GI 4 Flashcards

Question

Choledocholithiasis & Cholangitis: Describe these conditions

Answer 1

1) 15% of patients with gallstones have stones in their CBD; increases with age 2) Most originate in gallbladder; may form in bile duct after cholecystectomy 3) Symptoms (pain, jaundice, n/v)& cholangitis if obstruction present 4) May have h/o biliary pain or jaundice

Answer 2

1) RUQ & epigastric tenderness 2) Elevated aminotransferases (ALT, AST) > 1000 units/L 3) Elevated serum bilirubin & bilirubinuria (Coca-Cola urine; clay-colored stools) elevation of ALP 4) Hyperprothrombinemia (secondary to obstruction) 5) Charcot’s Triad (indicates biliary obstruction)– RUQ pain, fever/chills and jaundice if add AMS/ hypotension = Reynold’s Pentad

Answer 3

1) Elevated lipase +/- amylase 2) Leukocytosis/ fever

Answer 4

1) Bacterial infection in patients with biliary obstruction Organisms ascend (usually) from duodenum 2) Etiology: Bile duct stones, benign biliary stricture, malignancy, post-ERCP, post-surgical -a) Extrinsic: Pancreatitis, cystic duct stone, duodenal diverticulum, tumor in gb, CBD, or pancreas -b) Intrinsic: blood clots, parasites

Answer 5

Leukocytosis, cholestatic pattern of liver tests (elevated ALP & bilirubin)

Answer 6

1) Evidence of systemic inflammation with one of the following: -a) Fever and/or rigors -b) Lab evidence of inflammatory response (ex/ abnormal WBC, increased CRP) 2) AND both of the following: -a) Evidence of cholestasis -b) Imaging shows biliary dilation or evidence of the underlying etiology (stricture, stone, or stent)

Answer 7

Admission, IV hydration/correct electrolyte abnormalities, analgesia, observe for organ dysfunction & shock

Answer 8

1) IV Antibiotics: tailored to culture & susceptibility results 2) Biliary drainage: timing based on severity; most within 24-48 hours -Procedure of choice: Endoscopic sphincterotomy (ERCP) with stone extraction and/or stent insertion -ERCP failure or not possible: biliary drain placement (EUS, PTC) or surgical drainage – patient must be hemodynamically stable to undergo procedure.

Answer 9

1) U/S: dilated bile ducts 2) HIDA: impaired bile flow (“non vis”) 3) EUS, CT & MRCP: patients with intermediate risk -ERCP with sphincterotomy & stone extraction is procedure of choice if a high likelihood that obstruction caused by stone. Or ERCP with stent placement if caused by mass.

Answer 10

1) Endoscopic (ERCP) sphincterotomy & stone extraction 2) Cholecystitis: Laparoscopic cholecystectomy within 72 hours 3) Without cholecystitis: Laparoscopic cholecystectomy within 2 weeks

Answer 11

1) Gluten intolerance 2) Lactose intolerance

Answer 12

1) Syndrome of symptomatic response to gluten ingestion with neg Celiac testing 2) Abdominal pain/cramping, bloating, bowel changes 3) Hours to few days after ingestion of gluten (compare with wheat allergy & Celiac)

Answer 13

1) Placebo or FODMAPs- group of fermentable carbs and sugars that cause many unpleasant GI symptoms 2) NCGS, FODMAP reduction, and/or placebo

Answer 14

1) Celiac disease is a small bowel disorder characterized by mucosal inflammation, villous atrophy 2) Diagnosed by endoscopic biopsies of the small bowel and serum tissue transglutaminase (tTG)-IgA and genetic testing

Answer 15

1) Chronic or recurrent diarrhea or constipation, malabsorption, unexpected weight loss, abdominal pain, distension, or bloating. 2) Fatigue, recurrent headaches, low birthweight offspring, dental enamel hypoplasia, metabolic bone disease and premature osteoporosis, idiopathic peripheral neuropathy, or pubertal delay.

Answer 16

1) Test for Celiac disease & IgE-mediated wheat allergy 2) Test before eliminating gluten (false negative tests) 3) No test to distinguish NCGS from IBS 4) Anti-Gliadin Ab or other biomarkers cannot identify NCGS 5) Relies on patient-reported symptoms, food diary, or gluten-challenge.

Answer 17

1) Patient education before gluten-free diet 2) Involve dietician

Answer 18

1) Failure of the small bowel to absorb ingested lactose due to lactase deficiency 2) The intestinal brush border (villa) lactase enzyme activity is lower than that of normal individuals 3) Clinical syndrome in which ingestion of lactose or lactose-containing food (milk, milk products) causes symptoms such as abdominal cramping, bloating, flatulence, pain and diarrhea

Answer 19

1) Higher prevalence in African Americans, Hispanics, Asians, Asian Americans, & Native Americans -Lowest prevalence in Europeans & European Americans 2) Prevalence low in children younger than six years & increases with age

Answer 20

**Other gastrointestinal disorders that affect the proximal small intestinal mucosa:** Crohn’s disease, celiac disease, viral gastroenteritis, giardiasis, short bowel syndrome, & malnutrition

Answer 21

1) Malabsorbed lactose is fermented by intestinal bacteria, producing gas (hydrogen/ methane)& organic acids 2) Nonmetabolized lactose & organic acids result in an increased stool osmotic load with an obligatory fluid loss=diarrhea

Answer 22

Hydrogen breath test: 1) Ingest 50 g lactose 2) Positive test = rise in breath hydrogen >20 ppm in 90 minutes

Answer 23

1) Hydrogen breath test 2) Empiric trial of a lactose-free diet for 2 weeks -Resolution of symptoms (bloating, flatulence, diarrhea) suggests lactase deficiency

Answer 24

1) Goal is to achieve patient comfort 2) Define “Threshold of intake” at which symptoms occur -High lactose foods: milk, ice cream, cottage cheese -Aged cheeses have lower lactose content -Unpasteurized yogurt contains bacteria that produce lactase & generally well tolerated 3) Spread intake of dairy throughout the day

Answer 25

1) Widely available milk pretreated with lactase (making it 70-100% lactose-free) and non-dairy milks 2) Lactase enzyme replacement available OTC 3) Restriction or elimination of milk products **may increase risk of osteoporosis** -Consider calcium supplementation

Answer 26

1) Bacterial deconjugation of bile salts-->decreased fat absorption-->steatorrhea & malabsorption of fat-soluble vitamins (A, D, E, K) -Reduced absorption of B12 & carbohydrates 2) Epithelial cells & brush border

Answer 27

Diarrhea & increased flatulence

Answer 28

1) Overgrowth of bacteria in stomach & proximal small bowel (mostly aerobic) 2) Predominantly anaerobic

Answer 29

1) Gastric achlorhydria (absent or low HCl) 2) Anatomic abnormalities of the small intestine with stagnation 3) Small intestine motility disorders (ex/ IBS, exercise, viruses…) 4) Gastrocolic or colo-enteric fistula

Answer 30

Prevalence is unclear, but the incidence increases with age.

Answer 31

1) Can be asymptomatic 2) Flatulence, weight loss, abdominal pain, diarrhea, & sometimes steatorrhea 3) Vitamin & mineral deficiencies

Answer 32

1) Stool sample to confirm steatorrhea 2) Labs: vitamin A, D, B12, serum iron 3) Noninvasive- breath hydrogen & methane tests 4) CTE, MRE, barium x-ray: rule out mechanical factors 5) Empiric antibiotics >

Answer 33

1) Treat underlying anatomic defect, if applicable 2) Empiric PO antibiotic x 1-2 weeks a) **Rifaximin (xifaxan) 1 PO TID for 14 days** *b) Ciprofloxacin 500 mg PO BID c) Amoxicillin clavulanate 875 mg PO BID d) Metronidazole + Bactrim DS 250mg PO TID + 160/800 BID* 3) Recurrent symptoms off antibiotics: Cyclic therapy (1 week out of 4)

Answer 34

1) PT/INR, PLT, & albumin are synthetic markers 2) Prothrombin time (PT) – usually calculated & reported as international normalized ratio (INR) 3) Bilirubin 4) Gamma-glutamyltransferase (GGT) 5) Alanine aminotransferase (ALT) 6) Aspartate aminotransferase (AST) 7) Alkaline phosphatase

Answer 35

Elevated bilirubin level (nl <1.0) with normal serum aminotransferases (nl ALT 7-55, nl AST 10-40, nl alk phos 44-147) and alkaline phosphatase

Answer 36

1) Hereditary/genetic, mild, harmless disorder of bilirubin processing. 2) Will cause isolated mild hyperbilirubinemia (increases with fasting) stays consistent throughout life, U/S=nl

Answer 37

1) Both hepatocellular AND cholestatic liver disease 2) Hepatocellular diseases

Answer 38

1) Low albumin: a chronic process (eg, cirrhosis or cancer) 2) Normal albumin: a more acute process (eg, viral hepatitis or choledocholithiasis)

Answer 39

1) Vitamin K deficiency due to prolonged jaundice & intestinal malabsorption of vitamin K 2) Significant hepatocellular dysfunction.

Answer 40

1) Metabolic dysfunction-associated steatohepatitis (MASH) 2) AST>ALT

Answer 41

1) Alcoholic fatty liver disease: AST <8x ULN; ALT <5x ULN 2) Metabolic dysfunction-associated fatty liver disease (MAFLD): AST & ALT <4xULN 3) Acute viral hepatitis or toxin-related hepatitis with jaundice: AST & ALT >25x ULN 4) Ischemic hepatitis (ischemic hepatopathy, shock liver, hypoxic hepatitis): AST & ALT >50x ULN (LDH also often markedly elevated)

Answer 42

1) **Chronic hepatitis C:** variable; normal-to-2xULN (rarely >10xULN) 2) **Chronic hepatitis B:** variable; normal-to-2xULN (>10x ULN during acute exacerbations)

Answer 43

Liver tests >10xULN, prolonged PT (INR >1.5)

Answer 44

1) Frequently have acute hepatitis 2) May have underlying chronic liver disease (ex/ hepatitis B) AST/ALT >5,000 U/mL usually due to ischemic or drug-inducted hepatitis; also rhabdomyolysis & heat stroke

Answer 45

Alcoholic fatty liver a) Alcoholic hepatitis b) Alcoholic cirrhosis

Answer 46

1) Increased lipogenesis 2) Impaired beta-oxidation & tricarboxylic acid cycle (TCA) activity (makes necessary components for ATP production) 3) Increased expression of key lipogenic enzyme regulators (ie, makes more fat)

Answer 47

1) Toxic metabolic products of alcohol (acetaldehyde) and alcohol damage hepatocytes 2) Acute or chronic inflammation & parenchymal necrosis of the liver induced by alcohol 3) Most common precursor of cirrhosis in U.S

Answer 48

1) Abstinence from alcohol is ESSENTIAL 2) Monitor for alcohol withdrawal (hospitalize patients) 3) Provide adequate nutrition 4) Micronutrient supplementation (folic acid, thiamine, zinc) 5) Avoid nephrotoxic drugs in patients with severe hepatitis 6) Need vaccination for hepatitis A & B

Answer 49

1) In patients who have not yet progressed to cirrhosis, abstinence may allow for reversal of some of the hepatic changes induced by alcohol. 2) In patients with cirrhosis, alcohol abstinence decreases the risk of hepatic decompensation and improves survival. Patients should be referred for treatment for alcohol abuse or dependence to increase the likelihood of successful abstinence.

Answer 50

Drugs are common cause of liver injury >1000 medications & herbal supplements implicated ~10% of all cases of acute hepatitis

Answer 51

Adults > children, F > M, alcohol use disorder, malnutrition

Answer 52

DILI (drug induced liver injury)

Answer 53

1) Disproportionate elevation ALT & AST compared with ALP + Sr bilirubin elevation + Abnormal synthetic liver function tests (INR, PT) 2) Disproportionate elevation ALP compared with ALT & AST + Sr bilirubin elevation + Abnormal synthetic liver function tests

Answer 54

Predictable, dose-related severity, latent period, susceptibility in all (ie, acetaminophen, alcohol, mushrooms)

Answer 55

(Most severe cases): unpredictable, less dose-related, variable latency, ~associated with allergic reaction (ie, amiodarone, ASA, diclofenac, levofloxacin)

Answer 56

Exacerbation of pre-existing liver disease (ie, HBV reactivation with immunosuppressive therapy for non-hepatic autoimmune disease)

Answer 57

1) Many asymptomatic 2) Symptomatic patients: malaise, low-grade fever, n/v, RUQ pain, jaundice, acholic stools, dark urine 3) Pts with cholestasis may have pruritis > scratching > excoriations 4) Possible hepatomegaly 5) Severe cases: coagulopathy, hepatic encephalopathy (indicating acute liver failure) 6) Chronic DILI: fibrosis --> cirrhosis

Answer 58

False; many are asymptomatic

Answer 59

1) Fever, rash, pseudomononucleosis 2) Toxicity to other organs (ie, bone marrow, kidney, lung, skin )SJS,) blood vessels)

Answer 60

1) Liver biopsy not needed if testing negative & history suggests drug associated with hepatic injury 2) Liver biopsy indications: -Diagnosis remains uncertain -Severity of injury uncertain -Clinical evidence of chronic liver disease

Answer 61

1) Thorough history (emphasis on drugs, herbals, supplements) 2) Labs to assess for other causes of hepatic injury 3) If cholestasis, imaging to assess for biliary obstruction 4) Liver biopsy not needed if testing negative & history suggests drug associated with hepatic injury

Answer 62

1) No, none 2) Drug exposure preceded onset -Underlying liver disease excluded -D/c of drug results in improvement in liver injury -Rapid & severe recurrence may occur with repeated exposure (re-challenge not advised)

Answer 63

1) Hepatitis: viral infection, alcoholic liver disease, MAFLD, AIH… 2) Cholestasis: biliary obstruction… 3) Steatosis: MAFLD, MASH, alcoholic liver disease, acute fatty liver of pregnancy 4) Granulomatous hepatitis: infections, sarcoidosis, other primary liver diseases

Answer 64

1) Withdrawal of offending drug 2) Assess severity & monitor for acute liver failure 3) N-acetylcysteine for acetaminophen toxicity 4) L-carnitine for valproic acid overdose 5) Possible role of glucocorticoids with hypersensitivity reactions 6) Bile acid sequestrant for cholestatic liver disease with pruritis 7) Serial biochemical measurements until liver tests normalize 8) **Hepatology and/or GI consultation if concern for acute liver failure, signs of chronic liver disease, or if diagnosis uncertain after eval

Answer 65

1) N-acetyl-p-aminophenol (APAP; paracetamol) 2) Acute liver failure (ALF) 3) 28%

Answer 66

Stage I (0.5 to 24 hours) Stage II (24 to 72 hours) Stage III (72 to 96 hours) Stage IV (four days to two weeks

Answer 67

1) Nausea, vomiting, diaphoresis, pallor, lethargy, & malaise 2) Some asymptomatic 3) Labs typically normal 4) AST & ALT may rise in 8-12 hours

Answer 68

1) Stage I symptoms resolve, appear to improve 2) Most have elevated ALT & AST within 24 hours; all within 30 hours 3) RUQ pain, liver enlargement & tenderness 4) Elevations of PT & total bilirubin, oliguria, & renal function abnormalities may become evident 5) Some cases of acute pancreatitis

Answer 69

1) *Abnormal liver tests peak; stage I Sx return 2) Jaundice, confusion (hepatic encephalopathy) 3) Marked elevation in hepatic enzymes, hyperammonemia, & bleeding diathesis 4) May develop signs of severe hepatotoxicity; acute renal failure in 10-25% 5) *Death usually occurs in this stage, usually from multi-system organ failure

Answer 70

1) Recovery phase 2) Begins by day 4; ends by day 7 3) Symptoms & labs may take several weeks to resolve 4) Recovery is complete; chronic hepatic dysfunction is not a sequela of acetaminophen poisoning

Answer 71

1) Obtain a good history: dose, intent of use, pattern of use, time of ingestion, and comorbid conditions 2) Serum acetaminophen concentration should be measured in every patient suspected of an intentional or unintentional overdose 3) Serum concentration should also be obtained four hours following the time of acute ingestion or presentation

Answer 72

1) Electrolytes, BUN & Cr, Sr total bilirubin, PT/INR, AST, ALT, lipase, & urinalysis 2) Toxic screening of blood & urine for other ingested drugs

Answer 73

1) Modified Rumack-Matthew nomogram 2) Line indicates level at which toxicity is possible after acetaminophen overdose

Answer 74

N-acetylcysteine (NAC)

Answer 75

1) 20-hour IV protocol (most common) 2) Simplified 20-hour IV protocol (2 bag instead of 3 bag regimen) 3) 72-hour oral protocol 4) 12-hour protocol

Answer 76

Total of 300 mg/kg over 20 to 21 hours