GI SAQ Flashcards

1
Q

A 52-year-old woman presents with abdominal pain, fever, loose stool and blood mixed with stool for 3 days.
1. List 4 differentials
2. Augmentin 2 weeks ago for new CAP. What is most likely dx now?
3. Name 1 Ix to confirm dx
4. 1 complication if untreated
5. Name 2 medical treatment for condition
6. If failed aforementioned treatment, what treatment can be offerred?

A
  1. Pseudomembranous colitis, bacterial dysentery/inflammatory gastroenteritis, ulcerative colitis, diverticular bleeding, CRC
  2. Pseudomembranous colitis
  3. Stool for clostridium difficile toxin
  4. Toxic megacolon, sepsis, colonic peforation
  5. Oral metronidazole (mild-moderate symptoms), oral vancomycin (if severe) –> not given IV as not as effective
  6. Surgery
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2
Q

Middle-aged man presented with melena. He drinks half bottle of whisky per day. PE no stigmata of chronic liver disease.
Blood with Hb 9.x, MCV 102,
LFT has normal albumin, bilirubin, raised GGT, raised AST and ALT, AST higher than ALT.
1. 2 ddx for macrocytic anemia
2. Name 2 ddx for melena considering the whole clinical picture
3. 1 contraindication for upper endoscopy, which is found on X ray or bloods

A
  1. Non megaloblastic (large normal nucleus, matuer RBCs): liver disease, alcohol use, hypothyroidism, hereditary spherocytosis
    Megaloblastic (structurally abnormal nucleus resulting in large, immature RBCs): B12 deficiency, folate deficiency, fanconi anemia
    Reticulocytosis: haemolysis (zieve syndrome: secondary to aclohol induced liver injury)
  2. Peptic ulcer, esophageal varices, mallory weiss tear
  3. Pneumoperitoneum: gree gas under diaphragm found on erect CXR
    Absolute contraindications: perforated bowel, peritonitis, toxic megacolon in unstable patient
    Relative contraindications: severe neutropenia, coagulopathy, severe thrombocytopenia or impaired platelet function (seen in bloods)
  4. Perforation/bleed/infection, sedation related
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3
Q
A
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4
Q

M/52, 4/7 Hb 12.6 MCV 97 Albumin 44 Bilirubin 9 ALT 31 AST 23 Transient elastography stiffness 14.45 (cirrhosis), contrast 335dB (steatosis) HbsAg pos, HbeAg neg
1. Question to ask in history taking
2. Would you start hep b treatment? why?
3. What Ix would you perform with reasons
4. 3 years after treatment, HBsAg -ve. Is this patient cured>
5. What does the HBsAg-ve result indicate for his Mx (implication of HBsAg -ve to patient)

A
  1. HPI (sx of liver disease: jaundice, tea colored urine, pruritis, bleeding tendency), constitional sx
    drug Hx: steroids, TCM, hepatotoxic drug
    social Hx: alcohol, IVDU with needle sharing, unsafe sex
    family Hx: hx of HCC, HBV status of partner/children, HBV vaccination status of partner/children
  2. Yes, cirrhosis
    All patients HBeAg+ve or -ve with ALT >ALN and DNA>2000iu/ml with moderate necroinflammation/fibrosis
    Patients with cirrhosis with anydetectable HBV DNA irrespective of ALT levels
    HBeAg+ve patients with high HBV DNA but persistently normal ALT
  3. AFP for HCC screening, PIVKA (tumor marker) available in HA now, liver USG for HCC screening. Upper endoscopy for esophageal varices screening. HBV DNA for pretreatment baseline
  4. No
  5. Resolved infection, occult hep B
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5
Q

Oesophageal varices M/60, chronic Hep B with no regular follow-up. Chronic alcohol drinker(non + 1 I recall NO alcohol history?). Positive shift dullness. Non-drinker. BP 85/50, HR 110 Blood test results: Hb 8.0 MCV 102 PLT 45 Urea 16
1. Reason for high MCV
2. Why thrombocytopenia?
Endoscopy confirmed eso varices, red wale sign but no active bleeding. No gastric ulcer.
3. Explain the reason for oesophageal varices
4. Other than esophageal varices, what other possible features specific to cirrhosis would you expect to find on upper endoscopy?
5. one 1st line intervention during endoscopy

A
  1. Reticulocytosis due to bone marrow compensation for acute blood loss. Liver cirrhosis.
  2. Hypersplenism (portal hypertension causing congestion), decreased thrombopoietin production in liver (decreased megakaryopoiesis) –> reduced platelet production –> thrombocytopenia
  3. Collateral portosystemic venous shunting due to portal hypertension, dilatation of submucosal veins
  4. Gastric varices, portal hypertensive gastropathy
  5. Endoscopic band ligation. (IV terlipressin, PPI, prophylactic antibiotics. B blocker for secondary prevention: carvedilol)
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6
Q
A

a) Types of accomodation, activities, inset bite, needle/blood exposure, sex history, soil/water contact, chemoprophylaxis
b) Malaria, dengue, typhoid, rickettsiosis, leptospirosis, melioidosis
c) Malaria caused by anopheles mosquito
d) Thin blood smear (after POCT)
e) P. falciparum treatment: Artemisinin combination therapies (ACTs): artesunate + doxycycline, artesunate + mefloquine. There is quinine resistant P. falciparum so not as effective.
PV, PM and PO (majority): cloroquine 600mg base, mefloquine for chloroquine resistant PV
f) haemolysis, jaundice, thrombocytopenia, pancytopenia, SIRS, acute respiratory distress, acute renal failure

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7
Q
A

a) non alcoholic fatty liver disease
b) obesity, T2DM, hypertriglyceridemia, metabolic syndrome
c) Abdominal ultrasound, fibroscan (elastography)
d) HCC, PCOS, hypertension, early atheroclerosis, nephropathy, OSA

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8
Q
A

a) TB lung
b) Lateral flow urine lipoarabinomannan (LF-LAM) assay, sputum culture (ziehl neelson stain) or sputum smear microscopy
c)
2 tests for latent TB:
IGRA (inferon gamma release assay): WBC infected with M. tuberculosis with release IFNgamma when mixed with antigens derived from M.tuberculosis
Tuberculin skin test: (>5mm if HIV positive/high risk, >15mm if no known risk factors for TB)
d) Immunodulators + biologics for fistulizing CD
Immunomodulators: thiopurines (azathioprine), methotrexate

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9
Q
A

a)Accomodation, insect bite, needle exposure, sex history, TOCC
b) Dengue, typhoid, rickettsiosis, leptospirosis
c) Thin blood smear
d) artesunate + doxycycline, mefloquine

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10
Q
A

a) myelosuppresion (pancytopenia)
b) levofloxacin, tazocin (piperacillin +tazobactam) + oral fluconazole
c) TPMT and NUDT15 in HK locality
d) Other immunomodulator: methotrexate
Biologics: anti TNFa (infliximab, etanercept), natalizumab, vedolizumab (mAb vs integrin alpha 4 beta 7 peyers patch adhesion molecule)

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11
Q
A

a) needle exposure, sex history
b)
c) fibroscan, AFP
d) non alcoholic steatohepatitis

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12
Q

A 60+/M presents to you for regular checkup. He has a history of diabetes and hypertension on metformin and losartan. On this checkup, his blood pressure is 150/90mmHg and his BMI is 35 kg/m2. His blood tests are as follows (elevated HbA1c, elevated creatinine, elevated AST/ALT
a. Other than the deranged LFT, what are the clinical problems that this patient has? Give 4.
b. What is the likely cause of his liver condition?
c. What non-invasive investigation can you perform to confirm your diagnosis?
d. What other diabetes drug can you give to improve his liver condition? (2) What is the mechanism?

A

a. hypertension, obese, DM, renal impairment
b. NASH
c. Transient elastograph with CAP (controlled attenuation parameter), USG liver
d. TZD (pioglitazone) been shown to reverse severe liver cirrhosis, GLP1 agonist (liraglutide)

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13
Q

A 50+/M is a chronic drinker who drinks whiskey and beer on a daily basis. He presents to you with epigastric discomfort. His laboratory results are as follows (normal CBC, elevated AST>ALT ~200-300/ALP, markedly elevated GGT, serum glucose normal). Temperature: 37.5 degree. He regularly drinks but admits that he hasn’t been drinking as much these past few days as he has run out of cash (I’m not sure if this is from medicine or psychiatry).
a. Give 3 differential diagnoses for his liver biochemistry (3)
b. List 3 immediate examinations (3)
He has been agitated since admission. RG 5.3.
He suddenly collapses and develops a GTCS.
c. What is the condition he is suffering from? (1)
d. What should have been given to prevent this condition from developing? (1)
e. What is the general management of his condition? (2)

A

a. Alcoholic hepatitis, NASH, acute hepatitis (Hep A,E, acute on chronic HBV), drugs
b. Neurological examination: cerebellar signs
c. Wernickes encephalopathy ?? (delirium tremens)
d. High dose IV thiamine
e. Monitor BP and temperature (hypo/hyperthermia, hypotension and tachycardia can occur). Monitor neurological signs (opthalmoplegia can be resolved within hours) Treat any concurrent illnesses (e.g. delirium tremens, hepatic encephalopathy, sepsis)

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14
Q

A 50+/M has severe knee pain. He has been prescribed naproxen by his GP. The knee pain has worsened and he has increased his intake of naproxen. Now he presents to you with epigastric pain. An OGD is performed, biopsy is taken and H. pylori is identified. He is also given triple therapy. After 8 weeks, the H pylori has been confirmed to be eradicated.
a. Name 2 methods to diagnose H pylori on OGD biopsy
b. List 2 other gastroduodenal diseases caused by H pylori apart from gastric ulcer
c. What is included in the triple therapy he has been given?
d. List 2 complications of gastric ulcer
e. List 2 methods to reduce PUD in the future if he needs to continue taking anti-inflammatory medication

A

a. rapid urease test, culture, microscopy
b. gastric cancer, hyperplastic polyp, gastric MALT lymphoma
c. Amoxicillin, clarithromycin, omeprazole
d. Gastric cancer, perforation, hemorrhage
e. Give PPI with NSAID, use COX2 selective NSAIDS (celecoxib –> has better pharmaco profile), stop NSAID

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15
Q
A
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