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Royal College Studying > GI > Flashcards

GI Flashcards

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1
Q

ROME criteria for constipation

A

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

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2
Q

is digital disimpactions recommended

A

No

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3
Q

Is there evidence for docusate in constipation

A

no

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4
Q

recommended fiber titntake for children

A

0.5g/kg/day

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5
Q

is there evidence for probiotics for treating onstipation

A

no

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6
Q

can you use mineral oil in infants

A

no due to risk for aspiration

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7
Q

how long to treat children wtih constipation for

A

minimum 6 months

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8
Q

What % of normal newborns pass meconium within 24h of lifw

A

90%

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9
Q

How to manage rumination disorder

A

reinforce the correct eating behaviour while minmizing attention to rumination diaphragmatic breathing adn postprandial gum chewing, no pharm evidence

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10
Q

functional GI disorder characterized by effortless regurgitation of ingested food into the mouth after moth meals

A

Rumination disorder

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11
Q

ROME 4 criteria for urminatinos disorder

A

○ 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)

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12
Q

Standard formula calories

A

29kcal/30ml

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13
Q

What is cronobacter sakazakii related to

A

powdered formula in premature infants

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14
Q

INdications for soy formula

A

galactosemia, preference for a vegetarian diet and hereditary lactase deficiency

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15
Q

What is goats milk low in

A

folate

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16
Q

At what age should you start screening for NAFLD

A

all obese children 9-11 and for overweight children with additional risk factors

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17
Q

screening test for NAFLD

A

ALT

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18
Q

What is the most common cause of inherited colorectal cancer

A

Lynch syndrome

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19
Q

How is lynch syndrome inherited

A

AD

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20
Q

What types of cancer increased risk for with lynch syndrome

A
  • CRC, endometrial cancer, sebaceous neoplasms, ovarian cancer, pancreatic cancer, brain cancer
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21
Q

Autosomal dominant syndrome with multiple hamartomas polyps in the GI tract, mucocutaneous pigmentation and an increased risk of GI and non GI cancer

A

Peutz Jeghers

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22
Q

How to diagnose Peutz Jeghers

A

histologically proven hamartomatous plyps if 2 of the following are met: positive family history wiht AD inheritenace pattern, mucocutaenous hyperpigementation and small bowel polyposiss

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23
Q

When should surveillance begin in Peutz Jeghers

A

Around age 8 or when symptoms occur with upper
and lower endoscopy

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24
Q

How is FAP inherited

A

AD

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25
Q

Types of cancer with FAP

A
  • Colorectal, thyroid, stomach and small intestinal cancer, hepatoblastoma
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26
Q

Gene for FAP

A

APC

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27
Q

Does breastfeeding reduce the risk for celiac disease

A

No

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28
Q

Does earlier introduction of gluten impact cumulative incidence of celiac disease

A

No

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29
Q

Extraintestinal manifestations of celiac disease

A

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

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30
Q

Who should you test for celiac disease

A

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

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31
Q

Next steps for patient with IgA TTG autoantibodies <10 times upper limit of nornmal

A

scope adn biopsy

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32
Q

TTG >10 times upper limit of normal

A

HLA and EMA, if positive, celiac disease

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33
Q

How to test for celiac disease in asymptomatic patients

A

duodenal biopsies

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34
Q

biopsy finding in celiac disease

A

villous atrophy

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35
Q

Treatment for rumination disorder

A

Chewing gum
Diaphragmatic breathing

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36
Q

Work-up for rumination

A

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

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37
Q

Cronobacter sakazakii is associated with

A

Contaminated formula

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38
Q

INdications for soy formula

A

Galactosemia, preference for vegetarian diet, hereditary lactase deficiency

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39
Q

Is there value for soy formula for colic, fussiness or atopic disease

A

No

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40
Q

Goats milk is low in

A

Folate

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41
Q

Preferred screening test for NAFLD

A

ALT

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42
Q

Is there a specific diet recommended for treatment of NASH

A

No

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43
Q

Most common inherited cause of colorectal cancer

A

Lynch syndrome

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44
Q

Types of cancers with Peutz-Jeghers

A

Colorectal, brain, reproductive tumors

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45
Q

Precancerous lesions within the surface epithelium of the intestine displaying various degrees of dysplasia

A

Andeomatous polyps

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46
Q

Cancers at risk for in FAP other than colon in young and older patients

A

Hepatoblastoma in BBs
Follicular or papillary thyroid cancer in teens

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47
Q

Gardner syndrome

A

Also APC mutations
Multiple colorectal polyps

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48
Q

Turcot syndrome

A

Colorectal polyposis and primary brain tumors (medulla lasts a)

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49
Q

How often to screen patients with FAP

A

Every 1-2 years with scope, every year once polyps identified

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50
Q

Treatment for FAP

A

Prophylactic protocols to my

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51
Q

Most common GI malignancy in pediatric population

A

Lymphoma

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52
Q

What to consider in patient older than 3 with intussuception

A

Lymphoma

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53
Q

How to diagnose carcinoid tumor

A

Elevated urinary 5-hydrocindoleacetic acid

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54
Q

Acute liver failure definition

A

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

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55
Q

Causes of neonatal acute liver failure

A

Gestational alloimmune liver disease, tyrosinemia, familial HLH, congenital HSV infection

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56
Q

Who is at high risk with Hep E infection

A

Pregnant women

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57
Q

MArkers of autoimmune hepatitis

A

ANA, ASMA, liver-kidney microsomal antibody or soluble liver antigen and possible elevated IgG

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58
Q

What does liver biopsy show in autoimmune hepatitis

A

Interface hepatitis and plasma cell infiltrate

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59
Q

What is GALD

A

Gestational alloimmune liver disease
Maternal IgG antibodies bind to fetal liver antigens and activate the terminal complement cascade resulting in hepatocyte injury and death

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60
Q

What does acute liver failure look like on biopsy

A

Patchy or confluence massive necrosis of hepatocytes and multilobular or bridging necrosis

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61
Q

What is centrilobular damage associated with in liver failure

A

Tylenol overdose or circulatory shock

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62
Q

Microvesciular fatty infiltrate of hepatocytes is observed in

A

Reye syndrome, B oxidation defects and tetracycline toxicity

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63
Q

What is an ominous sign in liver failure

A

Rapid decrease in liver size without clinical improvement

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64
Q

Stages of hepatic encephalopathy

A

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

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65
Q

Does serum aminotransferase activity correlate with the severity of illeness in liver failure

A

No

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66
Q

Antidote for liver failure in a Anita mushrooms

A

Penicillin

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67
Q

GALD treatment

A

Double volume exchange transfusion to remove existing reactive antibody followed immediately by IgG 1g/kg

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68
Q

Treatment for hyperammonemia

A

Lactose or rica I’m in

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69
Q

Increased mortality risk factors in acute liver failure

A

Age <1, stage 4 encephalopathy, INR >4, low factor 5 levels and need for dialysis before transplant

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70
Q

Is pre0transplant bill or height of hepatic enzymes predictive of post transplant survival

A

No

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71
Q

How many kids get aplastic anemia after idiopathic acute liver failure

A

10%

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72
Q

What nutritional deficiencies are Vegas at risk for

A

Iron, B12
Insuf. Fatty acids
Calcium and vitamin D

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73
Q

Pellagra

A

Vitamin B3 deficiency
Raw skin, sun exoposed rash, diarrhea, dementia

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74
Q

Who gets B3 deficiency (pellagra(

A

Alcoholics, anorexia, bariatric surgery or mlabsorptive disease

75
Q

What medication can cause pellagra

A

Isoniazid

76
Q

Beriberi

A

Thiamine deficiency

77
Q

What does infantile beri beri look like

A

Fulminant cardiac syndrome with cardiomegaly, tachycardia, loud piercing cry, cyanosis, dyspnea, vomiting, pulmonary hypertension

78
Q

Who can get beri beri

A

Infants on soy based formulas

79
Q

Is CVS more common in girls or boys

A

Girls

80
Q

Criteria for CVS

A

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

81
Q

SCreening test in CVS

A

Lutes, glucose, upper GI radiographs to exclude Mal rotation

82
Q

Do you need routine endoscopy in CVS

A

No unless they have chronic symptoms in between or large hematemesis

83
Q

Which patients with CVS should be evaluated for a metabolic disorder

A

Under 2
Vomiting associated with interucrrent illness, fasting, increased protein intake
Neuro findings
Labs like hypoglycemia, anion gap, alkalosis, hyperammonemia

84
Q

Who should get prophylactic therapy in CVS

A

Episodes more than every 1-2 months, severe enough to require repeat hospitalization, fail to respond to abortive therapy

85
Q

Treatment for CVS

A

Cyproheptadine under 5
Amitryptiline over 5
Propranolol is second line for both age groups

86
Q

RF with cyprohepatdine

A

Enhanced appetite

87
Q

What do you have to monitor in patient on amitryptiline

A

QTC

88
Q

Vitamin A deficiency manifestations

A

Eye lesions, can be late finding with corneal keratinization, susceptibility to infection, xeropthalmia, Bitot spots (plaques on conjunctival membrane)
Major cause of blindness

89
Q

Vitamins B6 deficiency

A

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

90
Q

Does breast milk contain vitamin C

A

Yes

91
Q

Scurvy manifestations

A

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

92
Q

Upper limits for vitamin D in younger children <1 and adults

A

1000 and 2000

93
Q

Vitamin D overdose

A

Nausea, vomiting, poor feeding, cosntipation, abdo pain, pancreatitis, hypertension, decreased QT interval
Lethargy, hypotonia, confusion, psychosis, hallucinations

94
Q

Esophagitits with dysphasia is an indication for

A

Scope

95
Q

Triad for Chloedocal cyst

A

Abdo pain, jaundice and palpable mass

96
Q

What is choledocal cyst associated with

A

Increased cancer risk mostly cholangiocarcinoma but also pancreatic and gallbladder cancers

97
Q

Type 5 choledocal cyst

A

Caroli disease

98
Q

Is biliary atresia usually associated with other abnormalities

A

No

99
Q

Biliary atresia with splenic malformation syndrome

A

Associated with situs I versus, Mal rotation, polysplenia, interrupted inferior vena cava and congenital heart disease
Poor prognosis

100
Q

Triangular cord sign

A

Seen in biliary atresia which represents a cone shaped fibrin mass cranial to the bifurcation fo the portal vein

101
Q

Biliary atresia biopsy findings

A

Bile duct Al proliferation, presence of bile plugs and portal or perilobular edema and fibrosis with the basic hepatic lobular architecture intact

102
Q

When is success rate for kasha better

A

Before 8 weeks of age

103
Q

What vitamin deficiency can you get with biliary atresia

A

Vitamin E with neuromuscular syndrome inc progressive areflexia, cerebella ataxia, ophthalmologist and decreased vibratory sensation

104
Q

achalasia cause

A

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

105
Q

Chagas’ disease

A

Can look like loss of intramural ganglion cells similar to achalasia

106
Q

How to diagnose achalasia

A

Esophageal nanometers showing incomplete relaxation of the LES and aperistalsis in the distal 2/3 of the esophagus

107
Q

What should be performed in achalasia

A

Should also do endoscopic evaluation to exclude malignancy at esoagogastric junction that can mimic achalasia

108
Q

How many eosinophils to see on endoscopy in EOE

A

Over 15 per HPF

109
Q

Lab abnormalities in EOE

A

Pierpheral eosinophilia and elevated IgE

110
Q

Serum trypsinogen used for

A

Exocrine pancreatic insufficiency will be low in CF and Shwachmann diamond

111
Q

Diagnostic test for protein losing enteropathy

A

Stool A!AT

112
Q

Mechanism of injury in button battery

A

Generation of hydroxide radicals in the mucosa resulting in caustic injury from high ph instead of electrical thermal injury

113
Q

How long until necrosis starts in button battery ingestion

A

15min

114
Q

Who is at increased risk for injury from button battery ingestion

A

Children younger than 5 with battery over 20mm ingested and multiple button batteries

115
Q

Who to observe with gastric button battery

A

Duration of ingestion <2h, size of battery < 20mm, absence of clinical symptoms and child over 5 years

116
Q

How to manage large button battery

A

Should be checked by radiograph and removed if in place after 48h

117
Q

Where is most common site for perforation with sharp objects

A

Ileocecal region

118
Q

How to manage esophageal food impacting

A

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

119
Q

What coin size likely to be impacted

A

Over 23.5mm (basically bigger than a quarter)

120
Q

How to manage gastric coins

A

Manage expectantly,
Monitor stools with repeat X-rays in 1-2 weeks
Consider removal if retained longer than 2-4 weeks

121
Q

What kind of intussuception do you get post-operatives surgery

A

Ileoileal

122
Q

Who gets ileoileal intussuception

A

Post-op and HSP, HSP often resolves on its own without treatment

123
Q

Juvenile polyposis syndrome

A

Autosomal dominant
Hamartomatous/juvenile polyps
Increased risk of GI malignancy

124
Q

Criteria for juvenile polyposis syndrome

A

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

125
Q

Mutation for juvenile polyposis

A

SMAD4. BMPR1A

126
Q

What are patients with SMAD4 mutation in juvenile polyposis at risk for

A

Hereditary hemorrhagictelangectasia

127
Q

What are you at increased risk for in Peutz Jeghers syndrome

A

Intussuception and malignancy

128
Q

Who should you test for H. Pylori

A

Patients with symptoms of PUD
NOT those with functional abdominal pain
Refractory iron deficiency
Chronic ITP
NOT short stature

129
Q

How long to wait before H pylori testing when on PPI and antibiotics

A

2 weeks of PPI and 4 weeks of antibiotics

130
Q

How many gastric biopsies for H pylori

A

6

131
Q

Who to treat with H pylori

A

Patients with PUD, ulceration, scarring and H pylori
Maybe natural modularity, gastritis, incidental finding???

132
Q

Treatment for H pylori

A

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

133
Q

Risk factors for drug induced hepatopathy

A

Age (very young)
Abnormal renal function
Concurrent use of other hepatotoxic agents
Drug interactions
Pre-existing live disease

134
Q

Most common injury pattern in drug induced acute liver failure

A

Hepatic Elul are

135
Q

Management of acute liver failure

A

Consider PICU admission if encephalopathy or INR >4
Frequent lab monitoring
Avoid bentos unless patient intubated and ventilated
Avoid hypoglycemia
Restrict TFI
Liver transplantation

136
Q

Kings college criteria - acetaminophen

A

Arterial ph < 7.3
INR >6.5 and serum creatinine > 300 and grade 3-4 hepatic encephalopathy

137
Q

Kings college criteria for non0aceatamonphen

A

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

138
Q

NAtural history of autoimmune liver disease

A

50% mortality at 5 years and 90% at 10 years

139
Q

Which type of autoimmune hepatitis is acute liver failure more common with

A

Type 2, anti LKM-1 positive

140
Q

Alagille syndrome mutation

A

JAG1 in up to 94% of patients
NOTCH2 in some JAG1 negative patients

141
Q

Alpha 1 anti trypsin inheritance

A

AD

142
Q

A1AT clinical presentation

A

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

143
Q

Wilson disease inheritance

A

AR

144
Q

Wilson disease presentation

A

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

145
Q

Gilbert syndrome

A

Recurrent episodes of jaundice, otherwise asymptomatic
Triggered by dehydration, fasting, intercurrent illness, menstruation, over exercise
Unconjugated hyperbilirubinemia
Increased risk cholelithasis

146
Q

What causes GIlbert syndrome

A

Defect in promotor gene encoding uridine diphosphoglucuronate-glucuronosyltranferase 1A! 9UGT1A1) that conjugated bilirubin to glucuronic acid

147
Q

How to diagnose Hep A

A

Hep A IgM
IgG= pst infection or immunization

148
Q

HbsAg Negative
AntiHBc Positive
Anti-HbS Positive

A

Immune due to past infection

149
Q

HbsAG NEgative
Anti0HbC Negative
Anti-HbS Positive

A

Immune due to vaccination

150
Q

HBsAg Positive
Anti-HBc Negative
Anti-HBs negative

A

Acutely infected

151
Q

HBsAg Positive
Anti-HBc POsitive
IgM anti-HBc Negiatve
Anti-HBs Negative

A

Chronically infected

152
Q

HbsAg Negative
Anti-HBc POsitive
Anti-HbS Negative

A

Resolved or resolving acute infection
Low level chronic infection

153
Q

How many children exposed to Hep C develop chronic infection

A

60-80%

154
Q

How to diagnosed Hep C in infants

A

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

155
Q

Signs of EOE on scope

A

Esophageal furrowing, rings (trachealization), exudates, linear furrowing

156
Q

Treatment options for achalasia

A

pneumatic dilation
Laparaoscopic surgery/Kyoto my
Botulism toxin injection into LES
Pharmacological therapies
Per-oral endoscopic Kyoto my

157
Q

Who should get a funds

A

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

158
Q

Risks of fundo

A

Gas blot, early satiety, dysphasia, retching, dumping syndrome, worse aspiration from esophageal stasis, wrap slip

159
Q

Who to test for celiac disease

A
  • 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
160
Q

Associated conditions of celiac disease

A

T1Dm
autoimmune thyroid it is
Down syndrome
Turner syndrome
Williams syndrome
Selective IgA deficiency
First degree relatives of celiac patients

161
Q

Celiac disease monitoring

A

TTG after 6 months of gluten free diet to demonstrate decrease in antibody
TTG if symptoms
TTG yearly in asymptomatic individuals

162
Q

Associated conditions with crowns disease

A

Turner syndrome
GSD 1b

163
Q

What 5 things would make you think this is NOT uC

A

Fistulizing disease
Perinatal skin tags
Deep ulcerations, cobble stoning or stenosis
Evidence of J or illegal inflammation
Granuloma anywhere in the GI tract

164
Q

Why do patients with IBD get kidney stones

A

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

165
Q

What screening to do in patient with newly diagnosed IBC

A

Stool infectious studies
Baseline infectious serology and manitou
CXR
EGD and colonoscopy
Fecal cal
Small bowel imaging

166
Q

Side effects ASA

A

Headaches, N/V/ anorexia, yellow/orange coloring, abdo pain, joint pain
Pericarditis, pneumonia is, SJS, hepatitis, nephritis, keukopenia, pancreatitis

167
Q

Azathioprine SE serious

A

BM suppression, immunosuppressive, pancreatitis, hepatitis, cancer

168
Q

Methotrexate side effects

A

Hair loss, mouth sores, photosensitivity,y teratogenic, anti-folate
BM suppression, immunosuppressive, hepatotxocity, nephrotoxicity, lung disease

169
Q

5 immunosuppressive medications to treat BD

A

Biological
Azathioprine
6-MP
Methotrexate
Corticosteroids

170
Q

Who is at increased risk for colon cancer with UC

A

Longer duration and extent of disease (>10 years, pancolitis)
PSC
Onset < 15 years

171
Q

Colon cancer surveillance in CD/UC

A

Surveillance colonoscopy for patients with over 8-10 years of colitis

172
Q

FPIES

A

Non IgE medication gut reaction to ingested foods

173
Q

CLinical presentation FPIES

A

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

174
Q

Common food triggers for FPIES

A

Milk, soy, rice

175
Q

Natural history of FPIES

A

They will grow out of it at 2 years of age

176
Q

Allergic proctocolitis, food protein induced proctocolitis

A

CMPA

177
Q

COmmon medications causing pill esopahgitis

A

Doxycycline, tetracycline
ASA
Bisphosphonates
KCl

178
Q

Non-infectious complications that can be seen post liver transplant

A

acute/chronic rejection
) Recurrence of primary disease
3) Malignancy
4) PTLD
5) Thrombosis (ie of portal vein)

179
Q

5 red flags that vomiting is NOT GERD

A

1) Abdominal distension
2) Fever
3) Dehydration
4) Peritoneal findings
5) Toxic appearance
6) FTT

180
Q

Birds beak

A

achalasia

181
Q

Dysphagia in a teenager ddx

A

Esophageal web/ring, Extrinsic compression due to malignancy, Extrinsic compression due to LN (ie TB), Peptic stricture, peritonsillar abscess, eosinophilic esophagitis

182
Q

Derm manifestations of IBD

A

Erythema nodosum, oral aphthous ulcers, anal fissures/fistulae, pyoderma gangrenosum, Sweet syndrome, acrodermatitis enteropathica, vitilgo, psoriasis

183
Q

Gilberts syndrome

A

reduced bilirubin UGT activity
present with intermittent episodes of mild jaundice, often triggered by infection, physical exertion or fasting
benign prognosis
normal variant

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