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PPC2 Exam 3 > GI 1 > Flashcards

GI 1 Flashcards

1
Q

Osmotic Diarrhea (5)

A
  1. Caused by failure to absorb luminal solutes with resulting secretion of fluids and net water retention across osmotic gradient
    ex: Toddler’s diarrhea
  2. Volume <200 cc
  3. Fasting will result in resolution of the diarrhea
  4. Lower stool sodium and chlorides than secretory
  5. Osmolality greater this serum osmolality indicates osmotic diarrhea
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2
Q

Secretory Diarrhea

A
  1. Net secretion of electrolytes and fluids from intestine without compensatory absorption
  2. Increased volume of stool
  3. Fasting does not effect the diarrhea
  4. Higher stool sodium and chloride than osmotic
  5. Stool osmolality Na + K multiplied by 2
    * Electrolytes are pushed into the intestine leading to dehydration
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3
Q

Dysmotility Diarrhea

A

Occurs in a setting of intact absorption but transit time is changed and time allowed for absorption is minimized

Example short gut syndrome and small intestinal bacterial overgrowth (SIBO)

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4
Q

Inflammatory Diarrhea (2)

A
  1. Malabsorption of dietary nutrients which cause luminal osmotic gradient
  2. Flattened; less absorption need to give protein for balance again
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5
Q

Chronic Diarrhea (3)

A
  1. Lasting greater than 14 days
  2. Due to nutrient malabsorption and/or excessive fluid intake of juices or fructose containing drinks
  3. Use of probiotics is becoming increasing popular
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6
Q

Fecal Calprotein

A
  1. Calcium binding protein with bacteriostatic and
  2. Migration of neutrophils to the intestinal mucosa, which occurs during intestinal inflammation, including inflammation caused by inflammatory bowel disease.
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7
Q

Fecal Elastase (5)

A
  1. Elastase (EL1) concentration in stool
  2. Five times higher than pancreatic juice
  3. Reflects the amount of enzyme secreted from the pancreas.
  4. Diagnostic test for pancreatic function
    i. Chronic pancreatitis
    ii. DM
    iii. Cystic fibrosis
    iv. Cholelithiosis
  5. Whereas serum pancreatic levels quantify EL1 for the diagnosis or exclusion of an acute pancreatitis or an inflammatory episode of chronic pancreatitis or gallstone induced pancreatitis, the fecal EL1 level allows the diagnosis or exclusion of pancreatic exocrine insufficiency
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8
Q

Helicobacter pylori (4)

A
  1. Spiral-shaped gram-negative bacteria
  2. Highly motile because of multiple unipolar flagella.
  3. Microaerophilic and potent producers of the enzyme urease
  4. One of the most common infections found in humans worldwide; Largely hispanic practice, go back and forth between countries
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9
Q

H. Pylori Lab Tests (4)

A
  1. Urea Breath Test
    * Must administer urea, skipping pretreatment with citric acid decreases the accuracy
    * More likely to be negative if they are taking H 2 blocker or PPI
  2. Stool tests
    * HpSA tests Different commercial tests have different sensitivity and specificity (Leal et al., 2008)
    - Sensitivity: 86-95%
    - Specificity: 91-95%
  3. Monoclonal antibody tests (WB)
    - Sensitivity: 92-87%
    - Specificity: 98%
  4. Helicobacter serology: Limited role
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10
Q

H. Pylori Tx (3)

A
  1. TWO WEEK DURATION
  2. Triple therapy is considered to be the standard treatment for children
    * Amoxicillin, clarithromycin, and a proton pump inhibitor for 2 weeks.

Other regimens
3. Proton pump inhibitor combined with clarithromycin and metronidazole or amoxicillin and metronidazole.

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11
Q

Adaptive H. Pylori (6)

A
  1. Shape and motility
  2. Reduced oxygen requirement
  3. Adhesion molecules that are trophic to certain gastric cells
  4. Urease production.
  5. Bacterial urease converts urea to ammonium and bicarbonate, neutralizing gastric acid
  6. Protective in hostile, highly acidic gastric environment
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12
Q

What is Celiac Disease? (3)

A
  1. An autoimmune enteropathy associated with gluten intake in predisposed individuals
  2. Gluten is a protein component found in wheat, rye, and barley and potential cross-contamination with oats
  3. Ingestion of gluten leads to an autoimmune response causing chronic inflammation and damage to the villi of the small intestine
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13
Q

What occurs with Celiac Disease? (3)

A
  1. Gluten consumption will continue to cause inflammation of intestine and breakdown of the villi
  2. Subsequently leads to micronutrient deficiencies and associated complications
  3. May be asymptomatic or have signs and symptoms that mimic other diseases
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14
Q

CD Etiology (3)

A
  1. CD is a result of both genetic and environmental factors
  2. 97% of CD patients express the human leukocytic antigens HLA-DQ2 or HLA- DQ8
    * Must have exposure to gluten to develop CD
  3. Confirm dx with HLA testing
    * If Negative for these two then they generally do not have celiac disease
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15
Q

CD Categories (5)

A
  1. Classic
  2. Atypical
  3. Silent
  4. Potential form
  5. Latent
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16
Q

Classic CD Presentation (9)

A
  1. Age of presentation (6-24months)
  2. Chronic or recurrent diarrhea
  3. Abdominal distention
  4. Irritability/anorexia
  5. Failure to thrive
  6. Weight loss
  7. Abdominal pain
  8. Vomiting
  9. Constipation
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17
Q

When to consider CD? (7)

A

a. Short stature/ Delayed puberty
b. Osteoporosis
c. Dental enamel defects
d. Anemia
e. Brain calcifications/Ataxia/Seizures
f. Psychiatric and mood disorders
g. Delayed puberty

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18
Q

Atypical CD (4)

A
  1. Asymptomatic children identified because of positive family history
  2. Dental enamel defects
  3. Dermatologic manifestations (itching, Dermatitis Herpetiformis)
  4. Arthritis
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19
Q

Diseases associated with CD (10)

A
  1. Addison’s disease
  2. Graves disease
  3. Type 1 diabetes mellitus
  4. Myasthenia gravis
  5. Scleroderma
  6. Sjögren syndrome
  7. Lupus erythematosus
  8. Pancreatic insufficiency
  9. Turner syndrome
  10. Down syndrome/Williams syndrome
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20
Q

Eosinophilic Esophagitis: General (6)

A
  1. Characterized by family history of asthma, eczema or food allergies.
  2. Predominantly male disease
  3. Food antigen induced eosinophilia
  4. Male disease
  5. Needs endoscopy
  6. Pathology examination will show > 15 eosinophils per high power field
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21
Q

Eosinophilic Esophagitis: Presentation (5)

A
  1. food aversion and intolerance with vomiting
  2. Reflux refractory to medical management
  3. Food impactions
  4. Dsyphagia
  5. Failure to thrive
22
Q

Eosinophilic Esophagitis: Treatment (4)

A
  1. PPI: Can work sometimes but needs to be a 6-8 week course
  2. 6 food elimination diet
  3. Elemental formulas and reintroduction of foods can be another way to go
  4. COMPLICATIONS needs to stressed: stricture and stenosis
23
Q

Pediatric Nonalcoholic Fatty Liver Disease (4)

A
  1. Abnormal lipid deposition in hepatocytes (steatosis) in the absence of excess alcohol intake
  2. Ranges from simple steatosis to nonalcoholic steatohepatitis leading to fibrosis and cirrhosis
  3. Once cirrhosis is present, liver cancer can occur
  4. Elevated insulin level is a sensitive predictor of progressive liver disease and severe extra hepatic disease
24
Q

Pediatric Nonalcoholic Fatty Liver Disease Diagnosis (4)

A
  1. Diagnosed using serum aminotransferase in conjunction with negative markers for other signs of liver disease
  2. Heavy infiltration is required for abnormalities in serum aminotransferases to occur
  3. MRI findings of fatty liver infiltrates will be before changes in transaminases
  4. The higher the ALT levels, the higher the risk of NASH
25
Q

Liver function labs: ALT (6)

A
  1. Enzyme a more specific indicator of liver injury
  2. In young children, ALT can be elevated because of growth spurts.

Other possible causes for elevated ALT besides liver damage

  1. Rhabdomyolysis
  2. Hemolysis
  3. Muscular dystrophy
  4. Liver cancer
26
Q

Liver function labs: AST (4)

A
  1. Enzyme that is found in high concentrations in the liver
  2. Found in other parts of the body
  3. Heart
  4. Skeletal muscles.
27
Q

Liver function labs: Alkaline phosphatase (3)

A
  1. No bone disease–elevated in alkaline phosphatase and biliary obstruction
  2. Injury to bile duct epithelium
  3. Cholestasis.
28
Q

Alkaline phosphatase for bones (6)

A
  1. Elevations of alkaline phosphatase due to bone disease
  2. Paget disease of the bone
  3. Metastatic disease
  4. Hyperparathyroidism
  5. Rickets
  6. Sarcoma
29
Q

Laboratory Evaluation of NAFLD (8)

A
  1. ALP and GGT can determine if there is a cholestatic problem and the fractionated bilirubin is also important
  2. Abnormal Direct bilirubin is a value that >20% of the total bilirubin
  3. Serum aminotransferases are mild to moderately elevated usually less than 1.5 times normal
  4. ALT:AST ratio is usually > 1 Our patient was 2.15
  5. Total and direct bilirubin are normal
  6. GGTP and alkaline phosphatases mildly elevated in 50% of patient with NAFLD
  7. Hepatocellular injury is AST and ALT
  8. Bile duct problems is bilirubin, alkaline phosphatase, and gamma glutamyl transpeptide (GGT) as well as 5- n7u5cleotidase to identify cholestatic disease
30
Q

Autoimmune liver disease work-up (3)

A
  1. Antinuclear Antibodies
  2. Smooth Muscle Ab w/Reflex
    i. Related to liver cell damage
    ii. Sometime associated with viral hepatitis, active chronic hepatitis, primary biliary cirrhosis, and cryptogenic cirrhosis
  3. Soluble Liver Antigen
    i. Antibodies to SLA associated with AIH type 1
31
Q

Wilson’s Disease work-up

A

Ceruloplasmin (falselow if albumin is low)

32
Q

hemochromatosis work-up

A

serum ferritin

33
Q

Gold Standard for Steatosis

A

Liver biopsy

34
Q

Hepatobiliary iminodiacetic acid (HIDA) scan (4)

A
  1. Second line test
  2. 2 test
  3. Radiotracer taken up by liver and excreted
  4. If liver can’t take up tracer needs liver biopsy needed
35
Q

Dif Dx of NAFLD (6)

A
  1. Wilson’s
  2. Alpha-1antryspin deficiency
  3. Viral hepatitis
  4. Autoimmune hepatitis
  5. Fatty acid oxidation defect
  6. Medication
36
Q

Metabolic Syndrome Features (3)

A
  1. Increased risk of cardiovascular disease
  2. Associated with insulin resistance
  3. Type 2 diabetes mellitus
37
Q

NAFLD Treatment

A
  1. Slow weight loss through diet and exercise (1lb/week)
  2. Vitamin E monotherapy
  3. Orlistat
  4. Metformin

^The drugs require further studies

38
Q

Most common cause of GI bleed

A

Anal fissure in first two years of line; superficial tear of squamous lining, large constipation stool, child learns to hold back

39
Q

cow’s milk protein intolerance

A
  1. Cow’s milk and soy are most often responsible

2. Child appears healthy and has normal weight gain

40
Q

Allergic eosinophilic gastroenteritis (5)

A

a. RARE
b. Infiltration of GI tract with eosinophil
c. May have iron deficiency anemia, FTT
d. Watery diarrhea
e. Postprandial vomiting

41
Q

Polyps (3)

A
  1. Beyond two years of age, polyps are most common cause of painless lower gT Bleeding
  2. Poly will outgrow its blood supply and slough off of its stalk
  3. Usually left sided and solitary
42
Q

Familial polyposis (3)

A
  1. Peutz Jegher syndrome
  2. Multiple gastric polys
  3. Autosomal dominant inherited disorder characterized by intestinal hamartomatous polyps in association with a distinct pattern of skin and mucosal macular melanin deposition
43
Q

Ulcerative Colitis: General (2)

A
  1. Starts at rectum and involves various parts of rectum

2. Mucosal ulceration in the colon is continuous

44
Q

Genetic Syndromes associated with IBD (3)

A
  1. Turner syndrome
  2. Hermansky-Pudlak syndrome (recessive disorder - oculocutaneous albinism, abnormal platelet aggregation w/ bleeding diathesis, pulmonary fibrosis)
  3. Glycogen storage disorders (Type IB)
45
Q

Epidemiology of IBD (5)

A
  1. Western
  2. Risk for UC and CD is greater for Jewish people of Middle European origin
  3. Blacks less commonly affected than whites
  4. Males and females equally affected
  5. Increasing incidence in young children
46
Q

Crohn’s Disease (7)

A
  1. Cyclical disease
  2. Chronic inflammation w/ periods of remission followed by relapse
  3. Characterized by “skip lesions” or granulomatous inflammations occurring in any part of the intestine or GI tract
    * FROM MOUTH TO ANUS!; Focal and asymmetrical
  4. Often diagnosed in childhood and adolescence, most commonly in peripubertal years
  5. Height and weight are significantly reduced in CD with a low BMI in some children
    * Growth failure more common in CD than UC
  6. No hx of bloody stools
  7. Rarely occurs less than 5 years
47
Q

CD Ulcers and Involvement (10)

A
  1. Ulcers are worse in smokers
  2. Perianal is only seen in CD
  3. Granulomas not found in majority even though lesion is pathogonomic for CD
  4. Terminal ileum involvement in 20- 30%
  5. Colon only: 20%
  6. Both ileum and colon (40-50%)
  7. Multiple pseudopolyps
  8. Noncaseaating granuloma pathognomonic lesions
  9. Aphthous ulcer
  10. Intermittently normal mucosa
48
Q

CD History (5)

A
  1. Abdominal pain (99%)
    a. Pain is more severe
    b. Occurs at any time of day
    c. Wakens the child
    d. Right lower quadrant (ileal or ileocecal disease
    e. Periumbilical (colon or generalized small bowel disease)
  2. Weight loss (80%)
  3. Diarrhea (50-77%)
  4. Hematochezia (60%)
  5. Growth failure (30%)
49
Q

CD Physical Exam (4)

A
  1. Aphthous-like oral lesions
  2. Abdominal mass
  3. Peri-anal disease
    a. Fissures
    b. Anal tags
    c. Fistula
    d. Abscess
  4. Growth failure – Early feature with decrease in height velocity antedated GI symptoms
50
Q

Common nutritional deficiencies in children with active CD (11)

A

a. Calcium
b. Folate
c. Vitamin B12
d. Zinc
e. Selenium
f. Iron
g. Vitamin D
h. Vitamin K
i. Carbohydrates
j. Fats
k. Protein

PPC2 Exam 3 (14 decks)

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