GI Flashcards
ROME criteria for constipation
2 or fewer defectations in the toilet per week, at least one episode of fecal incontiencne per week, history of retentive posturing or excssive volitional stool retntion, history of painful or hard bowel movements, presence of a large fecal mass in the rectum, history of large diameter stool
is digital disimpactions recommended
No
Is there evidence for docusate in constipation
no
recommended fiber titntake for children
0.5g/kg/day
is there evidence for probiotics for treating onstipation
no
can you use mineral oil in infants
no due to risk for aspiration
how long to treat children wtih constipation for
minimum 6 months
What % of normal newborns pass meconium within 24h of lifw
90%
How to manage rumination disorder
reinforce the correct eating behaviour while minmizing attention to rumination diaphragmatic breathing adn postprandial gum chewing, no pharm evidence
functional GI disorder characterized by effortless regurgitation of ingested food into the mouth after moth meals
Rumination disorder
ROME 4 criteria for urminatinos disorder
○ Persistent or recurrent regurgitation of recently infested food into the mouth with subsequent spitting or mastication and swallowing
○ Regurgitation is not preceded by retching
○ Clinical features not required but supportive of rumination syndrome: effortless regurgitation not preceded by nausea, recognizable food that may have a pleasant taste, cessation of rumination when material becomes acidic
○ Should not occur during sleep (peds)
Should not respond to standard medical therapy for reflux (peds)
Standard formula calories
29kcal/30ml
What is cronobacter sakazakii related to
powdered formula in premature infants
INdications for soy formula
galactosemia, preference for a vegetarian diet and hereditary lactase deficiency
What is goats milk low in
folate
At what age should you start screening for NAFLD
all obese children 9-11 and for overweight children with additional risk factors
screening test for NAFLD
ALT
What is the most common cause of inherited colorectal cancer
Lynch syndrome
How is lynch syndrome inherited
AD
What types of cancer increased risk for with lynch syndrome
- CRC, endometrial cancer, sebaceous neoplasms, ovarian cancer, pancreatic cancer, brain cancer
Autosomal dominant syndrome with multiple hamartomas polyps in the GI tract, mucocutaneous pigmentation and an increased risk of GI and non GI cancer
Peutz Jeghers
How to diagnose Peutz Jeghers
histologically proven hamartomatous plyps if 2 of the following are met: positive family history wiht AD inheritenace pattern, mucocutaenous hyperpigementation and small bowel polyposiss
When should surveillance begin in Peutz Jeghers
Around age 8 or when symptoms occur with upper
and lower endoscopy
How is FAP inherited
AD
Types of cancer with FAP
- Colorectal, thyroid, stomach and small intestinal cancer, hepatoblastoma
Gene for FAP
APC
Does breastfeeding reduce the risk for celiac disease
No
Does earlier introduction of gluten impact cumulative incidence of celiac disease
No
Extraintestinal manifestations of celiac disease
iron deficiency anemia, short stature, osteoporosis, delayed pubtery, arthritis and arthrlagia, epilepsy wth bilateral occipital calcifications, peripheral nueropathies, isolated hypertransaminasemia, dental enamel hypoplasia and pathous stomatitis
Who should you test for celiac disease
unexplained abdo symptoms persistent
faltering growth
prolonged fatigue
unexpected weight loss
severe or persistent mouth ulcers
unexplained iron, vitamin B12 or foalte deficiency
T2DM
autoimmune thyroid disease
IBS
first degree relative of people with celiac disease
dermatitis herpetiformis
Next steps for patient with IgA TTG autoantibodies <10 times upper limit of nornmal
scope adn biopsy
TTG >10 times upper limit of normal
HLA and EMA, if positive, celiac disease
How to test for celiac disease in asymptomatic patients
duodenal biopsies
biopsy finding in celiac disease
villous atrophy
Treatment for rumination disorder
Chewing gum
Diaphragmatic breathing
Work-up for rumination
Exclude mechanical obstruction with up GI endoscopy and if uncertain CT/MR enterorrpathy
Upper endoscopy is usually normal
Do NOT need gastric emptying study for diagnosis, majority have normal gastric emptying
Cronobacter sakazakii is associated with
Contaminated formula
INdications for soy formula
Galactosemia, preference for vegetarian diet, hereditary lactase deficiency
Is there value for soy formula for colic, fussiness or atopic disease
No
Goats milk is low in
Folate
Preferred screening test for NAFLD
ALT
Is there a specific diet recommended for treatment of NASH
No
Most common inherited cause of colorectal cancer
Lynch syndrome
Types of cancers with Peutz-Jeghers
Colorectal, brain, reproductive tumors
Precancerous lesions within the surface epithelium of the intestine displaying various degrees of dysplasia
Andeomatous polyps
Cancers at risk for in FAP other than colon in young and older patients
Hepatoblastoma in BBs
Follicular or papillary thyroid cancer in teens
Gardner syndrome
Also APC mutations
Multiple colorectal polyps
Turcot syndrome
Colorectal polyposis and primary brain tumors (medulla lasts a)
How often to screen patients with FAP
Every 1-2 years with scope, every year once polyps identified
Treatment for FAP
Prophylactic protocols to my
Most common GI malignancy in pediatric population
Lymphoma
What to consider in patient older than 3 with intussuception
Lymphoma
How to diagnose carcinoid tumor
Elevated urinary 5-hydrocindoleacetic acid
Acute liver failure definition
Biochemical evidence of acute liver injury (<8 weeks duration) with no evidence of chronic liver disease and hepatic based coagulopathy defined as INR > 1.5 with encephalopathy not corrected by vit K and INR > 2 without encephalopathy
Causes of neonatal acute liver failure
Gestational alloimmune liver disease, tyrosinemia, familial HLH, congenital HSV infection
Who is at high risk with Hep E infection
Pregnant women
MArkers of autoimmune hepatitis
ANA, ASMA, liver-kidney microsomal antibody or soluble liver antigen and possible elevated IgG
What does liver biopsy show in autoimmune hepatitis
Interface hepatitis and plasma cell infiltrate
What is GALD
Gestational alloimmune liver disease
Maternal IgG antibodies bind to fetal liver antigens and activate the terminal complement cascade resulting in hepatocyte injury and death
What does acute liver failure look like on biopsy
Patchy or confluence massive necrosis of hepatocytes and multilobular or bridging necrosis
What is centrilobular damage associated with in liver failure
Tylenol overdose or circulatory shock
Microvesciular fatty infiltrate of hepatocytes is observed in
Reye syndrome, B oxidation defects and tetracycline toxicity
What is an ominous sign in liver failure
Rapid decrease in liver size without clinical improvement
Stages of hepatic encephalopathy
Stage 1- period of lethargy and euphoria, day night reversal, normal EEG
Stage 2- drowsiness, inappropriate behavior, agitation, wide mood swings, disorientation, asterisks, incontinence
Stage 3- stupor but arousable, confused, incoherent speech, asterisks, hyper reflexes, rigidity, markedly abnormal EEG
Stage 4- coma, Areflexia
Does serum aminotransferase activity correlate with the severity of illeness in liver failure
No
Antidote for liver failure in a Anita mushrooms
Penicillin
GALD treatment
Double volume exchange transfusion to remove existing reactive antibody followed immediately by IgG 1g/kg
Treatment for hyperammonemia
Lactose or rica I’m in
Increased mortality risk factors in acute liver failure
Age <1, stage 4 encephalopathy, INR >4, low factor 5 levels and need for dialysis before transplant
Is pre0transplant bill or height of hepatic enzymes predictive of post transplant survival
No
How many kids get aplastic anemia after idiopathic acute liver failure
10%
What nutritional deficiencies are Vegas at risk for
Iron, B12
Insuf. Fatty acids
Calcium and vitamin D
Pellagra
Vitamin B3 deficiency
Raw skin, sun exoposed rash, diarrhea, dementia
Who gets B3 deficiency (pellagra(
Alcoholics, anorexia, bariatric surgery or mlabsorptive disease
What medication can cause pellagra
Isoniazid
Beriberi
Thiamine deficiency
What does infantile beri beri look like
Fulminant cardiac syndrome with cardiomegaly, tachycardia, loud piercing cry, cyanosis, dyspnea, vomiting, pulmonary hypertension
Who can get beri beri
Infants on soy based formulas
Is CVS more common in girls or boys
Girls
Criteria for CVS
At least 5 attacks in any interval or 3 i 6 months
Episodic attacks of nausea/vomiting lasting 1h-10d days and occuring at least one week apart
Stereotypical pattern in the patient
Vomiting during attacks occurs at least 4 times per hour for at leas tone hour
Return to baseline bttween episodes
Not attributed to another disorder
SCreening test in CVS
Lutes, glucose, upper GI radiographs to exclude Mal rotation
Do you need routine endoscopy in CVS
No unless they have chronic symptoms in between or large hematemesis
Which patients with CVS should be evaluated for a metabolic disorder
Under 2
Vomiting associated with interucrrent illness, fasting, increased protein intake
Neuro findings
Labs like hypoglycemia, anion gap, alkalosis, hyperammonemia
Who should get prophylactic therapy in CVS
Episodes more than every 1-2 months, severe enough to require repeat hospitalization, fail to respond to abortive therapy
Treatment for CVS
Cyproheptadine under 5
Amitryptiline over 5
Propranolol is second line for both age groups
RF with cyprohepatdine
Enhanced appetite
What do you have to monitor in patient on amitryptiline
QTC
Vitamin A deficiency manifestations
Eye lesions, can be late finding with corneal keratinization, susceptibility to infection, xeropthalmia, Bitot spots (plaques on conjunctival membrane)
Major cause of blindness
Vitamins B6 deficiency
Some seizure syndromes are dependent on vitamin B6 so should give to all babies with seizures
Can have skin lesions, gloss it is, seborrheic dermatitis
Does breast milk contain vitamin C
Yes
Scurvy manifestations
Irritability, MSK pain, tenderness in legs, leg swelling, pseudo paralysis, rosary at Costco Cho drawl junction
Petechiae, purport, ecchymoses, gum bleeding
Poor wound healing, arthralgia and muscle weakness
Upper limits for vitamin D in younger children <1 and adults
1000 and 2000
Vitamin D overdose
Nausea, vomiting, poor feeding, cosntipation, abdo pain, pancreatitis, hypertension, decreased QT interval
Lethargy, hypotonia, confusion, psychosis, hallucinations
Esophagitits with dysphasia is an indication for
Scope
Triad for Chloedocal cyst
Abdo pain, jaundice and palpable mass
What is choledocal cyst associated with
Increased cancer risk mostly cholangiocarcinoma but also pancreatic and gallbladder cancers
Type 5 choledocal cyst
Caroli disease
Is biliary atresia usually associated with other abnormalities
No
Biliary atresia with splenic malformation syndrome
Associated with situs I versus, Mal rotation, polysplenia, interrupted inferior vena cava and congenital heart disease
Poor prognosis
Triangular cord sign
Seen in biliary atresia which represents a cone shaped fibrin mass cranial to the bifurcation fo the portal vein
Biliary atresia biopsy findings
Bile duct Al proliferation, presence of bile plugs and portal or perilobular edema and fibrosis with the basic hepatic lobular architecture intact
When is success rate for kasha better
Before 8 weeks of age
What vitamin deficiency can you get with biliary atresia
Vitamin E with neuromuscular syndrome inc progressive areflexia, cerebella ataxia, ophthalmologist and decreased vibratory sensation
achalasia cause
Progressive degeneration of ganglion cells in myenteric plexus in the esophageal wall leading to failure of relaxation of the LES accompanied by a loss of peristalsis in the distal esophagus
Chagas’ disease
Can look like loss of intramural ganglion cells similar to achalasia
How to diagnose achalasia
Esophageal nanometers showing incomplete relaxation of the LES and aperistalsis in the distal 2/3 of the esophagus
What should be performed in achalasia
Should also do endoscopic evaluation to exclude malignancy at esoagogastric junction that can mimic achalasia
How many eosinophils to see on endoscopy in EOE
Over 15 per HPF
Lab abnormalities in EOE
Pierpheral eosinophilia and elevated IgE
Serum trypsinogen used for
Exocrine pancreatic insufficiency will be low in CF and Shwachmann diamond
Diagnostic test for protein losing enteropathy
Stool A!AT
Mechanism of injury in button battery
Generation of hydroxide radicals in the mucosa resulting in caustic injury from high ph instead of electrical thermal injury
How long until necrosis starts in button battery ingestion
15min
Who is at increased risk for injury from button battery ingestion
Children younger than 5 with battery over 20mm ingested and multiple button batteries
Who to observe with gastric button battery
Duration of ingestion <2h, size of battery < 20mm, absence of clinical symptoms and child over 5 years
How to manage large button battery
Should be checked by radiograph and removed if in place after 48h
Where is most common site for perforation with sharp objects
Ileocecal region
How to manage esophageal food impacting
Can Delane removal up to 24h, should have biopsies done at time of scope
Repeat X-ray before scope to remove because often it will move on its own
No good evidence for glucagon only try if can’t get a scope right away
What coin size likely to be impacted
Over 23.5mm (basically bigger than a quarter)
How to manage gastric coins
Manage expectantly,
Monitor stools with repeat X-rays in 1-2 weeks
Consider removal if retained longer than 2-4 weeks
What kind of intussuception do you get post-operatives surgery
Ileoileal
Who gets ileoileal intussuception
Post-op and HSP, HSP often resolves on its own without treatment
Juvenile polyposis syndrome
Autosomal dominant
Hamartomatous/juvenile polyps
Increased risk of GI malignancy
Criteria for juvenile polyposis syndrome
5 or more juvenile polyps in the colon or rectum OR
JPs in other parts of the GI tract
OR
Any number of junvenile polyps and positive family history
Mutation for juvenile polyposis
SMAD4. BMPR1A
What are patients with SMAD4 mutation in juvenile polyposis at risk for
Hereditary hemorrhagictelangectasia
What are you at increased risk for in Peutz Jeghers syndrome
Intussuception and malignancy
Who should you test for H. Pylori
Patients with symptoms of PUD
NOT those with functional abdominal pain
Refractory iron deficiency
Chronic ITP
NOT short stature
How long to wait before H pylori testing when on PPI and antibiotics
2 weeks of PPI and 4 weeks of antibiotics
How many gastric biopsies for H pylori
6
Who to treat with H pylori
Patients with PUD, ulceration, scarring and H pylori
Maybe natural modularity, gastritis, incidental finding???
Treatment for H pylori
PPI, clarithromycinand amoxicillin for 14 days
If resistant to cla—> PPI, Amos, metronidazole
If resistant to met —> PPI, Amos, clarithro
If resistant to clarithromycin and metronidazole—> PPI, Amos, metronidazole with high dose Amos or bismuth based
Risk factors for drug induced hepatopathy
Age (very young)
Abnormal renal function
Concurrent use of other hepatotoxic agents
Drug interactions
Pre-existing live disease
Most common injury pattern in drug induced acute liver failure
Hepatic Elul are
Management of acute liver failure
Consider PICU admission if encephalopathy or INR >4
Frequent lab monitoring
Avoid bentos unless patient intubated and ventilated
Avoid hypoglycemia
Restrict TFI
Liver transplantation
Kings college criteria - acetaminophen
Arterial ph < 7.3
INR >6.5 and serum creatinine > 300 and grade 3-4 hepatic encephalopathy
Kings college criteria for non0aceatamonphen
INR > 6.5
OR
3 of the following:
Age <10 or >40
Serum bilirubin >300
INR >3
Duration of jaundice to HE > 7 days
Etiology: non hepatitis A/B or idiosyncratic drug reaction
NAtural history of autoimmune liver disease
50% mortality at 5 years and 90% at 10 years
Which type of autoimmune hepatitis is acute liver failure more common with
Type 2, anti LKM-1 positive
Alagille syndrome mutation
JAG1 in up to 94% of patients
NOTCH2 in some JAG1 negative patients
Alpha 1 anti trypsin inheritance
AD
A1AT clinical presentation
Often notice first 1-2 months
Neonatal hepatitis with priorities, increased direct bile, ALT/AST/GGT, hepatomegaly
Can have alcoholic stool
Spontaneous regression common, only small % develop cirrhosis
Wilson disease inheritance
AR
Wilson disease presentation
10-25% psychiatric disturbance initial presentation
Ataxia, reduced functional capacity, tremor
Bradykinesia, rigidity, cognitive impairment
Dyskinesia dysarthria
Dystopia, dysphasia, fixed grin, facial grimacing, stereotypic gestures
Choreiform, athetoid movements rare
Seizures, ingrained headache
Sensory function, intelligence unaffected
Proximal tubular dysfunction
DAT negative hemolytic anemia
Liver failure
Gilbert syndrome
Recurrent episodes of jaundice, otherwise asymptomatic
Triggered by dehydration, fasting, intercurrent illness, menstruation, over exercise
Unconjugated hyperbilirubinemia
Increased risk cholelithasis
What causes GIlbert syndrome
Defect in promotor gene encoding uridine diphosphoglucuronate-glucuronosyltranferase 1A! 9UGT1A1) that conjugated bilirubin to glucuronic acid
How to diagnose Hep A
Hep A IgM
IgG= pst infection or immunization
HbsAg Negative
AntiHBc Positive
Anti-HbS Positive
Immune due to past infection
HbsAG NEgative
Anti0HbC Negative
Anti-HbS Positive
Immune due to vaccination
HBsAg Positive
Anti-HBc Negative
Anti-HBs negative
Acutely infected
HBsAg Positive
Anti-HBc POsitive
IgM anti-HBc Negiatve
Anti-HBs Negative
Chronically infected
HbsAg Negative
Anti-HBc POsitive
Anti-HbS Negative
Resolved or resolving acute infection
Low level chronic infection
How many children exposed to Hep C develop chronic infection
60-80%
How to diagnosed Hep C in infants
HCV Ab not recommended before 18 months (will be moms)
HCV RNA recommended for diagnosis < 18 months but should be obtained > 2 months
ACtive infection confirmed with HCV RNA
Signs of EOE on scope
Esophageal furrowing, rings (trachealization), exudates, linear furrowing
Treatment options for achalasia
pneumatic dilation
Laparaoscopic surgery/Kyoto my
Botulism toxin injection into LES
Pharmacological therapies
Per-oral endoscopic Kyoto my
Who should get a funds
Life threatening complications
Symptoms refractory to therapy after evaluation with alternate diagnoses
Chronic conditions with significant risk of GERD complications
Need for chronic pharmacotherapy to control signs and symptoms
Risks of fundo
Gas blot, early satiety, dysphasia, retching, dumping syndrome, worse aspiration from esophageal stasis, wrap slip
Who to test for celiac disease
- persistent G symptoms
Non GI symptoms of celiac disease (dermatitis herpetiformis, dental enamel hypo plasma, osteoporosis , short stature, delayed puberty, IDA resistant to oral iron)
Those with associated conditions
Associated conditions of celiac disease
T1Dm
autoimmune thyroid it is
Down syndrome
Turner syndrome
Williams syndrome
Selective IgA deficiency
First degree relatives of celiac patients
Celiac disease monitoring
TTG after 6 months of gluten free diet to demonstrate decrease in antibody
TTG if symptoms
TTG yearly in asymptomatic individuals
Associated conditions with crowns disease
Turner syndrome
GSD 1b
What 5 things would make you think this is NOT uC
Fistulizing disease
Perinatal skin tags
Deep ulcerations, cobble stoning or stenosis
Evidence of J or illegal inflammation
Granuloma anywhere in the GI tract
Why do patients with IBD get kidney stones
Terminal ideal disease leads to malabsorption of fatty acids, fatty acids enter colon and bind calcium, frees up oxalate for absorption leading to enteric hyperoxaluria
What screening to do in patient with newly diagnosed IBC
Stool infectious studies
Baseline infectious serology and manitou
CXR
EGD and colonoscopy
Fecal cal
Small bowel imaging
Side effects ASA
Headaches, N/V/ anorexia, yellow/orange coloring, abdo pain, joint pain
Pericarditis, pneumonia is, SJS, hepatitis, nephritis, keukopenia, pancreatitis
Azathioprine SE serious
BM suppression, immunosuppressive, pancreatitis, hepatitis, cancer
Methotrexate side effects
Hair loss, mouth sores, photosensitivity,y teratogenic, anti-folate
BM suppression, immunosuppressive, hepatotxocity, nephrotoxicity, lung disease
5 immunosuppressive medications to treat BD
Biological
Azathioprine
6-MP
Methotrexate
Corticosteroids
Who is at increased risk for colon cancer with UC
Longer duration and extent of disease (>10 years, pancolitis)
PSC
Onset < 15 years
Colon cancer surveillance in CD/UC
Surveillance colonoscopy for patients with over 8-10 years of colitis
FPIES
Non IgE medication gut reaction to ingested foods
CLinical presentation FPIES
Onset typically in infancy but later than cows milk protein allergy
Severe reaction with profuse vomiting and diarrhea, over 1-6 h from ingestion of the trigger food
Can also have lethargy, shock, hypotension, hypoalbuminemia
Common food triggers for FPIES
Milk, soy, rice
Natural history of FPIES
They will grow out of it at 2 years of age
Allergic proctocolitis, food protein induced proctocolitis
CMPA
COmmon medications causing pill esopahgitis
Doxycycline, tetracycline
ASA
Bisphosphonates
KCl
Non-infectious complications that can be seen post liver transplant
acute/chronic rejection
) Recurrence of primary disease
3) Malignancy
4) PTLD
5) Thrombosis (ie of portal vein)
5 red flags that vomiting is NOT GERD
1) Abdominal distension
2) Fever
3) Dehydration
4) Peritoneal findings
5) Toxic appearance
6) FTT
Birds beak
achalasia
Dysphagia in a teenager ddx
Esophageal web/ring, Extrinsic compression due to malignancy, Extrinsic compression due to LN (ie TB), Peptic stricture, peritonsillar abscess, eosinophilic esophagitis
Derm manifestations of IBD
Erythema nodosum, oral aphthous ulcers, anal fissures/fistulae, pyoderma gangrenosum, Sweet syndrome, acrodermatitis enteropathica, vitilgo, psoriasis
Gilberts syndrome
reduced bilirubin UGT activity
present with intermittent episodes of mild jaundice, often triggered by infection, physical exertion or fasting
benign prognosis
normal variant
