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172 Cards in this Set
- Front
- Back
Why do you need to order IgA when you order ttf antibodies in coeliac's disease?
|
if you are IgA deficient anti-ttg will give you a false negative result
|
|
What are the 3 types of gastric carcinoma?
|
Adenocarcinoma
Sarcoma (GIST) Lymphoma |
|
Adenocarcinoma is divided into 2 types. What are they and what are their features?
|
1. Intestinal
Common in Japanese Preceded by chronic gastritis Related to diet of nitrites, salt, smoking less aggressive 2. Diffuse Sporadic, stronger genetics, Poorly differentiated, and more aggressive |
|
How does gastric carcinoma usually present?
|
Often asymptomatic, insidious or late onset of symptoms
haematemesis, posprandial abdominal fullness, vague epigastric pain anorexia, weight loss burping, N/V, dyspepsia, dysphagia |
|
What is virchow's node?
Sister mary joseph node Irish's node Blumer's shelf |
Virchow's: Left supraclavicular node
Sister mary joseph node: umbilical met Irish's node - left axillary node Blumer's shelf - mass in pouch of douglas |
|
What are the surgical options for management of gastric cancer?
|
1. Total gastrectomy (can be a struggle to keep weight on, only do if cancer is in body, fundus, cardia)
2. subtotal gastrectomy - leave little bit of fundus to anastomose - better outcome - lower risk of leaking BOTH take greater omentum and lymphadenectomy |
|
Where does gastric carcinoma commonly met to?
|
liver
lung brain |
|
How do you stage gastric carcinoma?
|
1. mucosa and submucosa
2. extension to muscularis propria 3. extension to regional nodes 4. distant mets or involvement of continuous structures |
|
What does GIST stand for? What cells is it derived from?
|
gastrointestinal stromal tumour
Derived from interstitial cells of cajal (these cells are associated with Auerbach's plexus and have autonomous pacemaker function co-ordinate peristalsis throughout the GIT tract) |
|
What pattern of spread to GIST"s have?
|
locally and haematogenously
therefore you don't need to worry about lymph nodes when you resect |
|
Which mutations are associated with GIST?
|
C-KIT mutations
|
|
Where are GIST most common found?
|
Stomach (50%)
Proximal SI (25%) Can occur anywhere along GIT |
|
Management of GIST
|
Not all GIST are malignancy but have the potential to become so RESECT
High recurrence rate even with clear margins Don't need to do lymphaedenectomy as rarely met to nodes |
|
Which chemotherapy is used for GIST?
|
imatininb mesylate (tyrosine kinase inhibitor)
Targets C-KIT |
|
Which genetic mutation is involved in celiac disease?
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HLA-DQ2 (chromsome 6)
also assoc. with HLA-DQ8 |
|
Which part of the bowel is celiac disease most severe in? Which nutrients are affected in absorption?
|
proximal bowel
iron, calcium, folic acid |
|
What is celiac disease associated with
|
dermatitis herpetiformis skin eruption (itchy bumpy blistery rash)
epilepsy myopathy infertility metabolic bone disease depression paranoia IgA nephropathy AI thyroid disease type 1 diabetes |
|
What might you see on a small bowel biopsy of someone with celiac disease
|
villous atrophy and crypt hyperplasia
increased plasma cells and lymphocytes in lamina propria |
|
What serological tests should be performed in someone with suspected celiac disease
|
Serum anti-TTG, IgA (serum protein electrophoresis)
NB: IgA deficiency patients have falst negative anti TTG |
|
What is bacterial overgrowth of the small bowel?
|
proliferation of bacteria in small bowel to concentrations > 10(4) bacterial /ml of bowel tissue
--> malabsorption and diarrhoea |
|
Aetiology of bacterial overgrowth?
|
anatomic factors
(jejunal diverticulae, fistulae, strictures (CD), obstruction) decreased motility (Scleroderma, DM, hypothyroid) Achlorhydria Decribed in elderly patients without known aetiology |
|
What are the clinical features of bacterial overgrowth of small bowel
|
--> steatorrhea (bacteria deconjugate bile salts impairing micellar lipid formation)
--> diarrhea (bowel mucosa damaged by bacterial products) megaloblastic anaemia - bacteria take up B12 --> bloating, flatulence may be asymptomatic |
|
How do you investigate small bowel overgrowth?
|
Gold standard = mixed bacterial cultures from the jejunum
|
|
Which nutrients are absorbed in the jejunum?
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Upper jejunum
iron, calcium Jejunum folic acid carbohydrates protein |
|
What is absorbed in the ileum?
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B12
fat soluble vitamin |
|
What is absorbed in the duodenum?
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Iron (also in upper jejunum)
Caclcium (also in upper jejunum) carbohydrate (also in jejunum) |
|
What does vitamin E deficiency lead to?
|
retinopathy
Neurological problems |
|
What does vitamin A defieicny lead to?
|
night blindness
dry skin keratomalacia |
|
What is the most frequent cause of mesenteric ischaemia?
|
Ischaemic colitis
|
|
What supplies blood to the colon?
|
SMA (ileocolic - proximal ascending colon, right colic - proximal ascending colon and hepatic flexure)
IMA (left colic, sigmoid, superior rectal) |
|
How do patients with acute colonic ischaemia present?
|
rapid onset of mild abdominal pain and tenderness over the affected bowel, most often involving the left side
mild to moderate rectal bleeding or bloody diarrhea cf. small bowel ischaemia - more severe pain, felt peri-umbilically |
|
MOA of lactulose
|
= non-absorbable disacharide
Increases gut transit and acidifies gut pH --> traps ammonia by converting ammonium ion which decreases ammonia absorption |
|
What metabolic derangements do you get with acute liver failure?
|
hypoglycaemia
hypophosphataemia metabolic acidosis |
|
What complications are associated with acute liver failure?
|
encephalopathy
cerebral oedema sepsis (immunological derangements) renal failure hepatic hydrothorax - associated with portal HTN and cirrhosis metabolic derangements coagulopathy |
|
Is serum albumin a good marker of acute liver failure?
|
NO.
It detects prolonged (weeks) of hepatic dysfunction |
|
What are some causes of decreased serum albumin?
|
malnutrition
renal or GI losses acute illness Chronic liver failure |
|
What happens to urea in chronic liver failure?
|
it goes down
it is synthesised in the liver |
|
What are the most common organisms in spontanous bacterial peritonitis associated with ascites?
|
gram negatives 70%
E.Coli Strep Klebseilla |
|
What is MEN 1?
|
3 Ps
hyperparathyroidism pituitary pancreas (insulinoma, gastrinoma) associated with ZE syndrome |
|
How does Zollinger-Ellison syndrome present?
|
epigastric pain + diarrhea
multiple duodenal ulcers malabsorption |
|
What is Peutz-Jeghers syndrome?
|
autosomal dominant condition with hemartoamtous polyps in GI tract
freckles and pigmented lesions on lips, palms, soles presents with rectal bleeding 50% will die from GI cancer |
|
What are anal fissures?
|
longitudinal or elliptical tears in squamous lining of distal anal canal
|
|
What is the common diagnosis of isolated hyperbilirubinemia?
|
Gilbert's syndrome
|
|
Which enzyme is decreased in Gilbert's syndrome?
|
glucoronyl transferase
|
|
What is a common trigger for hyperbilirubinemia in Gilbert's sydnrome?
|
viral infection
|
|
What is the urinalysis if raised unconjugated bilirubin?
|
normal, unconjugated bilirubin cannot be excreted via urine
|
|
What is the most useful prognostic marker in acute liver failure (paracetamol overdose, etc.)?
|
PT (prothrombin time)
|
|
What do you need to measure in acute liver failure?
|
BGL due to severe hypoglycemia
|
|
Treatment of esophageal varices
|
1. endoscopic variceal band ligation
2. Sengstaken-Blakemore tube if uncontrolled hemorrhage 3. Tranjugular intrahepatic portosystemic shunt if above measures fail Prophylaxis includes ocreotide or propanolol |
|
Treatment of non-dysplastic change in esophagus
|
high dose proton pump inhibitor
|
|
Treatment of dysplastic change in esophagus
|
1. endoscopic ablation
2. mucosal resection 3. esophagectomy |
|
Drug-induced cause of choelstasis
|
flucloxacillin + co-amoxiclav
erythromycin nitrofurantoin OCP sulphonylureas |
|
Liver tests in obstructive/cholestatic disease
|
ALP and GGT are raised
|
|
Common cause of dysphagia from both solids and liquids
|
achalasia = failure of esophageal peristalsis and relaxation of LOS due to degenerative loss of ganglia from Auerbach's plexus
|
|
Treatment of achalasia
|
Botox injection
myomectomy balloon dilation |
|
Which disease is most associated with primary sclerosing cholangitis?
|
ulcerative colitis
|
|
Tell me about FAP
|
autosomal dominant, leads to formation of 100s of polyps by 30 years old, mutation of tumor suppressor gene APC, on chromosome 5, Rx w/ colectomy w/ ileo-anal pouch in 20s
|
|
Tell me about HNPCC
|
autosomal dominant, most common form of inherited colon cancer, 90% develop cancer, often proximal, poorly differentiated, aggressive, gene mutations = hMLH1 & hMSH2
|
|
Risk factors for gastric cancer
|
H Pylori, Blood group A, gastric polyps, pernicious anemia, smoking, nitrates in diet
|
|
What type of cancers are cholangiocarcinomas?
|
mucin producing adenocarcinomas that arise from bile ducts
Can be: Intrahepatic hilar (central) - 65% Peripheral or distal - 30% |
|
How do cholangiocarcinomas most often present?
|
painless jaundice, often with pruritus or weight loss and acholic stools
|
|
Which tumours markers can be useful for monitoring therapy for cholangiocarcinomas?
|
CEA
CA-19.9 Ca-125 |
|
Investigations in suspected cholangiocarcinoma?
|
US
MRCP or helical CT ERCP is needed to obtain a biopsy |
|
Treatment of cholangiocarcinoma
|
Generally palliative
Lower third lesions - whipple procedure Further up - bile duct resection and lymphadenectomy High rate of locoregional recurrence - RT Surviuval isn't great - local and met recurrences - lung and liver |
|
What are the 3 types of pancreatic carcinoma?
|
Adenocarcinoma (arising from ductal epithelium) - 90%
Ampullary or periampullary adenocarcinoma (rare arising from ampulla of vater or adjacent duodenum) Mucinous cystadenocarcinoma - very rare, arising from head of pancreas |
|
What are the RF for pancreatic carcinoma
|
Smoking
DM Chronic pancreatitis Family history |
|
What are the most common sites of distant mets in pancreatic carcinoma?
|
Liver
Lung Peritoneum less frequently bone |
|
Complications with pancreatic cancer?
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Hypercoagulable state (Trousseau's syndrome)
High incidence of thromboembolic events |
|
What stage of pancreatic disease can be surgically resected?
|
Stage I-IIB
I.e. limited to the pancrease and peripancreatic nodes |
|
What pharmacological management can be given to control variceal haemorrhage while waiting for more definitieve treatment?
|
terlipressin
helps initial haemostasis and preventing rebleeding |
|
How many months does HbsAg need to be present for to imply chronic HBV?
|
> 6 months
|
|
What does anti HbsAg imply in HBV?
|
Immunity or previous immunisation
|
|
What does anti-HbC imply in HBV?
|
Acute or past infection
Generally appears early on and lasts for 6 months |
|
What does HbeAg imply in HBV?
|
Result of breakdown of infected liver cells so is a marker of infectivity
|
|
Which infection is a gastric MALT lymphoma associated with?
|
H, Pylori
|
|
Which patients are at increased risk of developing hepatotoxicity after paracetanol overdose?
|
Chronic alcohol
Anorexia nervosa patients on P450 enzyme inducers (phenytoin, carbamazepine, rifampicin) HIV |
|
Which traveller's diarrhoea organisms are responsiblve for watery diarrhoea?
|
E Coli
Cholera |
|
Which traveller's diarrhoea organisms are responsible for bloody diarrhoea?
|
Shigella
Amoebiasis Campylobacter |
|
Does giardia present with bloody diarrhoea?
|
NO
|
|
What are the main features of chronic pancreatitis?
|
Steatorrhea
Pain after meals DM develops usually 20 years after onset of symptoms |
|
How do HCC usually present?
|
Usually no symptoms other than those of advancing cirrhosis
think abou it in a patient with previously compensated cirrhosis who decompensates Those without cirrhosis may present with abdominal pain and weight loss if tumour > 5cm |
|
What paraneoplastic syndromes are associated with HCC?
|
Hypoglycaemia
Erythrocytosis - tumour secretes EPO Hypercalacaemia Watery diarrhoea Cutanous features - dermatomyositis, multiple seborrheic keratoses |
|
Where does HCC usually spread to?
|
Lung
Bone Adrenal gland Brain - very rare |
|
Which tumour marker is seen in HCC?
|
Alpha fetoprotein
Produced by 60% of HCC Also rises in active HBV and HCV replication and is seen in acute hepatic necrosis Correlates with prognosis |
|
How do you investigate suspected HCC?
|
US first
Nodules < 1cm redo in 2-6 months If > 1cm - MRI or CT + contrast If typical appearance on CT - no further investigation If not typical for HCC - either CT or MRI (whicever was hot done before) OR biopsy Only perform biopsy when diagnostic imaging results are uncertain and result would have direct impact on management NB: in cirrhotic patients any dominant solid nodule that is not clearly a haemangioma should be considered an HCC unless proven otherwise |
|
What classification is used to assess the severity of liver disease?
What parameters does it use? |
Child Pugh classification
Ascites Bilirubin PT INR Encephalopathy |
|
What screening is available for HCC?
|
Screen every 6-12 months for high risk individuals
US + AFP |
|
Which patients are high risk for hepatocellular carcinoma and require screening?
|
Cirrhosis
Haemacrhromatosis Alcohol Alpha 1 anti-trypsin deficiency Wilson's disease |
|
Which cancers commonly met to the liver?
|
Colorectal
Breast Lung Stomach Pancreas Endometrium Melanoma |
|
What is more common primary liver cancer or mets?
|
mets
|
|
PHarmacological management of HCV?
|
pegylated interferon and ribavirin
|
|
SE of ribavirin?
|
haemolytic anaemia
Shouldn't fall pregnant on it |
|
SE of interfern alpha
|
Flu like symptoms
leukopenia Thrombocytopenia |
|
Which layers of mucosa does CD and UC affect?
|
UC affects mucosa and submucosa
CD - affects all layers including serosa |
|
Which IBD has crypt abscesses?
|
UC
|
|
What is the gold standard for investigating bacterial overgrowth?
|
small bowel aspiration and culture
|
|
Methotrexate is recommended as the management for which IBD?
|
Crohn's disease
|
|
What is the most common cause of biliary disease in patient's with HIV?
|
sclerosing cholangitis due to
CMV Cryptosporidium Microsporidia |
|
What is H.Pylori associated with?
|
MALT tumour
Peptic ulcer duodenal > gastric gastric cancer atrophic gastritis |
|
Risk factors for GORD
|
smoking
alcohol obesity hyperchlorydia gastric surgery radiotherapy |
|
What percentage of GORD patients have Barrett's at Dx?
|
10%
|
|
Indications for gastroscopy in GERD
|
rule out malignancy, peptic ulcer, infective esophagitis (all mimic GERD)
discern btwn esophagitis and non-esophagitis reflux dx Barrett's |
|
Most accurate test in GERD
|
24 hour pH monitoring
rarely required most useful if PPIs not helpful |
|
When do you do esophageal manometry in GERD?
|
dx abnormal persitalsis and/or decreased lower esophageal sphincter tone
DOESNT dx GERD |
|
Surgical management of GERD
|
fundoplication, used if PPIs not working or if large hiatus hernia
|
|
Management of Barrett's esophagus
|
surveillance gastroscopy w/ biopsy 1 yr after initial dx, then every 2-3 yrs
if dysplasia, Rx w endoscopic ablation, endoscopic mucosal resection followed by high dose acid suppression |
|
Complications of GERD
|
esophageal stricture
ulcer bleeding Barrett's esophagus |
|
Causes of dysphagia with solids AND liquids
|
neuromuscular disorder
intermittent: esophageal spasm progressive: scleroderma, achalasia |
|
Causes of dysphagia with solids only
|
mechanical obstruction
progressive: carcinoma (age >50), peptic stricture (if heartburn) intermittent: lower esophageal ring |
|
What is a Schatzi's ring?
|
ring of mucosa thickened at squamo-columnar junction in a patient w hiatus hernia, intermittent dysphagia with solids
|
|
What is psoas sign?
|
RLQ pain on hip extension w pt in left lateral position
sign of appendicitis |
|
What is the obturator sign?
|
RLQ pain on passive internal rotation of flexed right thigh
stretches obturator mm sign of appendicitis |
|
What is Rovsing's sign?
|
RLQ pain w palpation on left
sign of appendicitis |
|
Treatment of acute hepatitis B
|
supportive, vaccination of sexual and household contacts
|
|
Treatment of acute hepatitis C
|
pegylated interferon alpha
start within 12 weeks of symptoms to have high systemic response |
|
T/F Hepatitis A can relapse but can never become chronic
|
true
|
|
In Hep B, when does IgM change to IgG?
|
when disease changes from acute --> chronic
IgM begins to lower at 4 months, and is gone at 12 months |
|
When do you get Anti-HBs in Hepatitis B?
|
in resolved infection or immunized pts
|
|
What is the treatment goal in Hepatitis B?
|
reduce serum HBV-DNA to undetectable levels
|
|
What is chronic Hepatitis B defined as?
|
hepatitis B surface antigen (HBsAg) positivity for longer than 6 months
|
|
What is the HepBe Ag?
|
Unlike the surface antigen, the e-antigen is found in the blood only when the HBV virus is actively replicating. HBeAg is often used as a marker of ability to spread the virus to other people (infectivity). It may also be used to monitor the effectiveness of treatment. However, there are some types (strains) of HBV that do not make e-antigen; these are especially common in the Middle East and Asia. In areas where these strains of HBV are common, testing for HBeAg is not very useful.
|
|
What is the HepBe Ab?
|
In those who have recovered from acute hepatitis B infection, anti-HBe will be present along with anti-HBc and anti-HBs. In those with chronic hepatitis B, anti-HBe can be used to monitor the infection and treatment.
|
|
T/F Liver biopsy is recommended before starting chronic Hep B treatment
|
True
|
|
Pharmacological treatment of chronic Hepatitis B
|
entacavir
tenofovir peg-interferon alfa (used if low HBV DNA, high ALTS and favorable genotype) |
|
Routes of transmission in Hepatitis A, B, C
|
Hep A: fecal-oral route
Hep B: blood and vertical transmission high, sexual low Hep C: blood high, vertical and sexual low |
|
Breastfeeding in Hepatitis and HIV
|
HIV: no
Hep B: if child is vaccinated Hep C: yes if viral load is low |
|
When do you start treatment of chronic Hepatitis B?
|
if HBV DNA >2000 and raised ALT
|
|
How do you treat needlestick injury of Hep B?
|
1. vaccinate
2. give HepB IgG |
|
What is the most important predictor of HCV treatment response?
|
HCV RNA genotype
genotypes 2 and 3 have best response |
|
Treatment of chronic Hepatitis C
|
interferon alfa + ribavirin
|
|
SEs of ribavirin
|
hemolytic anemia
|
|
SEs of interferon alfa
|
neutropenia
thrombocytopenia |
|
Criteria for diagnosing auto-immune hepatitis
|
1. + ANA or + smooth muscle actin Ab or + LKM or + SLA
2. IgG 3. no viral hepatitis 4. liver histology like AIH |
|
Rx of autoimmune hepatitis
|
prednisolone
if moderate - severe, add mercaptopurine or azathioprine |
|
What treatment offer HCC pts the best long term survival?
|
liver transplantation
however most HCC pts are not suitable, if cirrhosis plus solitary nodule <5 cm, or less than 3 nodules each <3 cm (Milan criteria); generally not with extrahepatic disease or vascular invasion) |
|
What blood tests will be abnormal in HCC?
|
alpha fetoprotein
ALP bilirubin |
|
What are the blood results in chronic liver disease
|
fall in platelet count <150 is the earliest finding, followed many years later with rise in INR
fall in albumin rise in bilirubin fall in glucose level (pre-terminal event) |
|
Criteria for Irritable Bowel Syndrome
|
abdo pain for at least 3 days for the last 3 months + 2 of the following:
1. pain is relieved by defecation 2. onset of pain is associated with a change in bowel frequency (either diarrhoea or constipation) 3. onset of pain is associated with a change in appearance of the stool (loose, watery or pellet-like) |
|
Rx of Irritable Bowel Syndrome
|
1. Diet change
2. Treat diarrhea and/or constipation 3. Treat abdo pain with hycosamine, mebeverine, peppermint oil 4. TCAs, such as amitriptyline |
|
Which drugs cause pseudomembranous colitis?
|
Broad spectrum antibiotics:
2nd and 3rd gen cephalosporins clindamycin |
|
Rx for Clostridium dificile
|
metronidazole - AB against anaerobes and protozoa
|
|
Rx of ascites
|
1. spironolactone (or frusemide if ineffective)
2. paracentesis (tap) 3. TIPS 4. liver transplant |
|
Ranson's criteria for acute pancreatitis (GA LAW and C HOBBS)
Predicts mortality associated with AP |
on admission:
Glucose >10 Age >55 LDH >350 AST >250 WBC >16000 After 48 hrs: Calcium <2 Hematocrit decreased by 10% PaO2 <60 mmHg Base Excess >4 BUN increased >5 Sequestered fluid >6L |
|
Rx of portal hypertension
|
1. Beta blockers
2. TIPS |
|
Serum amylase __ times higher than normal almost always indicates pancreatitis or renal disease.
|
5
increased lipase is more specific |
|
Best investigation in pancreatitis
|
CT w/ contrast
contrast seen only in viable pancreatic tissue |
|
Rx of mild acute pancreatitis
|
1. pain relief - morphine, fentanyl
2. anti-emetic - metoclopramide, prochlorperazine 3. gut rest 4. fluids |
|
Rx of severe acute pancreatitis
|
managed in ICU
1. fluids 2. NG tube 3. parenteral nutrition 4. insulin 5. calcium gluconate 6. ERCP if biliary obstruction 7. drainage surgery, but try and wait 2 weeks to allow demarcation between viable and necrotic tissue *if necrotizing, treat w ABs: piperacillin +tazobactam |
|
What is a pseudocyst?
|
cavity lined by granulation tissue, containing pancreatic secretions and communicates with pancreatic duct
|
|
Rx of pseudocyst
|
may settle spontaneously if small
surgically drain if large |
|
Are amylase and lipase raised in chronic pancreatitis?
|
no!
|
|
Ix in chronic pancreatitis
|
Bloods: raised glucose, raised ALP, possibly raised bilirubin
imaging: look for calicfications and psuedocysts in all modalities fecal fat test gold standard = secretin test, measures exocrine fxn, but |
|
Rx of chronic pancreatitis
|
1. stop alcohol
2. pancreatic enzyme supplements/restrict fat 3. opiod pain relief if severe pain 4. ESWL to fragment pancreatic calculi 5. surgery to resect pancreas |
|
Rx of H Pylori
|
PPI + clarithromycin + amoxicillin
|
|
What is the most common extra-intestinal features of IBD
|
arthritis
|
|
What symptoms are related to disease activity in IBD
|
• Arthritis: pauciarticular, asymmetric
• Erythema nodosum • Episcleritis • Osteoporosis |
|
What symptoms are NOT related to disease activity in IBD
|
• Arthritis: polyarticular, symmetric
• Uveitis • Pyoderma gangrenosum • Clubbing • Primary sclerosing cholangitis |
|
What is the most common cause of traveller's diarrhea?
|
E Coli
|
|
Which GI bugs take more than 7 days for incubation
|
amoebiasis
giardia |
|
Which GI bugs have the shortest incubation period (1-6) hrs?
|
staph aureus
bacillus cereus |
|
Which GI bugs have an incubation time of 12-48 hrs?
|
E Coli
Salmonella |
|
What is a common SE of ERCP
|
pancreatitis, 3-5% get it!
|
|
What is painless jaundice in >55 year old?
|
pancreatic cancer until proven otherwise!
|
|
What is usually elevated in primary sclerosing cholangitis?
|
ALP, hallmark lab result
|
|
Difference between primary sclerosing cholangitis and primary biliary cirrhosis
|
PBC involves intra-hepatic ducts and PSC involves extra and intrahepatic ducts
PBC likely AI, increased ALP, GGT, cholesterol, +AMA Ab, normal ERCP PSC related to IBD, elevated ALP (hallmark), +pANCA, ERCP shows narrowing |
|
Rx of acute cholescystitis (which is the same for ascending cholangitis)
|
amoxiciliin + gentamicin
if obstruction present, add metronidazole |
|
Difference between primary and secondary gallstones
|
primary: formed in bile duct, indicated bile duct pathology, eg benign biliary stricture, sclerosing cholangitis, choledochal cyst
secondary: formed in gallbladder (85% of all cases) |
|
What is the most SENSITIVE investigation for gallstones?
|
HIDA scan
|
|
What on abdo xray is pathognomonic for chronic pancreatitis?
|
calcification
|
|
4 Ss associated with esophageal cancer?
Which type of tumor is it associated with? |
smoking, seeds (betel), scalding, spirits
squamous cell carcinoma |
|
Which type of esophageal cancer does Barrett's esophagus predispose you to?
|
adenocarcinoma
|
|
Rx of Wilsons disease
|
penicillin
trientine hydrochloride tetrthiomolybdate |