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Year 3 > Gastroenterology Block > Flashcards

Gastroenterology Block Flashcards

1
Q

What is Charcot’s Triad?

A

The combination of jaundice, RUQ pain, and fever = ascending cholangitis

  • Infection of the bile duct in the liver
  • E. coli is typically the causative organism of ascending cholangitis
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2
Q

What antispasmodic is typically used in gallstones?

A

Buscopan

- Should avoid NSAIDs

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3
Q

What condition is a risk factor for gallbladder cancer?

A

Chronic cholecystitis

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4
Q

What is a complication of acute cholecystitis?

A

Gallbladder empyema/mucosele

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5
Q

What is Sepsis 6?

A

Remember “3 in, 3 out”

3 in:

  • Oxygen
  • Fluids
  • IV antibiotics

3 out:

  • Blood cultures
  • Lactate
  • Urine output
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6
Q

What findings on ultrasound are consistent with gallstones?

A

Thick-walled gallbladder with pericholecystic fluid

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7
Q

What is the treatment for peptic ulcers?

A
  1. Antibiotics to kill H. Pylori -> i.e. amoxicillin, clarithromycin
  2. Block acid production (PPI)-> i.e. omeprazole, lansoprazole
  3. Reduce acid production (H2 antagonists) -> i.e. ranitidine, nizatidine
  4. Antacids to neutralise stomach acid
  5. Protect lining of stomach + small intestine -> i.e. misoprostol
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8
Q

What hematological values would be indicative of an upper GI bleed?

A

High urea with a normal creatinine

- Increased protein

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9
Q

What 3 things would you look for when investigating a DKA?

A
  1. Acidosis on ABG
  2. Raised glucose on ABG
  3. Raised ketones in urine/blood
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10
Q

What are the 3 main risk factors for kidney stones?

A
  1. Smoking
  2. High calcium
  3. Dehydration
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11
Q

What is the striking differential in a patient presenting with LIF pain?

A

Diverticulitis

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12
Q

What is the difference between diverticulosis, diverticular disease, and diverticulitis?

A

Diverticulosis = multiple out-pouching of the bowel without symptoms

Diverticular disease = symptoms associated after eating

Diverticulitis = pain, fever, and PR bleeding

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13
Q

What are the causes of epigastric pain?

A
  1. Pancreatitis
  2. Gastritis/duodenitis
  3. Peptic ulcer
  4. Gallbladder disease
  5. Aortic aneurysm
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14
Q

What blood test would be elevated in pancreatitis?

A

Lipase (more sensitive than amylase) + amylase

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15
Q

What are the causes of pancreatitis?

A

GET SMASHED

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion sting
Hypercalcemia/high cholesterol
ERCP (endoscopic retrograde cholangiopancreatography)
Drugs (i.e. sodium valproate, thiazide diuretics, amiodarone)

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16
Q

What is messenteric adenitis?

A

A mild condition that causes temporary pain in the abdomen, mainly in children. It usually clears on its own or requires antibiotics + painkillers.

Inflamed lymph glands in the abdomen

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17
Q

How can you differentiate small and large bowel obstruction?

A

Ask the patient if vomit or pain came first.

If pain = large bowel obstruction
If vomit = small bowel obstruction

Important to also ask when they last passed stool, diarrhoea, family history, weight loss, PR bleeding

Remember previous abdominal surgery is a risk factor for GI adhesions!

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18
Q

What is the 3-6-9 rule?

A

The diameter of the small intestine, large intestine, and cecum cannot be greater than 3cm, 6cm, and 9cm respectively. If so, then the bowel is dilated and is likely caused by an obstruction.

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19
Q

What is “drip and suck”?

A

In a patient with a GI adhesion, insert a nasogastric tube and cannula to try and get rid of stomach contents. If no change, then surgery is required to operate on adhesions.

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20
Q

What is permissive hypotension?

A

In the scenario of a gross haemorrhage, it has been found to be beneficial in some patients who are hypotensive to avoid giving IV fluids to the extent that reverses their hypotension.

Instead management is given so their SBP ≤ 80mmHg. This is to prevent thrombus dislodgement and help the body to stop the bleeding on its own without causing further fluid loss.

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21
Q

What is a cause of increased ADH secretion and decreased ADH secretion?

A

Increased ADH = SIADH (I.e. cancer)

Decreased ADH = Diabetes Insipidus

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22
Q

What’s the difference between transudate and exudate?

A

Transudate -> dealing with hydrostatic P
Exudate -> dealing with inflammation

Transudate:

  • Fluid shifts out b/c of low protein (increased hydrostatic P = leakage between endothelial cells)
  • Causes: CHF, Liver failure, Kidney failure, SVC obstruction, PE

Exudate:

  • Vessel dilates + stasis of fluid + proteins
  • Endothelial spaces are larger thus fluid + protein leaks out of the vessel
  • Causes: pleural effusion, pneumonia/infections, SLE, Cancer, PE, Pancreatic disease, Drug reactions

Test for transudate or exudate with Thoracentesis -> “Light’s criteria”:

  • Presence of cholesterol (LDH) + protein = exudate
  • No cholesterol/proteins = transudate
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23
Q

What are the BMI categories?

A 
< 18.5 = underweight
18.5-25 = on target
25-30 = overweight
30-40 = obesity
> 40 = morbidly obese
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24
Q

Name 9 conditions affecting the mouth?

A
  1. Leukoplakia = white patch on oral mucosa. Oral hairy leukoplakia is associated with HIV caused by EBV.
  2. Aphthous Ulcers = causes can be Celiac or Crohn’s Disease
  3. Candidiasis = risk factor is steroids (fluconazole for oropharyngeal thrush)
  4. Angular Stomatitis = denture problems, candidiasis, def of iron/vitamin B2
  5. Gingivitis = poor oral hygiene, pregnancy, drugs (phenytoin, cyclosporine, nifedipine), vitamin C deficiency, acute myeloid leukaemia, Vincent’s angina
  6. Microstomia = mouth is too small from thickening and tightening of perioral skin after burns or in epidermolysis bullosa
  7. Oral Pigmentation = Perutz-Jegher’s; Addison’s disease, drugs (antimalarials), malignant melanoma
  8. Teeth = blue line at gum-tooth margin is lead poisoning
  9. Tongue = Glossitis (B12/iron/folate deficiency), macroglossia (myxoedema, acromegaly, amyloid), tongue cancer (raised ulcer with firm edges. Smoking + alcohol are risk factors)
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25
Q

List causes of white intra-oral lesions in the mouth?

A
  • Idiopathic keratosis
  • Leukoplakia
  • Lichen plants
  • Poor dental hygiene
  • Candidiasis
  • Squamous papilloma
  • Carcinoma
  • Hairy oral leukoplakia
  • Lupus erythematosus
  • Smoking
  • Aphthous stomatitis
  • Secondary syphilis
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26
Q

List diagnostic and therapeutic indications for upper GI endoscopy

A

Diagnostic:

  • Hematemesis/melena
  • Dysphagia
  • Dyspepsia
  • Duodenal biopsy
  • Persistent vomiting
  • Iron deficiency (cancer)

Therapeutic:

  • Treatment for bleeding lesions
  • Variceal banding and sclerotherapy
  • Argon plasma coagulation for suspected vascular abnormality
  • Stent insertion, laser therapy
  • Stricture dilatation, polyp resection
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27
Q

What are the diagnostic and therapeutic indications for colonoscopy?

A

Diagnostic:

  • Rectal bleeding
  • Iron-deficiency anemia (bleeding cancer)
  • Persistent diarrhoea
  • Positive fecal occult blood test
  • Assessment or suspicion of IBD
  • Colon cancer surveillance

Therapeutic:

  • Hemostasis
  • Bleeding Anglo dysplasia lesion
  • Colonic stent deployment
  • Volvulus decompression
  • Pseudo-obstruction (polypectomy)
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28
Q

What are the causes of dysphagia?

A

Dysphagia is difficulty swallowing -> exclude malignancy!

Causes:

  • Oral, pharyngeal, or esophageal?
  • Mechanical or motility related?

Key questions to ask:
1. Was there difficulty swallowing solids + liquids from the start?
Yes = motility disorder (I.e. Achalasia - coordinated peristalsis lost, CNS, or pharyngeal causes)
No = solids then liquids suspect a stricture (benign or malignant)

  1. Is it difficult to initiate a swallowing movement?
    Yes = suspect bulbar palsy, especially if patient coughs on swallowing
  2. Is swallowing painful (odynophagia)?
    Yes = suspect ulceration (malignancy, esophagitis, viral infection, candida in immunocompromised, poor steroid inhaler technique) or spasm
  3. Is the dysphagia intermittent or constant and getting worse?
    Intermittent = suspect esophageal spasm
    Constant and worsening = malignant stricture
  4. Does the neck bulge or gurgle on drinking?
    Yes = suspect a pharyngeal pouch
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29
Q

What are risk factors for esophageal cancer?

A
  • Male
  • GORD
  • Tobacco
  • Alcohol
  • Barrett’s esophagus
  • Tylosis (palmar hyperkeratosis)
  • Plummer-Vinson syndrome (post-cricoid dysphagia, upper esophageal web + iron-deficiency)
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30
Q

What are the possible different appearances of vomit and what do they indicate?

A

Coffee grounds = upper GI bleed
Recognisable food = gastric stasis
Feculent = small bowel obstruction

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31
Q

What does the timing of the vomiting tell you about the condition?

A

Morning = pregnancy or increased ICP

1h post food = gastric stasis/gastroparesis (DM)

Vomiting that relieves pain = peptic ulcer

Preceded by loud gurgling = GI obstruction

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32
Q

Name an anti-emetic from each class

A

H1 - cyclizine

D2 - Metoclopramide

5HT3 - ONdansetron

Others - Hyoscine Hydrobromide

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33
Q

What are the symptoms of indigestion + peptic ulcer disease?

A

Epigastric pain often related to hunger, specific foods, or time of day, fullness after meals, heartburn (retrosternal pain), tender epigastrium

Beware of ALARM Symptoms:
Anemia (iron deficiency)
Loss of weight
Anorexia
Recent onset/progressive symptoms
Melena/hematemesis
Swallowing difficulty
34
Q

How do you treat H. Pylori?

A

Give appropriate PPI and 2 antibiotic combination

I.e. Lnassoprazole 30mg/12h PO, clarithromycin 250mg/12h PO, and amoxicillin 1g/12h PO for 1 week

35
Q

What are risk factors for gastric ulcers?

A 
H. Pylori (~80%)
Smoking
NSAIDs
Reflux of duodenal contents
Delayed gastric emptying
Stress
36
Q

List 6 differentials for dyspepsia

A
  1. Non-ulcer dyspepsia
  2. Oesophagitis/GORD
  3. Duodenal/gastric ulcer
  4. Gastric malignancy
  5. Duodenitis
  6. Gastritis
37
Q

What are the causes of GORD?

A
  • Lower esophageal sphincter hypotension
  • Hiatus hernia
  • Oesophageal dysmotility
  • Obesity
  • Gastric acid hypersecretion
  • Delayed gastric emptying
  • Smoking
  • Alcohol
  • Pregnancy
  • Drugs (tricyclics, anticholinergics, nitrates)
  • H. Pylori
38
Q

What are the symptoms of GORD?

A
  • Heartburn
  • Belching
  • Acid brash
  • Waterbrash
  • Odynophagia
  • Nocturnal asthma
  • Chronic cough
  • Laryngitis
  • Sinusitis
39
Q

What’s the difference between a sliding hernia and rolling hiatus hernia?

A

Sliding (80%):
- Gastroesophageal junction slides up into the chest. Acid reflux often happens as the lower oesophageal sphincter becomes less competent in many cases

Rolling (20%):
- Gastroesophageal junction remains in the abdomen but a bulge of stomach herniated up into the chest alongside the esophagus. As the GE junction remains intact, GORD is less common

40
Q

What are common causes of upper GI bleeds?

A
  • Peptic ulcers
  • Mallory-Weiss tear
  • Oesophageal varies
  • Gastritis/gastric erosions
  • Drugs (NSAIDs, aspirin, steroids, trombolytics, anticoagulants)
  • Esophagitis
  • Duodenitis
  • Malignancy
  • No obvious cause
41
Q

What are the pre-hepatic, intra-hepatic and post-hepatic causes of portal hypertension?

A

Pre-hepatic:
- Thrombosis (portal or splenic vein)

Intra-hepatic:

  • Cirrhosis (80% in UK)
  • Schistosomiasis (commonest worldwide)
  • Sarcoid
  • Myeloproliferative disease
  • Congenital hepatic fibrosis

Post-Hepatic:

  • Budd-Chiari syndrome
  • R heart failure
  • Constrictive pericarditis
  • Veno-occlusive disease
42
Q

What characteristics of diarrhoea indicate certain conditions?

A

Bloody diarrhoea: campylobacter, shigella/salmonella, E.coli, UC, Crohn’s Disease, Colorectal cancer, Colonic polyps, pseudomembranous colitis, ischemic colitis

Mucus: IBS, colorectal cancer, polyps

Frank pus: IBD, diverticulitis, fistula/abscess

Explosive: Cholera, Giardiasis, Yersinia, Rotavirus

Steatorrhoea: increased gas, offensive smell, floating/hard-to-flush stools (consider pancreatic insufficiency or biliary obstruction)

43
Q

What are common causes of diarrhoea?

A
  1. Gastroenteritis
  2. Traveller’s diarrhea
  3. C. Difficult
  4. IBS
  5. Colorectal cancer
  6. Crohn’s, UC, Celiac
  7. Thyrotoxicosis
  8. Autonomic neuropathy
  9. Addison’s Disease
  10. Drugs (antibiotics, propranolol, cytotoxic, laxatives, PPI, NSAIDs, Digoxin, Alcohol)
44
Q

Name an example of a constipation agent from each drug class

A

Bulking agents - Ispaghula husk, Methylcellulose

Stimulant Laxatives - Bisacodyl tablets, suppositories, senna, Docusate, Sodium picosulfate

Stool Softeners - Arachis oil enemas

Osmotic Laxatives - Lactulose, Macrogol/Movicol, Magnesium salts, Phosphate enemas (rapid evacuation)

If these don’t help…Prucalopride (5HT4 agonist)

45
Q

What are the symptoms of UC?

A
  • Episodic/chronic diarrhea
  • Crampy abdominal discomfort
  • Bowel frequency relates to severity
  • Urgency/tenesmus = proctitis
  • Systemic symptoms in attacks: fever, malaise, anorexia
46
Q

What is UC and what are the signs?

A

UC is a relapsing and remitting inflammatory disorder of the colonic mucosa.

Signs:

  • Clubbing
  • Aphthous oral ulcers
  • Erythema nodosum
  • Nutritional deficits
47
Q

What is the treatment for UC and Crohn’s?

A

Steroids

48
Q

What is Crohn’s disease? It’s symptoms and signs?

A

A chronic inflammatory disease characterised by transmutation granulomatous inflammation affecting any part of the gut from mouth to anus.

Unlike UC there is unaffected bowel between areas of active disease (skip lesions)

Symptoms:

  • Diarrhea
  • Abdo pain
  • Weight loss
  • Fever, malaise, anorexia

Signs:

  • Bowel ulceration
  • Abdo tenderness/mass
  • Perianal abscess/fistula/skin tags
  • Anal stricture
  • Clubbing, skin/joint/eye problems
49
Q

What type of anemia is present in Celiac disease?

A

B12 or iron deficiency

50
Q

List 4 nutritional disorders

A

Scurvy: Lack of vitamin C
- Signs = listlessness, anorexia, cachexia, gingivitis, bleeding from gums/nose/hair follicles/into joints/bladder, muscle pain/weakness, oedema

BeriBeri: Deficiency of B1 (thiamine)

  • Heart failure with general oedema = wet Beriberi
  • Neuropathy = dry Beriberi

Pellagra: Lack of nicotinic acid
- Classical triad: Diarrhoea, Dermatitis, Dementia

Xerophthalmia: Vitamin A Deficiency
- Cause of blindness in the tropics (Bitôt’s Spots)

51
Q

What are causes of chronic pancreatitis?

A 
Alcohol
Smoking
Autoimmune
familial, 
cystic fibrosis
Hemochromatosis
Pancreatic duct obstruction (tumour/stones)
Congenital (pancreas divisum)
52
Q

What is the drug treatment for chronic pancreatitis?

A
  1. Analgesia (celiac-plexus block may give brief relief)
  2. Lipase (I.e. Creon)
  3. Fat-soluble vitamins
  4. Insulin
53
Q

Name risk factors for pancreatic carcinoma

A
  • Smoking
  • Alcohol
  • Carcinogens
  • Diabetes
  • Chronic pancreatitis
  • Obesity
  • Genetics (95% have mutations in the KRAS2 gene)
54
Q

How does pancreatic cancer present?

A

Tumours in the head of the pancreas = painless obstructive jaundice

Tumours in body + tail of pancreas = epigastric pain

Either may cause:

  • Anorexia
  • Weight loss
  • Diabetes
  • Acute pancreatitis

Mean survival < 6mo

55
Q

What is jaundice and what causes it?

A

Yellowing of the skin, sclera, and mucosae from increased plasma bilirubin (visible at ≥60umol/L).

It’s classified by the site of the problem or by the type of circulating bilirubin

UNCONJUGATED HYPERBILIRUBINEMIA:
- Unconjugated bilirubin is water-insoluble, it doesn’t enter urine resulting in unconjugated hyperbilirubinemia

  1. Overproduction = hemolysis (I.e. malaria, DIC), ineffective erythropoiesis
  2. Impaired Hepatic Uptake = Drugs (paracetamol, rifampicin), ischemic hepatitis
  3. Impaired Conjugation = Eponymous syndromes: Gilbert’s, Crigler-Najjar
  4. Physiological Neonatal Jaundice = Caused by a combo of the above

CONJUGATED HYPERBILIRUBINEMIA:
- Conjugated bilirubin is water-soluble, it’s excreted in urine, making it dark. Less conjugated bilirubin enters the gut and the feces become pale. When severe, it can be associated with an intractable prurititus which is best treated by relief of the obstruction

  1. Hepatocellular Dysfunction: Viruses (Hepatitis, CMV, EBV), Drugs, Alcohol, Cirrhosis, Liver mets/abscess, hemachromatosis, autoimmune hepatitis, septicaemia, leptospirosis, syphilis, a1-antitrypsin deficiency, Budd-Chiari, Wilson’s disease, R heart failure, toxins (carbon tetrachloride, fungi)
  2. Impaired Hepatic Excretion (Cholestasis): Primary biliary cholangitis, primary sclerosis growth cholangitis, drugs, common bile duct gallstones, pancreatic cancer, compression of the bile duct, cholangiocarcinoma, Mirrizi’s syndrome (compression by a gallstone in the cystic duct on the common bile duct)
56
Q

Name examples of drugs that cause jaundice

A

Antimalarials -> Hemolysis

Paracetamol OD, TB treatment, Statins, Sodium valproate -> Hepatitis

Flucloxacillin, Steroids, Sulfonylureas -> Cholestasis

57
Q

What are the 5 broad causes of liver failure?

A

Infections: Viral hepatitis, yellow fever, leptospirosis

Drugs: paracetamol OD, halothane, isoniazid

Toxins

Vascular: Budd-Chiari syndrome, veno-occulusive disease

Others: Alcohol, fatty liver disease, primary biliary cholangitis, a1-antitrypsin deficiency

58
Q

What is primary biliary cholangitis?

A

Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing Cholestasis which may lead to fibrosis, cirrhosis, and portal HTN.

Patient is often asymptomatic and diagnosed after incidental finding of increased ALP (increased yGT, mildly increased AST + ALT). Lethargy, sleepiness, and pruritis may preced jaundice by years.

Signs:

  • Jaundice
  • Skin pigmentation
  • Xanthelasma
  • Xanthomata
  • Hepatosplenomegaly

Treatment:

  • Pruritis -> colestyramine; naltrexone + rifampicin may also help
  • Diarrhoea -> codeine phosphate
  • Osteoporosis prevention
  • Vitamin prophylaxis -> Vitamin A, D, K
  • High-dose ursodeoxycholic acid (UDCA) may improve survival + delay transplantation
59
Q

What is primary sclerosis cholangitis?

A

Progressive Cholestasis with bile duct inflammation and strictures

Symptoms/Signs:

  • Pruritis + fatigue
  • Ascending cholangitis, cirrhosis, and hepatic failure if severe
  • Associated with male sex and increased risk of colorectal malignancy

Also use Ursodeoxycholic Acid as it may improve LFT

60
Q

What diseases are associated with autoimmune hepatitis?

A
  1. Pernicious anemia
  2. Ulcerative colitis
  3. Glomerulonephritis
  4. Autoimmune thyroiditis
  5. Autoimmune hemolysis
  6. Diabetes
61
Q

Discuss the different LFTs

A
  1. TESTS OF HEPATOCELLULAR INJURY OR CHOLESTASIS
    Aminotransferases (AST, ALT):
    - Released in the bloodstream after HEPATOCELLULAR injury
    - ALT is more specific to hepatocellular injury (also in kidney + muscle)
    - AST also expressed in the heart, skeletal muscle, and RBCs
Alkaline Phosphatase (ALP):
- May originate from liver, bone (so raised in growing child), or placenta

yGT:

  • Present in liver, pancreas, renal tubules, and intestine - but not bone so it helps if a raised ALP is from bone (b/c yGT will be normal) or liver (yGT elevated)
  • It’s not specific to alcohol damage in the liver
  1. TESTS OF HEPATIC FUNCTION
    - Serum albumin
    - Serum bilirubin
    - PT (INR)

HEPATOCELLULAR PREDOMINANT LIVER INJURY
- Increased AST + ALT

CHOLESTASIS/OBSTRUCTION PREDOMINANT LIVER INJURY
- ALP + yGT are elevated, AST + ALT mildly elevated

62
Q

Discuss ALP, GGT, AST, ALT, Albumin, PT/INR

A

ALP:

  • Low specificity for cholestasis, increased in:
    1. Cholestasis
    2. Preganncy
    3. Bone growth (ie. Paget’s disease, prostate + breast cancer - blastic cancers)

GGT:

  • Cholestasis
  • Alcohol
    • Not raised in bone disease! Used to distinguish if ALP is increased.

Check total bilirubin: TB - DB = IB (indirect bilirubin to determine the location/cause of increased LFTs)
- DB > 50% = inrahepatic or extra hepatic cause

Gilbert’s Disease = low glucoronic transferase enzyme which converts IB to DB

AST: Enzyme made in liver. Low specificity for liver. Also raised in muscle breakdown

ALT: Enzyme made in liver. Increased specificity for liver.

Both AST + ALT are released when hepatocytes die

Albumin: Low in chronic liver disease. 1/2 life = 20 days

PT/INR: Most sensitive liver function test

Factor 2, 7, 9, 10, 1, 5 = related to Vitamin K/PT
- Warfarin or hemophilia will increase PT

ALT, AST, ALP, GGT = distinguish between hepatocellular damage and cholestasis

Albumin, Bilirubin, PT = assess liver synthetic function

63
Q

What are the steps to determine what the damage in the liver is coming from?

A
  1. Is ALT raised 10x or less? (hepatocyte damage)
  2. Is AST raised 3x or less? (cholestasis)
    - If both are raised = mixed picture
  3. Check GGT if AST is raised 3x b/c its more specific for cholestasis:
    - if raised = cholestasis
    - if normal = bone growth/pregnancy
  4. Normal ALT + AST? Check bilirubin levels = pre-hepatic cause of jaundice
    - Gilbert’s Syndrome
    - Hemolysis

Normal urine + normal stool = pre-hepatic cause
Dark urine + normal stool = hepatic cause
Dark urine + pale stool = post-hepatic cause (i.e. obstruction)

64
Q

What are causes of unconjugated hyperbilirubinemia?

A
  1. Hemolysis
  2. Impaired hepatic uptake (drugs, CHF)
  3. Impaired conjugation (Gilbert’s syndrome)
65
Q

What are causes of conjugated hyperbilirubinemia?

A
  1. Hepatocellular injury

2. Cholestasis

66
Q

What does the ALT/AST ratio tell you?

A

ALT > AST = chronic liver disease

AST > ALT (2:1) = cirrhosis/acute alcoholic hepatitis

67
Q

What are causes of acute hepatocellular injury?

A
  1. Paracetamol OD
  2. Infection (Hepatitis A + B)
  3. Liver ischemia
68
Q

What are causes of chronic hepatocellular injury?

A
  1. Alcoholic fatty liver disease
  2. Non-alcoholic fatty liver disease
  3. Chronic infection (Hepatitis B + C)
  4. Primary biliary cirrhosis
  5. A1 antitrypsin deficiency
  6. Wilson’s disease
  7. Hemachromatosis
69
Q

What tests are included in a liver screen?

A
  1. LFTs
  2. Coagulation screen
  3. Hepatitis serology (ABC)
  4. EBV
  5. CMV
  6. Anti-mitochondrial antibody (AMA)
  7. Anti-smooth muscle antibody (ASMA)
  8. Anti-liver/kidney microsomal antibody (anti-LKM)
  9. Anti-nuclear antibody (ANA)
  10. p-ANCA
  11. Immunoglobulins - IgM/IgG
  12. A1-antitrypsin
  13. Serum copper (for Wilson’s Disease)
  14. Ceruloplasmin (for Wilson’s Disease)
  15. Ferritin (for hemochromatosis)
70
Q

What bacteria causes stool to float?

A

Giardia Lamblia

  • fat malabsorption thus greasy stool floats in H2O
  • Resistant to chlorination -> risk of transfer in swimming pools
71
Q

When is ulcerative colitis severe?

A
  1. Blood in stool
  2. Stools > 7x/day
  3. > 37.8ºC temperature, HR > 90bpm, anemia, or ESR > 30mm/hr
72
Q

What is the most common organism found on ascetic fluid culture in spontaneous bacterial peritonitis?

A

E. coli

73
Q

What is the triad of symptoms/signs in mesenteric ischemia?

A
  1. CVD
  2. High lactate
  3. Soft + tender abdomen
74
Q

What tumours can cause Cushingoid features? Why?

A

Carcinoid tumours

  • Secrete ACTH
75
Q

What condition has a 3-5% annual incidence of hepatocellular carcinoma?

A

Liver cirrhosis 2º to hepatitis C

76
Q

What antibiotics have an increased risk of C. Diff infection and resulting diarrhea?

A

Clindamycin + cephalosporins

77
Q

What is the treatment for patients with ascites ([protein] ≤ 15g/l)?

A

Oral ciprofloxacin or norfloxacin to protect against spontaneous bacterial peritonitis

78
Q

What is the typical presentation of duodenal ulcers?

A

Pain when hungry + relieved by eating

79
Q

What is the treatment of acute severe alcoholic hepatitis?

A

Corticosteroids

80
Q

What should be prescribed first-line to those with suspected hepatic encephalopathy?

A

Lactulose

Year 3 (7 decks)

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