Gastroenterology Flashcards
Inducing remission in Crohns disease
- Steroids (e.g Oral pred/IV hydrocortisone) - or budoneside if mild disease
- Aminosalicylates e.g Mesalazine
- Azathioprine / Mercaptopurine / Methotrexate
- Infliximab
What must be checked prior to commencing treatment with Azathioprine or Mercaptopurine
TPMT - thiopurine methyltransferase.
If a pt is deficient in this then they cannot take azathioprine or Mercaptopurine. Consider methotrexate management instead.
Maintenance of remission in Crohn disease
- Azathioprine / Mercaptopurine
- Methotrexate (if TPMT deficient)
Inducing remission in Ulcerative colitis
- Rectal mesalazine +/- oral too if required (before adding a steroid)
- Oral prednisolone
If severe disease (i.e >6 stools per day + blood. or Systemic upset Temp >37.8, HR >100bpm, Hb <105, ESR >30) = INPATIENT
1. IV hydrocortisone
2. IV cyclosporin (if steroid can’t be tolerated or if no improvement in 72hrs with just steroids)
Maintenance of remission in Ulcerative Colitis
- Mesalazine (Rectal/Oral if L side or extensive)
If severe disease (or 2+ relapses in 1yr) = Azathioprine/Mercaptopruine
Histological findings in Crohn’s disease
Non-caseating granuloma formation
Lymphoid hyperplasia
Goblet cell hyperplasia
Histological findings in Ulcerative Colitis
Crypt abscesses
Goblet cell depletion
Crypt disorganisation
Radiological findings in Crohn’s disease
Small bowel enema shows;
- Kantor’s string sign (due to strictures)
- Rose thorn ulcers
- Proximal bowel dilation
- Fistulas
Radiological findings in Ulcerative Colitis
Barium enema shows;
- Loss of haustra
- Pseudopolyps
- Drainpipe colon: narrow and short colon in chronic disease
- Leadpipe sign: loss of haustra
- Thumb-printing sign: Thickened haustra folds
Endoscopic findings in Crohn’s disease
Deep ulcers with cobblestone appearance
Endoscopic findings in Ulcerative Colitis
Widespread ulceration, preservation of deep mucosa + pseudopolyps.
Distribution differences in IBD
Crohns = skip lesions
UC = continuous lesions
Is smoking protective or causative in UC
Protective
Extra-GI manifestations of IBD
Eyes = uveitis (more in UC) + episcleritis
Enteric arthritis
Skin = erythema nodosum + pyoderma gangrenosum
Clubbing
Osteoporosis
PSC (in UC only)
Age of onset in Chron’s disease
Bimodal - 15-40yrs and 60-80yrs
Age of onset in UC
20-40yrs
Indications for protocolectomy in UC
Protocolectomy = Colon + rectum removed. Ileostomy formed.
Indications = dysplastic transformation of the colon (long standing UC inc risk of colon cancer)
Indications for sub-total colectomy in UC
Sub-total colectomy = Portion of colon removed. Rectum remains in place. Temporary ileostomy formed.
Emergency/severe UC which has failed to respond to medical therapy
Restorative/Curative surgery in UC
Panprotocolectomy with Ileo-anal J pouch
Indications for surgery in Crohn’s disease
Fistulae, Abscess formation + Strictures
What is the main complication of a small bowel resection?
Short bowel syndrome
Severe peri-anal / Rectal Crohn’s disease surgical management
Proctectomy - with ileostomy
Why can ileo-anal J pouches not be used in Crohn’s disease
It carries a high risk of fistula formation + pouch failure
Terminal ileum Crohn’s disease surgical management
limited ileocaecal resection
What is the main risk/complication following limited ileocaecal resection in Crohn’s disease
Gallstone formation- due to Impairment of hepatic bile salt recycling
Most appropriate investigation to assess disease severity and therapeutic response in a Severe UC flare up
Flexible sigmoidoscopy
- less risk of perforation and can be done in emergencies without bowel preparation.
Investigation of choice for peri-anal fistula in patients with Crohn’s disease
MRI Pelvis - allows tract to be identified and any other abscesses
Hartmann’s procedure
Removal of sigmoid colon with end colostomy as emergency procedure.
Clinical Presentation of achalasia
Dysphagia of Solids AND liquids
Heartburn / regurgitation
1st line investigation + finding for achalasia
Manometry - demonstrates increased LOS tone which does not relax on swallowing
A bird-beak appearance on barium swallow is indicative of what disease?
Achalasia
What is the 1st line management of achalasia
Pneumatic balloon
Where does a pharyngeal pouch typically develop?
In the pharynx between the thyroid cartilage and Cricoid cartilage - Killian’s dehiscence
Sx of Pharyngeal pouch
Dysphagia
Halitosis
Neck swelling + gurgles on palpation
What is boerhaave’s syndrome?
Spontaneous rupture of the oesophagus resulting from repetitive vomitting
Sudden onset chest pain + Repetitive vomitting + Subcutaneous emphysema is indicative of what condition?
Boerhaave’s syndrome
Red flag Sx (2ww referral) in a pt presenting with dyspepsia
Dysphagia
Age > 55yrs
Weight loss
Treatment resistant dyspepsia
low Hb
Raised platelets
1st line Invx for GORD
Endoscopy
Gold standard Invx for GORD / further invx when endoscopy is inconclusive
24hr oesophageal pH monitoring
Medical treatment for GORD
PPI for 1-2 months (continue on lower dose prn if useful. If no response X2 the dose for 1 month and if still no response try a H2RA or prokinetic)
1st line investigation in any presentation of dyspepsia
H.pylori - Urea breath test or Stool antigen test
Note - must discontinue PPIs 2 weeks before and Abx 4 weeks before
Triple eradication therapy for H.pylori
PPI + Amoxicillin + Clarithromycin/metronidazole for 7 days
If pen allergic = PPI + Clarithromycin + Metronidazole
What is Barrett’s oesophagus?
Premalignant metaplasia or the lower oesophagus due to chronic reflux
Stratified squamous –> Columnar
What is the cancer risk in a pt with Barrett’s oesophagus
2-5 % inc risk of developing adenocarcinoma of oesophagus
Main complications of H.pylori infection
GORD
Gastritis
Peptic ulcers
Gastric cancer
Gastric MALT (b-cell lymphoma - eradication of h.pylori usually induces remission)
Pathophysiology of peptic ulcer formation
1) Loss of protective layer (due to meds e.g NSAIDs which inhibit COX-1 therefore inhibit prostaglandin synthesis)
2) Increased acid secreation
Differentiation in symptoms between Gastric and Duodenal ulcers
Gastric ulcers = pain worse after eating
Duodenal ulcers = pain relieved by eating
Diagnostic investigation for Peptic ulcer disease
H.pylori should be ruled out 1st line, then do an
Endoscopy = diagnostic +/- Rapid urease test/biopsy
Management for Peptic ulcer (-ve H.pylori)
PPIs until the ulcer is healed
Causes of Upper GI bleed
Mallory-weiss tears
Oesophageal cancer
Esophagitis
Oesophageal varices
Gastric ulcer
Gastric cancer
Dieluafoy lesion
Diffuse erosive gastritis
Duodenal ulcer
Aortic-enteric fistula
Diverticular disease
Scoring systems in upper GI bleed
1) Glasgow-blatchford score: based on clinical findings to determine risk of GI bleed. Points for Rise in urea, drop in Hb/SBP/Pulse. Melena, syncope, hepatic disease, cardiac failure
2) Rockall score = based on endoscopic findings and determines risk of re-bleed.
Acute management of GI bleed caused by Oesophageal varices
IV terlipressin + Abx
Definitive treatment of oesophageal varices
Band ligation or TPSS
Acute management of upper GI bleed caused by a bleeding ulcer?
Adrenaline +/- Endoscopic clipping
Causes of Lower GI bleeding
Colitis
Diverticular disease
Cancer
Haemorrhoids
Angiodysplasia
Indications for surgery in acute lower GI bleed
Age >60yrs
Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known CVD / Hypotension
Most common type of oesophageal cancer in UK
Adenocarcinoma
RF for oesophageal adenocarcinoma
GORD
Barrett’s
Smoking
Achalasia
Obesity
2ww referral for suspected oeseophageal cancer
New or changed dysphagia (any age)
Age >55 with weight loss + abdominal pain/reflux/dyspepsia
Diagnostic imvx for oesophageal cancer
Endoscopy + biopsy
Best imvx for TNM staging in oeseophageal cancer
CT TAP
Management of oesophageal cancer
Ivor-lewis type oesophagectomy + adjuvant chemo
Histology of gastric cancer
Signet ring cells - large vacuole of mucin displacing nucleus
Which lymph nodes are typically involved in gastric cancer
Virchow’s nodes - supraclavicular
sometimes sister may Jospeh nodes = periumbilical nodes
Surgical management choices in gastric cancer
Subtotal gastrectomy if cancer 5-10cm away from OGJ
Total gastrectomy if cancer <5cm from OGJ
Skin changes associated with coeliac disease
Dermatitis herpatiformis
Genetic associations to Coeliac disease
HLA-DQ2 & HLA-DQ8
Investigations for Coeliac disease
1) Total IgA - as if deficient can cause false -ve’s in the next two tests
2) Anti-TTG
3) Anti-endomysial antibodies
Why are coeliac patients considered immunocompromised
Functional Hyposplenism
Which cancer is associated with coeliac disease
Enteropathy-associated T cell lymphoma of intestines (EATL)
NICE diagnostic criteria for IBS
Abdominal pain
Bloating
Change in bowel habit (>6 months)
+ 2 of;
> abnormal stool passage (loose/constipated)
> Bloating
> Worsening sx after eating
> PR mucus
Medical management in IBS
Loperamide (if diarrhoea)
Laxatives (if constipation - avoid lactulose)
Hyoscine butyl bromide (for pain)
Risk Factors for Colorectal carcinoma
Fhx
FAP
HNPCC
IBD
Old age
Diet high in red meat / low in fibre
Obesity
Smoking
Alcohol
Familial adenomatous polyposis
Autosomal dominant mutation to the APC gene
results in 100’s of polyps in colon
Typically leads to cancer <40 yrs
pts require prophylactic panprotocolectomy
Lynch syndrome
-> Hereditary non-polyposis colorectal cancer
Autosomal dominant mutation to DNA mismatch repair genes / MHS2 gene /MLH1
Causes multiple undifferentiated tumours in proximal colon
also inc risk of endometrial/ovarian/prostate cancer
Gold standard investigation for colon canceer
Colonoscopy + biopsy
2ww referral criteria for colon cancer
+ve Faecal occult blood test
Age <50yrs with rectal bleeding + abdominal pain/change in bowel habit/weight loss/anemia
Age > 40yrs + unexplained weight loss + abdominal pain
Age > 50yrs + unexplained rectal bleeding
Age >60 yrs + iron deficiency anaemia/change in bowel habit
Anal fissures NOT in midline/posterior
What is the tumour marker in Colon cancer
CEA - Carcinoembryonic antigen
Ileostomy
opening of the small intestine. Usually located in the RIF.
Has a sprouted appearance
Output will be liquid
Colostomy
Opening of the colon
Location varies - more likely to be on L side of abdomen
Flushed appearance
Output will be solid
Risk factors for ischemic bowel disease
AF
Endocarditis
malignancy
Old age
Smoking
IBS
HTN
Cocaine use
Clinical Presentation of Acute mesenteric ischemia
Sudden severe abode pain which is out of keeping with physical examination findings.
Pt typically has AF
Thumb-printing sign on Abdo X-ray is indicative of what?
Ischemic colitis
Causes of Acute pancreatitis
idiopathic
Gallstones
Ethanol
Trauma
Scorpion sting
Mumps / malignancy
Autoimmune - SLE / Sjogrens
Steroids
Hyperlipidemia / Hypercalcemia / Hypothermia
ERCP
Drugs - azathioprine, furosemide + thiazide diuretics + Mesalazine
Indications of Severe disease in pancreatitis
Pa02 <8 kPa
Age > 55yrs
Neutrophils (wbc>15)
Calcium <2
Urea > 16
Enzymes (LDH >600 or AST/ALT >2000)
Albumin <32
Sugar (hyperglycaemia)
Cullens sign
Periumbilical discolouration
- can be seen in trauma (bleeding) or in pancreatitis
Turner’s sign
Flank discolouration
- can be seen in trauma or pancreatitis
Investigations for Acute pancreatitis
Bloods - FBC, U&E, LFT, calcium - for assessing severity
ABG
Amylase - will be 3x the norm. must be done <24hrs
Lipase - better test. Will be raised. Should be done >24hrs
Liver USS - to assess for presence of gallstones
CT abdomen - if you suspect any complications.
Complications of Acute Pancreatitis
Pancreatic fluid collection
Pseudocysts - 4 weeks after
Pancreatic abscess
Pancreatic necrosis
Haemorrhage
ARDS
1st line invx for chronic pancreatitis
Imaging (USS / CT/ Xray) = calcification
2nd line = Faecal elastase (if low it indicates exocrine insufficiency) can be done if imaging is inconclusive
Pancreatic enzyme replacement
Creon
Clinical presentation of Pancreatic cancer
Painless obstructive jaundice!!!!
-> yellow skin/sclera + dark urine + pale stools + pruritus
Palpable gallbladder
Rapid onset diabetes / worsening glycemic control
change in bowel habit
back pain
Courvoisiers law
Painless palpable gallbladder + jaundice = unlikely to be gall stones (pancreatic or cholangiocarcinoma more likely)
Trousseau’s sign
Migratory thrombophlebitis is indicated of pancreatic carcinoma
Diagnostic investigation for Pancreatic cancer
High-resolution CT TAP - may show a double-duct sign
Tumour marker in pancreatic cancer
CA19-9
Whipple’s procedure
radical pancreaticoduodenectomy = removal of head of pancreas + pylorus of stomach + duodenum + gallbladder + bile duct + lymph nodes
Which antibiotics cause C.Diff?
Cephalosporins e.g cefotaxime / cefaclor (most common)
Clindamycin
Ciprofloxacin / quinolones
Co-amoxiclav + penicillins
Treatment of C.diff
1st line = oral vancomycin
2nd line = oral Findoxomicin
Treatment of C.diff reinfection (recurrence)
If within 12 weeks of first = Findaxomicin
If > 12 weeks after first = Vancomycin
Treatment of life-threatening C.diff infection
high-dose vancomycin + IV metronidazole
Risk factors for small bowel overgrowth syndrome
Scleroderma
Structural abnormalities of GI tract e.g stricutes/diverticular
Altered motility e.g gastroporesis, surgery, radiation, pancreatitis etc
Medications - PPIs / antibiotics
Characteristic presentation of small bowel overgrowth syndrome
Intermittent loose stools + bloating, unrelated to type of food. Symptoms relieved by antibiotics
Diagnosis of small bowel overgrowth syndrome
hydrogen breath testing
Globus phyangis
Sensation of having a ‘lump in throat’ at all times. typically pain is worse when swallowing saliva and often relieved by food.
Gastric cancer and colorectal cancer can often present in a similar way (i.e abdominal discomfort and anaemia due to bleeding) but what simple blood test can differentiate the two.
Urea - if this is raised then gastric cancer is more likely.
- also - the blood is more likely to be melena as its coming from higher up whereas colorectal cancer is more often fresher blood
which area is most likely to be affected in ischemic colitis
Splenic flexure
Management of severe alcoholic hepatitis
Steroidss
Best investigation for pharyngeal pouch
Barium swallow + fluoroscopy
Prehepatic jaundice: Causes and Features
Haemolytic anemia
Sickle-cell anemia
Spherocytosis
Drugs - antibiotics + antiepileptics
Gilbert’s syndrome
Features = Unconjugated hyperbilirubinemia. Normal LFTs. Normal urine + Stool
Intra-hepatic jaundice: causes + features
Causes = Hepatocyte dysfunction, liver cirrhosis + most liver diseases e.g hep B, alcoholism, Wilson’s disease.
Features = mixed bilirubinema. Dark urine, normal stools.
Hepatic LFT picture = V high ALT/AST + mildly raised ALP
Post hepatic jaundice causes + features
Causes = Gallstones / Pancreatic cancer / Cholangiocarcinoma / Pancreatitis / Parasitic infection
Features = Conjugated bilirubinemia.
Obstructive LFTs = V high ALP, mildly raised ALT/AST. Dark urine & Pale stools
1st line investigation in pt presenting with jaundice
USS liver + Biliary tree
Cholestasis
Blockage to the flow of bile
Can be triggered by the COCP or Co-amoxiclav
Typical presentation of gallstones induced cholestasis
Severe biliary colic (RUQ) typically triggered by fatty meals.
Pt is often female + Fat + Fair + Forty + Fertile
Which type of IBD is a risk factor for gallstones
Crohn’s disease
Best investigations to find gallstones
USS + MRCP
Management of gallstones
no management if asymptomatic
Stones <5mm can be left
ERCP if stones are located in the bile duct
Acute Cholecystitis Clinical Features
= Inflammation of the gall bladder due to impaired drainage.
RUQ pain
Boa’s sign = Hyperaesthesia of R shoulder
Murphy’s sign
N&V
Tachycardia
Management of acute cholecystitis
NBM + IV fluids + Abs + NG tube (if vomitting)
Definitive management = cholecystectomy within 72hours.
Acute Cholangitis presentation
Charcot’s triad;
RUQ pain
Fever
Obstructive jaundice
+/- Confusion + hypotension (Reynolds pentad)
1st line investigation for Cholangitis
USS
Definitive management of cholangitis
ERCP cholangiopancreatography after 24-48hrs
(during this can do sphincterectomy, balloon dilation, stunting etc to relieve the bile duct)
If AST > ALT what does this indicate
Alcoholic liver disease
(ALT is normally higher than AST)
What causes a rise in ALP?
ALP is found in liver, biliary system and bone.
Liver disease
Bone disease
Renal disease
Lymphoma
Myeloma
Pregnancy
***Isolated ALP rise often indicates bony mets or vit D deficiency
Non hepatic causes of raised GGT
COPD
Renal failure
Post MI
Non invasive liver screen
USS liver
Hep B & C serology
Immunoglobulins
Ceruloplasmin
A1AT
Ferritin
Transferrin
Autoantibodies
Investigations to assess degree of liver fibrosis
Liver fibrosis blood test (HA + HIINP + TIMP1)
NAFLD fibrosis score
Fibroscan (transient elastography USS)
Medical management of NAFLD
Vit E
Pioglitazone
transplant
Gold standard investigation for alcoholic liver disease
Liver biopsy
*** this is required prior to steroid treatment
Autoimmune hepatitis Type 1
Women aged 40-50yrs
Sx = Fatigue + Features of liver disease (less acute presentation than T2)
Imvx = ANA + anti-smooth muscle antibody
Autoimmune hepatitis Type 2
Occurs in teens/early 20’s
Sx = acute hepatitis + jaundice
Invx = Anti-LKM1 antibodies
Which hepatitis is commonly caused through eating poorly cooked seafood
Hep A
Which hepatitis is common following a BBQ or eating pork
Hep E
Viral markers of active Hep B infection
HBsAG
HBcAB IgM
HbeAg = raised during replication
how to differentiate between acute or chronic hepatitis B
IgM high titre = acute, Low titre = chronic
Marker of Hep B immunity
HbcAb = past infection
HBsSb = Vaccination/previous infection
Complications of Hep B / Hep C
Liver cirrhosis
Hepatocellular carcinoma
Sjogren’s syndrome
Membranoproliferative GN
Drugs causing chronic liver disease
Think SAM
Sodium valporate
Amiodarone
Methotrexate
Tumor marker for hepatocellular carcinoma
Alpha fetoprotein
Liver USS findings in chronic liver disease
Corkscrew appearance to hepatic arteries
Enlarged portal vein
Ascites
Splenomegaly
Scoring systems for cirrhosis
Child-pugh score
MELD score
Prophylactic Abx for ascitic patients
Ciprofloxacin
What must you give to a patient undergoing ascitic tap/paracentesis
IV Human albumin
Management of Spontaneous bacterial peritonitis
IV cefotaxime (cephalosporin)
Management of hepatorenal syndrome
Desmopressin + IV albumin + TIPSS
Features of cholangiocarcinoma
Cancer symptoms + Painless jaundice + Palpable gallbladder + hepatomegaly
Pt may have PSC or a history of liver flukes
Cholangiocarcinoma tumor marker
CA 19-9
Carcinoid tumour presentation
Flushing + Diarrhoea + Bronchospasm + Hypotension
What is Wilson’ disease
An autosomal recessive condition resulting in copper accumulation in tissues due to inc absorption + decreased excretion
What mutation causes Wilson’s disease
ATP7B mutation on chromosome 13
Clinical Presentation of Wilson’s disease
Typically age 10-25yrs
Kayser-fleischer rings
Hepatic symptoms (hepatitis/cirrhosis)
Neurological symptoms - concentratio problems, dysarthria, dystonia, psychosis
Renal tubular acidosis
Wilson’s disease investigations
Serum Ceruloplasmic + Total serum copper = low
Gold standard = Liver biopsy
24hr urine copper assay = elevated
MRI brain to look for copper deposits
Management of Wilsons disease
Copper chelation - Penecilliamine 1st line
Trientene 2nd line
What is Gilberts disease
Autosomal recessive condition causing an unconjugated hyperbilirubinemia (due to decreased UDP glucoronsyltransferase)
Clinical Presentation of Gilberts syndrome
Jaundice typically following illness/hangover/exercise/fasting
Investigation = rise in bilirubin levels after a period of fasting or IV nicotinic acid
What is hereditary haemochromatosis
Autosomal recessive condition due to a mutation of the human haemochromatosis gene on chromosome 6.
Resulting in increased iron levels and deposition in tissue
Clinical Presentation of Hereditary haemochromatosis
Typical onset age 40
Bronze skin pigmentation, erectile dysfunction, fatigue
Chrondrocalcinosis
Mood/memory disturbance
Liver disease –> cirrhosis –> hepatocellular carcinoma
T1DM/Hypogonadism/Hypothyroidism
Dilated cardiomyopathy
Investigation findings in hereditary haemochromatosis
High Ferritin
High Transferrin
Low TIBC
Biopsy reveals Perl’s stain due to iron deposition
CT abdo = inc attenuation of the liver
Management of heriditary haemochromatosis
Weekly venesection.
Aim for transferrin/ferritin <50%
What would a liver biopsy show in A1AT deficiency
Acid schiff +ve staining
Primary Biliary Cholangitis
Chronic autoimmune destruction of the small bile ducts resulting in cholestasis + Fibrosis + Cirrhosis
Risk Factors for PBC
Middle aged women
RA / Systemic sclerosis / Sjogren’s syndrome
Autoimmune disease e.g thyroid/coeliac disease
Autoantibodies in PBC
Anti-mitochondrial antibodies
IgM
Complications of PBC
20x increased risk of hepatocellular carcinoma
Cirrhosis + Osteomalacia + Osteoporosis +
Primary sclerosing cholangitis
Stricture + fibrosis of bile ducts resulting in cholestasis + cholangitis.
Risk Factors for PSC
Male
Aged 30-40
Ulcerative colitis
Autoantibodies in PSC
P-ANCA
ANA
Anti-cardiolipin
Gold standard investigation for PSC
MRCP
Complications of PSC
Acute cholangitis
Cholangiocarcinoma
Colon cancer
Cirrhosis
Budd Chiari syndrome
= Hepatic vein thrombosis
usually seen with underlying haematological condition (e.g polycythemia) other procoagulant conditions (like thrombophilias) or associated with the COCP use
Presents with;
* Sudden onset severe abdo pain
* Ascites (SAAG >11)
* Tender hepatomegaly