regenerating nodules
69
if there was alpha-fetoprotein present in the serum of a cirrhosis patient, what would you suspect to be the cause of their cirrhosis?
hepatocellular carcinoma
70
what medications should be avoided when treating cirrhosis?
NSAIDs, opiates, sedatives
71
list 3 causes of cirrhosis
\*chronic alcohol abuse. \*HBV or HCV infection haemachromatosis alpha1-antitrypsin deficiency Budd-Chiari non-alcoholic steatohepatitis autoimmune - primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis. drugs - amiodarone, methyldopa, methotrexate.
72
give 3 clinical features of cirrhosis
pruritus jaundice raised LFTs leuconchyia Terry's nails clubbing palmar erythema hyperdynamic circulation Dupuytren's circulation spider naevia xanthelasma gynaecomastia atrophic testes loss of body hair parotid enlargement hepatomegaly
73
list 3 possible complications of cirrhosis
hepatic failure - coagulopathy, encephalopathy, hypoalbuminaemia, sepsis, SBP, hypogylcaemia. portal hypertension - ascites, splenomegaly, portosystemic shunt + oesophageal varices. increased risk of HCC.
74
what investigations would you carry out in cirrhosis? what would you find?
bloods - raised bilirubin/AST/ALT/alk phos, low albumin. liver ultrasound and duplex - small liver or hepatomegaly, focal liver lesions, ascites. MRI - big caudate lobe, small islands of regenerating nodules, right posterior hepatic notch. transient elastography scan. ascitic tap for urgent MC&S. liver biopsy - confirms diagnosis.
75
if a cirrhosis patient presented with ascites, how would you treat this?
bed rest, fluid and salt restriction, spironolactone ± furosemide.
76
how would cirrhosis be treated?
nutrition, alcohol abstinence, avoid certain drugs. colestyramine for pruritus. treat underlying cause. liver transplant.
77
what are the indications for liver transplant?
advanced cirrhosis secondary to - alcoholic liver disease, hepatitis (B, C, autoimmune), primary biliary cirrhosis, Wilson's disease, alpha1-atintrypsin deficiency, primary sclerosing cholangitis. hepatocellular cancer.
78
what are the contraindications for liver transplant?
extrahepatic malignancy, multiple tumours, severe cardiorespiratory disease, systemic sepsis, HIV infection, non-compliance (drug therapy or alcohol abstinence)
79
what immunosuppression would a liver transplant patient be put on?
ciclosporin or tacrolimus + azathioprine.
80
what's the difference between hyperacute and acute transplant rejection?
hyperacute - due to ABO incompatibility. acute - T cell mediated, 5-10d post-op, patient feels unwell with pyrexia and tender hepatomegaly - managed by altering immunosuppressives.
81
describe the underlying pathogenesis of primary biliary cirrhosis?
serum antimitochondrial antibodies (AMA) cause chronic autoimmune granulomatous inflammation damages interlobular bile ducts causing cholestasis, cirrhosis and portal hypertension.
82
give 2 risk factors for primary biliary cirrhosis
family history, frequent UTIs, smoking, past pregnancy, other autoimmune diseases, hair dye/nail polish
83
give 2 signs found in a patient with biliary cirrhosis
jaundice, skin pigmentation, xanthelasma, hepatomegaly, splenomegaly
84
what blood test results would you find in a patient with primary biliary cirrhosis?
\*\*very high alkaline phosphate - unique to PBC \*\*AMA ab +ve. raised AST/ALT increased Igs.
85
what other investigation, apart from blood tests, might you perform in primary biliary cirrhosis?
ultrasound
86
how would you treat primary biliary cirrhosis?
ursodeoxycholic acid. vitamin supplements for malabsorption. bisphosphonates for osteoporosis, colestyramine/rifampicin for pruritus.
87
give 3 diseases associated with primary biliary cirrhosis
scleroderma, thyroid disease, keratoconjunctivitis sicca, renal tubular acidosis, membranous glomerulonephritis, coeliac disease, interstitial pneumonitis
88
explain secondary biliary cirrhosis
destruction of biliary tracts due to prolonged large duct biliary obstruction, caused by gall stones, bile duct stones, sclerosing cholangitis.
89
how would you investigate secondary biliary cirrhosis?
US followed by ERCP.
90
what are the CAGE questions?
ever felt you should Cut down on your drinking? have people Annoyed you by criticising your drinking? ever felt Guilty about your drinking? ever had an Eye opener to help you get up in the morning?
91
what changes would you see on a liver biopsy of an alcoholic hepatitis patient?
fatty change and infiltration by polymorphonuclear leucocytes and hepatocytes in zone 3. Mallory bodies - dense cytoplasm and giant mitochondria.
92
what is "fatty change"?
first change in the alcoholic liver - hepatocytes contain microvesicular droplets of triglycerides. reversible, but will progress if alcohol isn't stopped.
93
what is the path of damage the alcoholic liver follows?
fatty change - alcoholic heptatitis - fibrosis - micronodular cirrhosis
94
what are the clinical features of alcoholic hepatitis?
SPIDER NAEVI. rapid onset jaundice, nausea, anorexia, RUQ pain, encephalopathy, fever, ascites, tender hepatomegaly
95
how would you manage an alcoholic hepatitis patient?
supportive - poss. NG tube. alcohol cessation - IV thiamine and diazepam if needed.
96
what causes hereditary haemachromatosis?
autosomal recessive inheritance with a mutation in the HFE gene (chromosome 6). mostly affects middle aged men.
97
what is the defining feature of hereditary haemachromatosis?
increased intestinal iron absorption leading to excess iron deposition in organs.
98
list 3 clinical features of hereditary haemochromatosis
erectile dysfunction, slate grey skin pigmentation, hepatomegaly, cirrhosis, dilated cardiomyopathy, osteoporosis, diabetes mellitus, hypogonadism
99
what would be the blood test results (iron, ferritin, total iron binding capacity) in hereditary haemachromatosis? what disease is this the same as?
increased iron and ferritin, low total iron binding capacity. the same as sideroblastic anaemia.
100
what staining would you use on liver biopsy in hereditary haemachromatosis?
Perl's staining
101
how would you treat hereditary haemachromatosis?
venesection - once a week, then a few times a year. desferrioxamine (iron chelator) if can't venesect. testosterone replacement. low iron diet, screen family members.
102
what is alpha1-antitrypsin?
glycoprotein that controls the inflammatory cascade. synthesised in the liver and protects lung tissue from damage by elastase.
103
what diseases does deficiency of alpha1-antitrypsin causes?
emphysema, COPD, chronic liver disease and HCC
104
what are the different genotypes you can inherit for alpha1-antitrypsin? which one brings about symptomatic disease?
PiMM - normal (M = medium) PiZZ - homozymgous, symptomatic (Z = very slow) PiMZ - heterozygous (slow)
105
give the clinical features of alpha1-antitrypsin deficiency
dyspnoea (emphysema), cirrhosis, cholestatic jaundice.
106
how would you diagnose alpha1-antitrypsin deficiency?
serum alpha1-AT levels. genotyping. liver biopsy.
107
what stain would you use on a liver biopsy in alpha1-antitrypsin defiency? what would you see?
Periodic Acid Schiff - PAS +ve globules.
108
what is the curative treatment of alpha1-antitrypsin deficiency?
liver transplant
109
what is Wilson's disease?
autosomal recessive disorder resulting in impaired excretion of copper in bile and faeces, leading to toxic accumulation of copper.
110
what system, apart from the liver, is affected by Wilson's disease? how does this present?
CNS - basal ganglia degeneration, depression, labile emotions, decreased libido, personality changes, tremor, dysarthria, dementia, decreased memory/IQ, delusions
111
what is a Kayser-Fleischer ring?
copper deposition in cornea - see in eyes of Wilson's disease patients
112
what investigations would you carry out in Wilson's disease? what would they show?
slit lamp eye exam. 24h urine copper - excretion high. liver biopsy - increased hepatic copper, hepatitis, cirrhosis. + genetic testing, serum copper/caeruloplasmin.
113
how would you treat Wilson's disease?
lifetime copper chelation - penicillamine. screen siblings (treatment whilst asymptomatic prevents liver damage).
114
name an infective cause of liver failure
EBV, hep B and C, yellow fever
115
name a drug cause of liver failure
paracetamol OD, halothane, isoniazid
116
name a toxin cause of liver failure
carbon tetrachloride, mushrooms
117
name a vascular cause of liver failure
Budd-Chiari, venous thrombosis
118
name an inherited cause of liver failure
primary biliary cirrhosis, haemachromatosis, autoimmune hepatitis, antitrypsin deficiency, Wilson's disease
119
name some other causes of liver failure
alcohol, fatty liver of pregnancy, malignancy
120
give 4 signs of fulminant hepatic failure
hepatomegaly, jaundice, splenomegaly, 'pear drop' smell, asterixis (flapping tremor) palmar erythema, clubbing, ascites, pruritus, portal hypertension
121
what is hepatic encephalopathy? explain it
a major complication of liver failure: liver fails - nitrogenous waste (ammonia) builds up in circulation - passes to brain - astrocytes clear it by converting glutamate to glutamine - excess glutamine causes an osmotic imbalance - cerebral oedema
122
what might you find on investigating the blood of a patient with liver failure?
high bilirubin and aminotransferases. low sodium, albumin, prothrombin, factor V
123
how would you manage a liver failure patient?
treat cause. treat complications: seizures - lorazepman. bleeding - vit K. ascites - diuretics. infection - blind abx = ceftriaxone. hypoglycaemia - IV glucose.
124
what tests would you run on ascitic fluid once aspirated?
cell count, MC&S, protein/albumin, cytology for malignancy, amylase to exclude pancreatitis.
125
give 3 causes of transudate ascites
portal hypertension (cirrhosis). hepatic outflow obstruction. Budd-Chiari syndrome. cardiac failure. tricuspid regurgitation. constrictive pericarditis. Meig's syndrome.
126
give 3 causes of exudate ascites
peritoneal carcinomatosis peritoneal TB pancreatitis nephrotic syndrome lymphatic obstruction
127
what would you find on abdo examination of a patient with ascites?
SHIFTING DULLNESS. fullness in flanks.
128
how would you manage a patient with ascites?
aspirate for testing. sodium restriction + oral spironolactone ± furosemide.
129
what would you seen on a liver biopsy of a patient with cirrhosis?
irregular nodules of fibrous tissues.
130
how would you investigate ascites?
paracentesis - investigation and intervention.
131
what would you see on biopsy in primary biliary cirrhosis?
bile duct granuloma
132
explain why gynaecomastia can be a feature of liver failure in males
failure of liver to eliminate steroid hormones
133
what would you find in the blood of a patient that would indicate they have carrier status for HBV?
HBsAg - surface antigen. present 1-6 months after exposure. present for \>6 months = carrier status.
134
what would you find in the blood of a patient that has recently (last couple of months) been infected with HBV? what does this mean?
HBeAg (e antigen) - present 1.5-3 months after exposure. implies high infectivity.
135
what might you find in the blood of a patient that indicates they have immunity to HBV through having previously been infected?
anti-HBc antibody
136
what might you find in the blood of a patient that indicates they have immunity to HBV through having been vaccinated?
anti-HBs antibody
137
what blood test would you do on an HBV patient to monitor progress?
HBV PCR
