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Medicine, Year 3, GI and Surgery > GI Flashcards > Flashcards

GI Flashcards

1
Q

ACUTE ABDOMEN

  1. What are causes of RUQ pain?
  2. What are causes of Epigastric pain?
  3. What are causes of LIF pain?
  4. What are causes of RIF pain?
  5. What are causes of flank pain?
  6. What are causes of umbilical pain?
  7. What are causes of suprapubic pain?
A
  1. Biliary colic, acute cholecystitis, acute cholangitis
  2. Pancreatitis, AAA, Peptic Ulcer Disease
  3. Diverticulitis, Ectopic pregnancy, Ovarian cyst
  4. Appendicitis, Ectopic pregnancy, Ovarian cyst, Meckel’s diverticulitis
  5. Renal colic, pyelonephritis, AAA (loin to groin)
  6. AAA, Intestinal obstruction, ischaemic colitis
  7. Urinary retention, PID
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2
Q

BILIARY COLIC

  1. What is it?
  2. What are the features of Biliary Colic?
  3. What are the risk factors of Biliary Colic?
  4. If a patient develops jaundice following a cholecystectomy for biliary colic, what has happened?
A
  1. When a gallstone passes through the biliary tree
  2. RUQ, worsened by eating fatty foods, may radiate to shoulder
  3. Fair, female, fat, forty, DM, Crohn’s Disease, COCP, rapid weight loss
  4. May have had a gallstone in CBD, has developed obstructive jaundice
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3
Q

ACUTE CHOLECYSTITIS

  1. What is it?
  2. What is it MAINLY caused by?
  3. What are other causes?
  4. What are the features of Acute Cholecystitis?
  5. Are LFTs normal in Acute Cholecystitis?
  6. What is the first-line investigation for Acute Cholecystitis?
  7. What is the management of Acute Cholecystitis?
  8. What is Murphy’s sign?
A
  1. Inflammation and infection of the gallbladder
  2. 90% are due to gallstones
  3. 10% are acalculous, more seen in hospitalised patients and those severely unwell. Also seen in immunocompromised patients
  4. RUQ, may radiate to shoulder. Fever. Positive Murphy’s sign
  5. Yes they are. If LFTs abnormal, consider Mirizzi’s syndrome
  6. Abdo US
  7. IV ABX, Lap chole within 1 week
  8. Arrest of breathing on gallbladder palpation
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4
Q

ASCENDING CHOLANGITIS

  1. What is it?
  2. What is it MAINLY caused by?
  3. What are the main features?
  4. What is Reynold’s pentad?
  5. What is the management?
A
  1. An infection of the BILIARY TREE
  2. E.Coli
  3. Charcot’s triad: Fever, RUQ, Jaundice
  4. Fever, RUQ, Jaundice + Hypotension/Bradycardia + Confusion
  5. IV ABX, Plus ERCP within 24-48 hours to relieve obstruction
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5
Q

APPENDICITIS

  1. In what patients does it commonly present?
  2. What are the clinical features?
  3. What may be seen on examination?
  4. What are some investigations to help diagnose it?
  5. What are some important differentials?
  6. What is the management?
A
  1. Young patients aged 10-20 years old
  2. Mild fever, peri-umbilical pain with radiation / migration
    to RIF. Some episodes of vomiting, anorexia, mild fever
  3. Generalised peritonitis, Rovsing positive, on DRE boggy sensation for pelvic abscess, Tenderness at McBurney’s point
  4. High CRP, Neutrophilia, Urine dip positive for leukocytes, negative for nitrites, Ultrasound - may see free fluid
  5. Ectopic pregnancy, ovarian cyst with torsion / rupture, Meckel’s diverticulitis, Mesenteric adenitis
  6. Prophylactic ABX, followed by Laparoscopic appendicectomy
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6
Q

MECKEL’S DIVERTICULUM

  1. What is it?
  2. What are the features?
  3. What are the rules of 2’s?
A
  1. A congenital diverticulum of the small intestine
  2. Abdominal pain, mimicking appendicitis. Painless rectal bleeding and intestinal obstruction
  3. 2% of the population, 2 feet from ileocaecal valve, 2 inches long, present before the age of 2, has 2 types of epithelial tissue (gastric and pancreatic)
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7
Q

PRIMARY SCLEROSING CHOLANGITIS

  1. What is it?
  2. What are the risk factors?
  3. What are the main features?
  4. What do the LFTs look like?
  5. What is the gold-standard imaging test? What is seen?
  6. What antibody is associated with it?
  7. What are some complications of PSC?
A
  1. A condition where the intra and extrahepatic ducts become strictured and fibrotic, causing an obstructive pattern preventing bile from leaving the liver leading to inflammation
  2. Ulcerative Colitis, less so Crohn’s Disease, HIV, family history, male, age 20-40
  3. Jaundice, RUQ, Hepatosplenomegaly, fatigue, pruritis / exocoriations, cirrhosis
  4. Elevated ALP and Bilirubin “cholestatic picture”
  5. MRCP > ERCP. Beaded appearance of intrahepatic and extrahepatic ducts
  6. pANCA
  7. Cholangiocarcinoma and colorectal cancer
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8
Q

PRIMARY BILIARY CIRRHOSIS / CHOLANGITIS

  1. What is it?
  2. What are the risk factors?
  3. What are the main features?
  4. What do the LFTs look like?
  5. What antibody is associated with it?
  6. What immunoglobulin is it associated with?
  7. What is FIRST-LINE management? MoA?
  8. What are other aspects of management?
A
  1. An autoimmune condition attacking the small ducts of the liver, causing obstruction of bile acids, billirubin, cholesterol
  2. Female, Sjorgren’s, RA, Thyroid disease, Systemic Sclerosis
  3. Being female, jaundice, pruritus / excoriations, hyperpigmented pressure points, xanthalesma, pale stools, cirrhosis, fatigue
  4. Elevated ALP and Billirubin “cholestatic picture”
  5. AMA
  6. IgM
  7. URSODEOXYCHOLIC ACID, reduces cholesterol absorption
  8. Liver transplantation, cholestyramine
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9
Q

HAEMOCHROMATOSIS

  1. What is it?
  2. What gene is mutated, on what chromosome?
  3. What is the inheritance pattern?
  4. What are some of the features?
  5. Why are women affected later than men?
  6. What is the ferritin, transferrin saturation and TIBC?
  7. What may be some other investigations?
  8. What is seen on CXR?
  9. What is first-line management?
  10. What is second-line management?
A
  1. An iron storage disorder of raised total body iron and deposition in tissues
  2. HFE gene, chromosome 6
  3. Autosomal recessive
  4. Bronze skin, hair loss, memory loss, mood disturbances, chronic tiredness, hypothyroidism, T2D, dilated cardiomyopathy, chronic liver disease, erectile dysfunction, amenorrhoea, arthralgia, arthritis
  5. Due to menstruation reducing iron overload regularly
  6. Raised ferritin, raised transferrin saturations, reduced TIBC
  7. Genetic testing for HFE, Liver biopsy with Perl’s stain, CT abdo / MRI
  8. Chondrocalcinosis
  9. Venesection
  10. Desferrioxamine
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10
Q

WILSON’S DISEASE

  1. What is it?
  2. What is the inheritance pattern?
  3. What are some of the features?
  4. What may investigations show?
  5. What is the management?
A
  1. Characterised by excess Cu deposition in body and tissues
  2. Autosomal recessive
  3. Kayser-Flescher rings, psychiatric issues, liver issues (cirrhosis, hepatitis), neurological issues (dementia, parkinsons)
  4. Reduced total serum copper, reduced serum caeruloplasmin, increased 24 hour copper excretion
  5. Penicillamine
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11
Q

NON-ALCOHOLIC FATTY LIVER DISEASE

  1. What is it?
  2. What are the different stages of NAFLD?
  3. What are the risk factors?
  4. What are the features?
  5. What is the first-line investigation?
  6. What is the management?
A
  1. The hepatic manifestation of the metabolic syndrome
  2. NAFLD, then NASH, then Fibrosis, then Cirrhosis
  3. Obesity, poor diet, low activity, T2D, hypercholesterolaemia, middle age and above, smoking, HTN, sudden weight loss or starvation
  4. Usually asymptomatic, may have hepatomegaly. May have ALT > AST, and increased echogenicity of liver
  5. ELF (Enhanced Liver Fibrosis) test
  6. Lifestyle changes i.e. weight loss, stop smoking, exercise. Monitoring the disease
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12
Q

GASTRO-OESOPHAGEAL REFLUX DISEASE

  1. What is it?
  2. What is the cell type of the Oesophagus and stomach?
  3. What are the presenting features?
  4. When might you refer a patient for Endoscopy urgently within 2 weeks?
  5. When might you refer a patient for Endoscopy non-urgently?
  6. If patients with dyspepsia do not meet criteria for Endoscopy, what are treatment options?
  7. If a patient has confirmed GORD on Endoscopy, what is the treatment?
  8. If a patient has no confirmed GORD on Endoscopy but has dyspepsia symptoms, what is the treatment?
  9. State the tests which can be formed for initial investigation of H pylori?
  10. What is the test of cure following H Pylori therapy? When would you do it?
  11. Outline the Urea Breath test?
  12. What things may interact with Urea Breath test?
  13. What type of bacteria is H.pylori?
  14. Outline the Rapid Urease test (CLO) test?
  15. What is the eradication therapy for H.pylori?
  16. What is the eradication therapy for H.pylori if penicillin allergic?
  17. What is a rare side-effect of PPI?
A
  1. Refers to when acid from stomach refluxes through the lower esophageal sphincter and irritates the lining of the oesophagus
  2. Oesophagus - stratified squamous. Stomach - Columnar
  3. Heart-burn, acid reflux, retrosternal / epigastric pain, nocturnal cough, hoarse voice
  4. Dysphagia, age over 55 years old, weight loss, upper abdominal pain / reflux
  5. Haematemesis, treatment resistant dyspepsia, nausea and vomiting, low Hb, raised platelets
  6. Full dose 1 month PPI or “test and treat” for H. Pylori
  7. 1-2 months of PPI, if response then continue on low dose. If no response consider double dose
  8. 1 month of PPI, if response then consider low dose PRN. If no response, consider prokinetic or H2RA for a month
  9. 13-Urea breath test, or stool antigen test
  10. 13-Urea breath test, ONLY if they still have symptoms
  11. Patient consumes a drink of 13-C urea, after 30mins will exhale into a glass tube
  12. PPIs and Antibacterial drugs, hence must be off PPI for 2 weeks or antibacterial for 4 weeks
  13. Gram negative, aerobic bacteria
  14. Performed during endoscopy. Biopsy is mixed with pH indicator and urea. Colour change = positive result
  15. PPI + Amoxicillin + Clarithromycin / Metronidazole
  16. PPI + Clarithromqycin + Metronidazole
  17. Hypomagnesemia - causing muscle aches
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13
Q

PEPTIC ULCER DISEASE

  1. What are some risk factors of Peptic Ulcer Disease?
  2. What are the general features?
  3. What is the pain for a Duodenal Ulcer?
  4. What is the pain for a Gastric Ulcer?
  5. What are the investigations?
  6. If patient is positive or negative for H. Pylori, what is the management?
A
  1. H. Pylori, NSAIDs, SSRIs, steroids, bisphosphonates, Zollinger-Ellison syndrome
  2. Epigastric pain, nausea
  3. Improved by eating
  4. Worsened by eating
  5. Test for H. Pylori, i.e. 13-C Urea breath test, stool antigen
  6. If positive, triple eradication therapy. If negative, PPI to allow ulcer to heal
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14
Q

BARRET’S OESOPHAGUS

  1. What is it?
  2. What are risk factors?
  3. What is the management?
A
  1. Transformation of stratified squamous epithelium to columnar epithelium in the oesophagus
  2. GORD, smoking, male, obesity
  3. Endoscopic surveillance, if metaplasia do this every 3-5 years. If dysplasia, consider resection and ablation. High dose PPI
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15
Q

BUDD-CHIARI SYNDROME

  1. What is it?
  2. What are the features?
  3. What are risk factors?
  4. What is the main-stay investigation?
A
  1. Hepatic vein thrombosis
  2. Sudden onset abdo pain, ascites, hepatomegaly
  3. COCP, procoagulant conditions i.e. Antiphospholipid syndrome, pregnancy
  4. US with Doppler flow studies
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16
Q

OESOPHAGEAL CANCER

  1. What is the most common cause in the UK? Where is it particularly found?
  2. What is the most common cause in the developing world? Where is it particularly found?
  3. What are the features?
  4. What are the main-stay investigations?
  5. What is the management?
A
  1. Adenocarcinoma, lower 1/3rd of oesophagus
  2. Squamous cell carcinoma, upper 2/3rd of oesophagus
  3. Dysphagia, weight loss, nausea, vomiting, cough, melena, change in voice
  4. Upper GI endoscopy, staging CT for chest, abdo, pelvis
  5. Ivor Lewis Oesophagectomy
17
Q

UPPER GI BLEEDING

  1. What are some causes of an Upper GI Bleed?
  2. What scoring criteria is used for a patient who has been admitted for an Upper GI Bleed? What score is significant?
  3. What scoring criteria is used for a patient who has just had an endoscopy to monitor their risk of re-bleeding?
  4. Features of an Upper GI Bleed?
  5. How would you management a patient with an Upper GI Bleed?
  6. For patients with a variceal bleed, what can they be given for treatment and also for prophylaxis?
  7. How do you manage an OESOPHAGEAL variceal bleed?
  8. How do you manage a GASTRIC variceal bleed?
A
  1. Variceal bleed, mallory weiss tear, Dieulafoy’s lesion, stomach and duodenal ulcers, stomach and duodenal cancer
  2. Glasgow Blatchford Score - anything greater than zero
  3. Rockall Score
  4. Haematemesis, melena, epigastric pain, sudden collapse, coffee ground vomit, haemodynamic instability
  5. ABATED mnemonic
    A - ABCDE approach
    B - Bloods: FBC, U&E, LFT, Cross Match, Group & Save, Clotting
    A - Access, IV, two wide-bore cannulas
    T - Transfuse the patient 2 units of blood
    E - Endoscopy within 24 hours, or immediately if unstable
    D - Drugs, stop NSAIDs, anticoagulants
  6. Terlipressin to stop the bleed and IV ABX, and Propranolol for prophylaxis
  7. Banding -> Sengstaken tube -> TIPS
  8. Cyanoacrylate injection -> Sengstaken tube -> TIPS
18
Q

ACUTE PANCREATITIS

  1. What is it?
  2. What are some causes of Acute Pancreatitis?
  3. What are the features of Acute Pancreatitis?
  4. What is Grey Turner’s sign?
  5. What is Cullen’s sign?
  6. What is a rare feature of Acute Pancreatitis?
  7. What are some investigations to help diagnose Pancreatitis?
  8. What are 3 scoring systems to help determine severity of Pancreatitis?
  9. Discuss the points of the most commonly used severity scoring system?
  10. What is defined as mild, moderate and severe Acute Pancreatitis?
  11. When should you consider admission to ICU in a patient with Acute Pancreatitis?
  12. What are some complications of Acute Pancreatitis?
  13. What are the general principles of management in such patients?
  14. Is Amylase a good prognostic indicator for severity of Amylase?
A
  1. Autodigestion of pancreatic tissue by pancreatic enzymes, leading to necrosis
  2. I GET SMASHED: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune / Ascaris Infection, Scorpion sting, Hypertriglyceridaemia / Hypercalcaemia / Hypothermia, ERCP, Drugs: Sodium Valproate, Bendroflumethiazide, Furosemide, Azathioprine, Mesalazine
  3. Epigastric pain, may radiate to back. Nausea, vomiting, low grade fever, Grey-Turner’s, Cullen’s, ischaemic retinopathy (rare)
  4. Bruising of flanks
  5. Bruising around umbillicus
  6. Ischaemic retinopathy
  7. Amylase, Lipase, Abdo US, CT Abdo, U&Es, LFTs
  8. Glasgow Score, Ransom Score, APACHE II
9. Glasgow Score
P - PaO2 < 60
A - Age >55
N - Neutrophils >15
C - Calcium <2
R - uRea >16
E - Enzymes LDH >600, AST/ALT >200
A - Albumin <32
S - Sugar / Glucose >10
  1. Below 2 = Mild, 2 = Moderate, Above 2 = Severe
  2. Glasgow Score above 1
  3. ARDS, Pancreatic necrosis, Chronic pancreatitis, Pancreatic pseudocysts, Pancreatic abscess
  4. Escalate care according to Glasgow Score, fluid resuscitation with IV crystalloids, analgesia with IV opioids, IV antibiotics if infective, enteral nutrition if vomiting / severe pancreatitis, endoscopic drainage of cysts, surgery to remove necrotic tissue
  5. NO
19
Q

CHRONIC PANCREATITIS

  1. What is the most common cause in 80% of cases?
  2. What are the 3 main features?
  3. What are some investigations?
  4. What is the screening performed for patients?
  5. What is the management?
A
  1. Alcohol
  2. Pain, worsened 15-30 mins after eating a meal, steatorrhoea, diabetes mellitus later on
  3. AXR, CT, will show pancreatic calcification. Faecal elastase for pancreatic exocrine insufficiency
  4. Pancreatic enzyme supplementation, and pain relief
20
Q

BOWEL ISCHAEMIA

  1. What are some risk factors of Bowel Ischaemia?
  2. What are features of Bowel Ischaemia?
  3. Where does Mesenteric Ischaemia affect?
  4. Where does Ischaemic Colitis affect?
  5. What is Mesenteric Ischaemia caused by?
  6. What is the management of Mesenteric Ischaemia?
  7. What is the management of Ischaemic Colitis?
  8. What is thumb-printing associated with?
  9. What are some investigations?
A
  1. AF, HTN, smoking, diabetes, age
  2. Abdominal pain, rectal bleeding, fever, diarrhoea
  3. Small bowel
  4. Large bowel
  5. An embolism in the artery supplying small bowel i.e. superior mesenteric artery
  6. Urgent surgery
  7. Conservative management
  8. Ischaemic Colitis
  9. FBC: Neutrophilia, CRP: Inflammation, ABG: Lactic acidosis, CT: Thumb-printing
21
Q

PANCREATIC CANCER

  1. What is the most common type of Pancreatic cancer?
  2. What are some risk factors of Pancreatic cancer?
  3. What is Courvoisier’s sign?
  4. Features of Pancreatic cancer?
  5. What is Trousseau’s sign of malignancy?
  6. What tumour marker is associated with Pancreatic cancer?
  7. Investigations for Pancreatic cancer?
  8. Management for Pancreatic cancer?
A
  1. Adenocarcinoma
  2. Age, smoking, diabetes, chronic pancreatitis, alcohol, MEN, BRCA2, HNPCC
  3. Painless jaundice + palpable gallbladder = unlikely to be gallstones
  4. Painless jaundice, dark urine, pale stools, pruritus, anorexia, weight loss, epigastric pain, steatorrhoea, diabetes
  5. Migratory thrombophlebitis, associated with pancreatic cancer
  6. CA19-9
  7. US Abdo, CT abdo “double-duct” sign, CA19-9 may be elevated. LFTs may show a cholestatic picture of elevated ALP and bilirubin
  8. Whipple’s procedure, chemotherapy, ERCP with stenting (palliative)
22
Q

CHOLANGIOCARCINOMA

  1. What is it?
  2. What is the main risk factor?
  3. What are the features?
  4. Where the two nodes found in Cholangiocarcinoma?
A
  1. Bile duct cancer
  2. Primary sclerosing cholangitis
  3. Persistent biliary colic, loss of appetite, jaundice, palpable mass in RUQ (Courvoisier’s sign), Sister mary joseph’s nodes and Virchow’s codes
  4. Sister mary joseph’s nodes = umbilical, Virchow’s = left supraclavicular
23
Q

COMMON BILE DUCT STONE

  1. What are features of a CBD stone?
A
  1. RUQ pain, jaundice. NO FEVER
24
Q

DIVERTICULITIS

  1. What is it?
  2. What are the risk factors?
  3. What features of Diverticular disease?
  4. What are features of Diverticulitis?
  5. What are some investigations and results?
  6. What is the management?
    7, What happens if patients do not respond to management?
  7. What investigation is contraindicated?
A
  1. Inflammation of the diverticulum; an outpouching of the intestinal mucosa
  2. Old age, lack of fibre, obesity (especially in young patients), sedentary lifestyle, smoking, NSAIDs
  3. Chronic history of LLQ pain, bloating and diarrhoea / constipation
  4. Severe LLQ abdominal pain, nausea and vomiting, constipation / diarrhoea, urinary frequency / urgency / dysuria, PR bleeding
  5. FBC will show increased WBC count, CRP will be high due to inflammation, erect CXR will show pneumoperitoneum for perforation, AXR may show dilated bowel loops, CT for abscess
  6. Oral ABX, liquid diet, analgesia
  7. If does not respond within 72 hours, consider IV ABX
  8. Colonoscopy
25
Q

VIRAL HEPATITIS

  1. Which Hepatitis strain is RNA?
  2. Which Hepatitis strain is DNA?
  3. What is the incubation period of Hepatitis A?
  4. What is the incubation period of Hepatitis B?
  5. What is the incubation period of Hepatitis C?
  6. What is the incubation period of Hepatitis E?
  7. Which Hepatitis strain(s) is transmitted faeco-orally?
  8. Which Hepatitis strain(s) is associated with Cirrhosis?
  9. Which Hepatitis strain(s) is associated with HCC?
  10. Which Hepatitis strain(s) have a vaccine?
  11. Which Hepatitis strain(s) are abrupt onset?
  12. Which Hepatitis strain is the most common in the world?
  13. How do you treat Hepatitis A?
  14. How do you treat Hepatitis B?
  15. How do you treat Hepatitis C?
  16. How do you treat Hepatitis D?
  17. How do you treat Hepatitis E?
  18. What are features on blood tests which may suggest a Hepatitis infection?
  19. What are features of Hepatitis?
  20. For HepB, which serology suggests acute infection?
  21. For HepB, which serology suggests current infection?
  22. For HepB, which serology suggests past infection?
  23. For HepB, which serology suggests infectivity?
  24. Which of the viral hepatitis strains are notifiable to PHE?
  25. Which Hepatitis can only survive in the presence of the other?
  26. What is the most common Viral Hepatitis in UK?
  27. What are general principles of management for patients with viral hepatitis, especially B and C?
A
  1. Hepatitis A, C, D, E
  2. Hepatitis B
  3. 2-4 weeks
  4. 6-20 weeks
  5. 6-9 weeks
  6. 3-8 weeks
  7. Hepatitis A and E
  8. Hepatitis B, C, D
  9. Hepatitis B, C
  10. Hepatitis A and B
  11. Hepatitis A, D, and E
  12. Hepatitis A
  13. Basic analgesia
  14. Pegylated interferon / other anti-virals
  15. Ribavirin and interferon alpha anti-virals
  16. Supportive care
  17. Supportive care
  18. Rise in ALT and AST compared to ALP “hepatic picture and elevated bilirubin
  19. Abdo pain, jaundice, fatigue, pruritus, nausea, vomiting, muscle and joint aches, fever
  20. HBsAg
  21. HBcAb IgM
  22. HBcAb IgG
  23. HBeAb
  24. All Viral Hepatitis
  25. Hepatitis D can only survive if patient has Hepatitis B
  26. Hepatitis C
  27. Have a low threshold for screening patients, test for Hepatitis A, B, HIV alongside STIs, refer to gastro / hepatology / infectious diseases, Notify Public Health, stop smoking and alcohol, test for complications i.e. Fibroscan for Cirrhosis and US for HCC
26
Q

AUTOIMMUNE HEPATITIS

  1. What are the two main types and in what sets of patients are they seen in?
  2. What antibodies is Type 1 autoimmune hepatitis associated with?
  3. What antibodies is Type 2 autoimmune hepatitis associated with?
  4. How can it be diagnosed?
  5. What is the management?
A
  1. Type 1: In women late 40-50s, around menopause. Type 2: In young children to early 20s
  2. ANA and SMA
  3. LKM1 or LC1
  4. Liver biopsy
  5. High dose steroids to induce remission, and Azathioprine lifelong
27
Q

LIVER CANCER

  1. What is the most common cause of Hepatocellular carcinoma worldwide?
  2. What is the most common cause of Hepatocellular carcinoma in UK / Europe?
  3. What are risk factors of Hepatocellular Carcinoma?
  4. How is screening for HCC done?
  5. What patients may be screened?
  6. What tumour marker is associated with HCC?
  7. What is the management?
A
  1. Hepatitis B
  2. Hepatitis C
  3. Liver cirrhosis, PBC, Alcohol, NAFLD, A1AT, COCP, DM, male
  4. Ultrasound + AFP
  5. Patients with liver cirrhosis secondary to alcohol, or secondary to Hepatitis B, C or haemachromatosis
  6. AFP
  7. Surgical resection if early, liver transplant, kinase inhibitors such as Sorafenib, Regofenib, Lanvatinib. Usually resistant to chemoradiation
28
Q

INHERITED JAUNDICE

  1. What are inherited causes of Unconjugated Hyperbilirubinemia?
  2. What are inherited causes of Conjugated Hyperbilirubinemia?
  3. What is the inheritance pattern of these?
  4. What is the pathophysiology of Gilbert’s Syndrome and Crigler-Najjar syndrome?
A
  1. Gilbert’s Syndrome & Crigler-Najjar syndrome
  2. Dubin-Johnson syndrome & Rotor syndrome
  3. All are autosomal recessive
  4. Gilbert’s is mild deficiency is UDP-Glucuronosyltransferase whereas Crigler-Najjar is absolute deficiency
29
Q

PRE-HEPATIC, HEPATIC and POST-HEPATIC JAUNDICE

  1. What are causes of Pre-Hepatic Jaundice?
  2. What are causes of Hepatic Jaundice?
  3. What are causes of Post-Hepatic Jaundice?
  4. What type of bilirubin is elevated in pre-hepatic jaundice?
  5. What type of bilirubin is elevated in hepatic jaundice?
  6. What type of bilirubin is elevated in hepatic jaundice?
  7. What does urine appear like in pre-hepatic jaundice?
  8. What does urine appear like in hepatic jaundice?
  9. What does urine appear like in post-hepatic jaundice?
A
  1. Haemolytic anaemia, Gilbert’s syndrome, Crigler-Najjar Syndrome
  2. Viral Hepatitis, Autoimmune Hepatitis, Alcoholic Liver Disease, Haemochromatosis, PBC, PSC, Hepatocellular carcinoma
  3. Cholangiocarcinoma, Pancreatic cancer, Gallstones
  4. Unconjugated
  5. Mixed
  6. Conjugated
  7. Normal, because unconjugated bilirubin is not water soluble
  8. Dark, because conjugated bilirubin is water soluble
  9. Dark, because conjugated bilirubin is water soluble
30
Q

COLORECTAL CANCER

  1. What are the symptoms?
  2. What are the risk factors?
  3. What are the three main causes?
  4. What are the bedside, blood, imaging and special tests?
  5. What is the medical and surgical management?
  6. How is a colorectal cancer patient managed later?
  7. Outline the 2WW referral for patients with suspected colorectal cancer
  8. Outline the features of the National Bowel Cancer Screening Programme
  9. A R hemicolectomy is for what cancer?
  10. A L hemicolectomy is for what cancer?
  11. A sigmoid colectomy is for what cancer?
  12. A anterior resection is for what cancer?
  13. A abdominoperineal resection is for what cancer?
  14. Outline the T in TNM staging
  15. Outline the N in TNM staging
  16. Outline the M in TNM staging
A
  1. Abdominal pain, weight loss, anorexia, progressive bowel habit change, tenesmus, melena, fatigue
  2. Age, family history, IBD, male, smoking, red meat diet, HNPCC, FAP
  3. Sporadic, HNPCC and FAP
  4. Bedside: Baseline Observations, 12-lead ECG
    Bloods: FBC (microcytic iron deficiency anaemia), B12 / Folate, U&Es, ferritin LOW, CEA, LFTs (liver mets), Imaging: Colonoscopy, Staging CT CAP, CT colonography (if unfit for colonoscopy)
    Special: FIT test
5.
Medical management: Chemotherapy, radiotherapy, palliative care input
Surgical: Depends on location of tumour
- R hemicolectomy
- L hemicolectomy
- Sigmoid colectomy
- Anterior resection
- Abdominoperineal resection
  1. CT CAP at 1, 2, 3 years, Colonoscopy at 1 and 5 years, and CEA 6 monthly for 3 years
  2. Patient >40 + weight loss + abdo pain
    Patient >50 + unexplained rectal bleeding
    Patient > 60 + iron deficiency anaemia / change in bowel
    Occult blood in faeces
  3. All men + women aged between 60 and 74 are entitled to a FIT test every 2 years, and a one-off flexible sigmoidoscopy at 55 years old
  4. Tumours of caecum, ascending bowel, and proximal transverse colon
  5. Tumours of distal transverse and descending colon
  6. Tumours of sigmoid colon
  7. Tumours of low sigmoid or high rectum
  8. Tumours of low rectum
14. 
Tx = Unable to assess
T1 = Extends to submucosa
T2 = Extends to muscularis propia
T3 = Extends to subserosa
T4 = Extends to tissues / peritoneum
15. 
Nx = Unable to assess
N0 = No nodal involvement
N1 = 1-3 nodes
N2 = >3 nodes

16.
Mx = Unable to assess
M0 = No metastasis
M1 = Metastasis

31
Q

BOWEL OBSTRUCTION

  1. What are the typical features of a Bowel Obstruction?
  2. How might a SBO differ to an LBO in presentation?
  3. What are some causes of a LBO?
  4. What are some causes of a SBO?
  5. What sign on AXR is associated with sigmoid volvulus?
  6. What are some bedside, blood tests and imaging to investigate a Bowel Obstruction?
  7. What is the medical management of a Bowel Obstruction?
  8. How do you specifically manage a Sigmoid Volvulus?
  9. How many you surgically manage a Bowel Obstruction?
  10. What is the normal diameter of the lumen of the small bowel, large bowel and caecum?
A
  1. Progressively worsening colicky abdominal pain, nausea and vomiting, absolute constipation, abdominal distension, bloating
  2. In SBO, nausea and vomiting may be an early sign and constipation develops later, however LBO will have constipation as an early sign and nausea and vomiting as a later complication
  3. Sigmoid volvulus, colorectal cancer, strictures
  4. Caecal volvulus, Crohn’s disease strictures, adhesions, paralytic ileus, incarcerated hernia
  5. Coffee bean sign
  6. Bedside: Baseline Observations
    Bloods: FBC, U&Es, CRP, Coag studies, Clotting, Ground & Save, Crossmatch, VBG (lactate), Blood cultures (if septic)
    Imaging: CXR (air under diaphragm, perforation), AXR, CT Abdo Pelvis, 12-lead ECG
  7. NBM patient, IV Fluids, IV analgesia, IV antiemetics, NG tube for decompression
  8. Rigid sigmoidoscopy with rectal tube insertion
  9. Treat underlying cause, i.e. bowel resection if cancer, adhesiolysis if adhesions, stricturoplasty if strictures, repair of hernia etc.
  10. Small bowel = 3cm, large bowel = 6cm, caecum = 9cm
32
Q

HAEMORRHOIDS

  1. What are they?
  2. Where are they commonly found?
  3. What is a 1st degree hemorrhoid?
  4. What is a 2nd degree haemorrhoid?
  5. What is a 3rd degree haemorrhoid?
  6. What is a 4th degree haemorrhoid?
  7. What are the classic features of a haemorrhoid?
  8. What is the conservative, medical and surgical management of haemorrhoids?
A
  1. Venous vascular cushions which have become enlarged due to increased pressure, i.e. straining
  2. At 3 o’clock, 7 o’clock and 11 o’clock
  3. No prolapse
  4. Prolapse on straining, but returns on relaxing
  5. Prolapse on straining, no return on relaxing but can be pushed back
  6. Permanent prolapse
  7. PAINLESS, FRESH RECTAL BLEEDING ON WIPING
  8. Conservative: Minimise straining, increase dietary fibre, increase fluid intake, peri-anal hygiene

Medical: Bulk forming laxatives, analgesia i.e. Paracetamol, local anaesthetics i.e. Lidocaine, Benzocaine, and topical corticosteroids

Surgical: Rubber band ligation, sclerotherapy, bipolar diathermy, haemorrhoidectomy, haemorrhoidal artery ligation

33
Q

ANAL FISSURE

  1. What is it?
  2. What are the risk factors?
  3. What are the features?
  4. What is an acute and chronic anal fissure?
  5. How do you manage an acute anal fissure?
  6. How do you manage a chronic anal fissure?
A
  1. A longitudinal / elliptical tear of the squamous lining of the anal canal
  2. Constipation, IBD (Crohn’s), STIs
  3. PAINFUL, FRESH RECTAL BLEEDING ON WIPING
  4. Acute < 6 weeks, chronic > 6 weeks
  5. Acute is treated with bulk forming laxatives i.e. ispaghula husk and osmotic laxatives i.e. lactulose, local anaesthetic i.e. Lidocaine, paracetamol / NSAIDs
  6. As above, plus GTN spray, Diltiazem, sphincterotomy / botox

Medicine, Year 3, GI and Surgery (12 decks)

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