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Gastroenterology > GI2 > Flashcards

GI2 Flashcards

1
Q

What are 3 steps to management of chronic constipation?

A
  1. complete evacuation of colon via use of oral stool softeners
  2. sustained evacuation via a regular stooling schedule, high fiber diet, oral stool softeners
  3. weaning of stool softeners as rectal tone recovers with continued stooling schedule and dietary management
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2
Q

Recurrent small pellet stools vs Infrequent massive stools - > what mechanism does it suggest

A

Recurrent small pellet stools - incomplete evacuation
infrequent massive stools - functional decal retention
Distal GI obstruction : abdo distention, narrow stool caliber, lack of encopresis

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3
Q

What age group is most likely to present with intusseption?

A

Oski says: most common in toddlers, intermittent episodes of severe generalized abdo pain, leathery may be a prominent finding
sausage shaped palpable RUQ mass, currant jelly stools - late finding

Nelson says - most common obstruction 3 month -6 year, most common abdo emergency in <2 year old

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4
Q

3 infectius aetiologies of esophagitis in immunocompromised patients?

A

Oski says:

  1. candida
  2. HSV
  3. CMV

also think of neutropenic enterocolitis (typhlitis), GVHD in immunocompromised patients with abdo pain

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5
Q

True or false - giving a patient with severe acute abdo pain morphine will interfere with your ability to establish the correct diagnosis

A

false - it should not interfere with your ability to establish the correct diagnosis

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6
Q

What is the most common cause of chronic and or recurrent abdominal pain in children?

A

functional abdominal pain - when no organic disease that explains the symptoms

Rome 3 criteria - categorizes functional abdo pain into 4 different disorders

  1. functional dyspepsia - above umbilicus, not better with poop, stool no change
  2. IBS: relieved by defecation, change in frequency or type or stool
  3. childhood functional abdo pain: episodic or continuous abdo pain, decreased activity, often other somatic complaints
  4. abdo migraine : paroxysmal episodes, >1 hour, in between normal, pain interferes with normal activities

can have other symptoms of migraine also (anorexia, nausea, vomiting, headache, photophobia)

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7
Q

Name other major causes of chronic or recurrent abdo pain in children?

A

functional abdo pain, lactose intolerance, constipation, MSK pain, parasites, reflux esophagitis, H. pylori gastrictis, PUD, mesenteric lymphadenitis, IBD (in order of prevalence)

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8
Q

What are two clinical signs of upper GI bleed?

A
  1. hematemesis

2. melena

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9
Q

What is the main clinical sign of lower GI bleed?

A

hematochezia (bright red blood from the bum)

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10
Q

How to tell the difference between upper and lower GI bleed ?

A

NG lavage - upper GI bleed - bloody, with lower GI will be clear

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11
Q

What is the best indicator of significant acute blood loss?

A

orthostasis is the best indicator of this
hematocrit is not a reliable indicator of acute blood loss
occur blood loss can lead to iron deficiency anemia - (low MCV, high RDW)

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12
Q

What is the Apt test?

A

used in neonates to determine the possibility of apparent GI bleeding
what it is : looks at the difference between maternal and fetal Hg (can be used prenatal too)
+ve means that it is baby’s blood, -ve means that it is mother’s blood 9Ie swallowed)

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13
Q

Two most common causes of bloody stools in infants <6 months?

A
  1. milk protein allergy

2. rectal fissure

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14
Q

Difference between lower GI bleed with abdo pain and without abdo pain?

A

with pain - intussuseption
without pain - Meckel’s

intestinal bleeding - late sign of obstruction

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15
Q

Differential diagnosis for rectal pain in children

A

hemorrhoids, anal fissure, infections (GAS dermatitis , tx with penicillin, bacterial abscess, pinworms), foreign body, rectal prolapse (CF), inflammatory (proctitis), IBD +-perianal fistula, neoplasm, trauma)

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16
Q

What is the scientific name and treatment for pinworm?

A

Enterobius vermicularis
can do the tape test
present with rectal itching
treatment is mebendazole

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17
Q

normal liver size in newborns? in children?

A

<2 cm in chilren

normal span: 4-5 cm in infants, 6-8 cm in oler chilren

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18
Q

True or false biliary atresia can result in hepatomegaly?

A

true - leads to a cholestatic picture - TPN cholestasis, choledochal cysts and CF can also lead to cholestasis and hepatomegaly

interestingly also malnutrition can lead to hepatomegaly in infants (Oski table 12.8)

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19
Q

Which test is more specific for hepatocellular injury, ALT or AST?

A

ALT is more specific for hepatocellular injury than AST

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20
Q

Patient with hepatomegaly, normal bill, and splenomegaly? Differentail diagnosis and investigations

A 
CBC and abdo US
DDx: 
1. storage diseases
2. leukemia
3. lymphoma
4. CHF
5. parasitic infections
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21
Q

Patient with hepatomegaly, normal bill, no splenomegaly. Differential diagnosis and investigations?

A

abdo US< serology, +/- liver biopsy

DDx:

  1. autoimmune/viral hepatitis
  2. infectious liver cysts/abscesses
  3. glycogen storage disease
  4. primary/metastatic tumours
  5. obesity/steatohepatitis
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22
Q

patients with hepatomegaly, hyperbilirubinemia, mainly unconjugated. Differential diagnosis?

A

OSKI says table 12.9

  1. Hemolysis
  2. sepsis
  3. DIC
  4. coagulopathy
  5. CHF

(not sure if all of these will cause haptometagly, discuss)

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23
Q

patient with hepatomegatly, elevated conjugated bilirubin, elevated transminases and slightly elevated ALP?

A 
inv:; viral serology, ceruoplasmin (low in Wilson), consider liver biopsy
DDx:
1. hepatitis
2. Wilson
3. Drugs/toxins
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24
Q

patient with hepatomegatly, elevated conjugated bilirubin, slight elevated transminases and greatly elevated y elevated ALP?

A

U/S or cholangiography (i.e. think obstruction)

DDx:

  1. biliary obstruction
  2. choledochal cyst/tumours
  3. parasitic infections
  4. parenteral nutrition
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25
Q

What type of hyperbili in alpha 1 antitrypsin

A

direct (i.e. conjugated) according to OSKI

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26
Q

most common of unconjugated hyper bill in non neonate?

A

Gilbert disease - mildly impaired bill conjugation in 5-10 % of the population

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27
Q

type of hyperbili in viral hepatitis?

A

direct and indirect hyperbili?

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28
Q

1st choice of imaging for direct hyperbili?

A

U/S first, further studies may in code CT, MRI, cholangiography, HIDA scan, hepatobiliary scintigraphy

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29
Q

Which type of TEF is the most common?

A

type A - proximal blind pouch with fistula connecting distal esophagus to the trachea(note that picture in Oski is not totally perfect)

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30
Q

Which type of TEF is more likely to present later in life?

A

type C - H type fistula (otherwise intact trachea and esophagus, more likely to present like aspiration

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31
Q

True or false - achalasia is common in young children

A

false - only 5% in children under 5 years old
loss of LES relaxation leading to high resting LES pressure and absent or non peristaltic oesophageal contractions
clinical: vomiting, regurg, dysphagia
dysphagia with solids then liquids as the disease progresses

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32
Q

An upper GI shows a bird beak appearance, what diagnosis do you think about

A

ahalasia

gold standard for diagnosis is manometry
Tx: balloon dilataion or surgical myotomy of LES

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33
Q

True or case - Premies are more likely to have GERD

A

true

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34
Q

What are some risk factors for GERD in older children and adolescents

A

obesity
tobacco/alcohol/drug use
anatomic abnormalities - ie hiatal hernia
neuro impairement

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35
Q

True or false - upper GI can diagnose reflux

A

no, it is done to look for anatomic abnormalities
other tests:
- esophageal pH monitoring - help with acid reflux, not with non acid reflux
- impedance probe- newer modality, detects any fluid in the esophagus
endoscopy -anatomic abnormalities, GERD related esophagitis

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36
Q

What is Sandifer syndrome?

A

rare but classic in infants

GERD and sterotypic repetitive stretching and arching movements

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37
Q

True or false - putting a baby in an infant seat can help reflux

A

No! apparently its bad and no longer recommended

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38
Q

What are 3 consequences of inadequately treated severe GERD

A
  1. esophageal strictures
  2. Barrett’s esophagitis
  3. adenocarcinoma
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39
Q

What are 4 types of esophagitis commonly encountered

A
  1. eosinophilic esophagitis
  2. infectious esophagitis
  3. pill esophagitis
  4. corrosive esophagitis - ingestion of caustic substances
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40
Q

What will the test results be in eosinophilic esophagitis

A

increased eosinophils and igE
endoscopy with biopsy - >15-20 eosinophils/hpf
treatment: eliminate inciting foods, steroids (topical?)
occurs mostly in males, presents with vomiting, chest/epigastric pain, strictures, dysphasia, associated with atopy and food allergies

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41
Q

What are the most common pathogens associated with infectious esophagitis?

A
  1. candida
  2. HSV
  3. CMV

rarer caues include: VZV, diphtheria, other bacteria
presentation: fever, dysphagia, odynophagia and retrosternal pain
candidal esophagitis, often associated with oral candidiasis

**if have oral candidal lesions, can try treating with oral fluconazole, otherwise need to do endoscopy with biopsy

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42
Q

What is pill esophagitis

A

meds with inadequate fluids, pill lodges in the oesophagus
doxycycline and other tetracycline derivatives are commonly associated
dx: odynophagia, retrosternal pain
tx: antacids and bland liquid diet until symptoms resolve

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43
Q

What are some causes of perforated oesophagus?

A

iatrogenic - endoscopy, NG/OG tube, suctioning
BOerhaave syndrome - increase in pressure from vomiting
blunt trauma

44
Q

What to do if X rays are normal (looking for free air/pneumomediastinum) but high degree of suspicion for esophageal perforation

A

esophagram with water - soluble contrast

management: NPO, gastric drainiage, broad spectrum Abx, if large need surgery

45
Q

Patient with known esophageal varicose presents with upper GI bleed. What to do?

A

present with hematemesis and/or melena
confirm via endoscopy

ABCs
octreotide
endoscopic - sclerotherapy, band ligation and/or thrombin injection
mechanical intervention - Sengstaken-Blakemore tube
severe or recurrent bleeding (vatical) may need surgery or shunt or liver transplant

Prevention: include sclerotherapy and beta-blockers

46
Q

Age group for pyloric stenosis?

A

peak age >3 weeks of age, can present as early as 1 week or as late as 5 months

47
Q

Risk factors for pyloric stenosis

A 
male
first born
white
\+ve family history
erythromycin exposure
48
Q

Risk of not correcting the alkalosis before surgery

A

risk of apnea

metabolic abnormality is hypochloremic, hypokalemic metabolic alkalosis, electrolytes are often normal

49
Q

What is the cause of most primary PUD?

A

healthy, usually associated with H. pylori (low SES, crowding, poor hygiene), duodenal in origin

conditions with increase the risk of PUD:

  • alcohol/caffeine/tobacco
  • gastrostomy tubes
  • NSAIDS
  • burn injuries
  • systemic illnesses
50
Q

Cause of secondary PUD?

A

usually gastric, caused by underlying disorder including hypergastrinemia and Zollinger-Ellison syndrome

51
Q

Clinically, how to tell the difference between gastric and duodenal ulcers?

A

gastric - pain worse with meals (especially spicy foods, caffeine)
duodenal - pain is better with meals
complications: bleed, perforation, obstruction

52
Q

What is the gold standard for diagnosis of H pylori?

A

gold standard - biopsy

noninvasive tests stool antigen testing and urease breath test (low specificity)

53
Q

What is Zollinger-Ellison syndrome

A

severe refractory PUD
autonomous gastrin secretion by a gastrinoma
often associated with MEN type I. recurrent, multiple atypically located ulcers and treated with PPI and octreotide to inhibit tumour growth

54
Q

Name 5 anomalies/conditions associated with duodenal atresia?

A 
Down syndrome
congenital heart disease
TEF
malrotation
renal anomalies
55
Q

Where is the cecum in malrotation

A

in the RUQ
therefore fixes the mesentery on a narrow base
small bowel at increased risk for twisting on the pedicle of mesentery (volvulus)->leads to compromised bowel vascularity, may lead to schema and necrosis
>90% present in the first year of life

56
Q

What is the embryonic origin of Meckel diverticulum?

A

remain of the embryonic yolk sac from the failure of the omphalomesenteric/vitelline duct to involute
1-3% of the population
most have ectopic gastric mucosa with secrete acid - leads to ulceration and bleeding of the adjacent intestinal mucosa
**can present with bleeding painless (most common), can also present with intussusception or volvulus

57
Q

Rule of 2s for Meckel divericulum

A

2% of infants
2inches in size
2 feet from ileocecal valve
detected in patients <2 years old

58
Q

Age group of intussusception

A

3 months to 3 years

59
Q

Most common cause of intusussception

A

usually idiopathic or related to hypertrophied Peyer patch (which are LN) (following viral illness)
In an OLDER child (not in the typical age group): think more of a specific lead point - i.e. Meckel, lymphoma, polyp

60
Q

What sign on abdo U/S may suggest intussuseption on abdo U/S or AXR?

A

target/crescent sign
gold standard is an air or contrast enema
observation for 24-48 hours is key

61
Q

Causes of ileum

A

infection
gut manipulation - ie surgery
metabolic abnormalities - hypercalcemia, hypokaelmia, acidosis, uremia and medications (ie loperamide, narcotics)
treatment: depending on aetiology - most resolve
ng decompression can help reliever symptoms

62
Q

A patient with CF presents with recurrent episodes of partial/complete intestinal obstruction due to thick intestinal contents. what condition do you think of?

A

distal intestinal obstruction syndrome

63
Q

A teenage boy is in a body cast after orthopaedic surgery and starts vomiting with severe abdominal pain . What is the likely diagnosis?

A

SMA syndrome
rare but series problem - occurs when SMA collapses onto and compresses the duodenum
rapid weight loss can lead to the SMA fat pad loss, predisposes the patient to SMA syndrome, especially in the supine position

64
Q

True or false - Crohn’s disease affects males and females equally

A

true - in contrast, UC is more common females

65
Q

Which is more common, Crohn’s or UC?

A

Crohn’s more common

66
Q

Which is more likely to have GI bleeding? UC or Crohns?

A

UC more likely bleeding, Crohns more likely nausea and vomiting

67
Q

Most common region involved in Crohn’s disease?

A

ileocolic (mouth to anus)

vs us is the colon

68
Q

Name extraintestinal manifestations of Crohn’s disease?

A

extra intestinal more common in Crohn’s

  1. spondyloarthropathy
  2. aphthous ulcers
  3. erythema nodosum
  4. pyoderma gangernosum
  5. uveitis
  6. primary sclerosing cholangitis

in UC, extra-intestinal is rare, pyoderma gangernosum and primary sclerosing cholangitis more common in US

69
Q

True or false both Crohn’s and UC are associated with toxic megacolon?

A

false - UC is strongly associated, no association with Crohn and toxic megacolon

70
Q

True or false, both Crohn’s and UC have same increase in risk of cancer?

A

nope, UC increases the risk way more, crown’s does slightly

71
Q

pANCA more likely in Crohn’s or UC?

A

more likely in UC

72
Q

What is the treatment for Crohn’s disease

A

(depends on location and severity)
Medical - steroids, mesalamine, sulfasalazine, azathioprine, methotrexate, infliximab (in order of increasing disease severity)
Surgery: for refracory and/or severe localized disease; surgical intervention also often needed for strictures and fistulas

73
Q

Treatment of UC

A

medical - similar to Crohn;s

Colectomy is CURATIVE for severe and/or refractory disease

74
Q

Name 5 conditions associated with celiac disease

A 
DM1
Down syndrome
Turner syndrome
autoimmune thyroiditis
IgA deficiency

usually presents age 2-3 can present at any age
gluten in wheat and related grains such as rye and barley

75
Q

Symptoms and Signs of celiac disease (table 12.11 Oski)

A

symptoms: FTT, weight loss, diarrhea, irritability, vomiting, anorexia or increased appetite, foul-smelling bulky stools, abdo pain adn/or distention, rectal prolapse
Signs: height <25th percentile, wasted muscles, abdo distention, edema, finger clubbing

76
Q

Please name some non intestinal manifestations of celiac disease

A 
osteopenia/osteoporosis
short stature (weight decreases before height)
delayed puberty
anemia
arthritis
hepatitis
dermatitis herpetiformis
dental enamel hypoplasia
brain calcifications
neuro sx
77
Q

Test for celiac disease

A

TTG - very specific
can be falsely negative with IgA deficiency
antigliadin antibodies - NOT useful because of low sensitivity and low specificity
t definitive dx : biopsy with villous atrophy

78
Q

Main Ddx that is often confused with celiac disease

A

autoimmune enteropathy (often misdiagnosed as celiac)

79
Q

true or false - congenital lactase deficiency is common

A

false - it is actually very rare

80
Q

Clinical findings in malabsorption

A

diarrhea, steatorrhea, abdo distention, flatulence, poor growth
can lead to vitamin deficiencies
decal fat will be elevated

81
Q

true or false diarrhea is present even in early lactose intolerance

A

false - usually presents with abdo pain and/or distention
best way to establish diagnosis - improvement with lctose-free diet and worse with lactose foods
tests include the breath hydrogen test, lactose tolerance test - too sensitive, common to have lots of case positives

82
Q

What is absorbed in the different parts of the bowel

A

proximal small bowel - protein, carbs, some vitamins (fat soluble)
distal ileum B12
colon - absorb water

83
Q

What are some common causes of shot-bowel syndrome

A

bowel resection - ischemic injury from NEC, malrotation, trauma etc
Congenital causes: multiple atresias, gastroschisis etc.

84
Q

Treatment for hemorrhoids

A

internal - above the dentate line - correct the aetiology, sclerosis therapy, band ligation
external - reassurance and proper anal hygiene

85
Q

How many imperforate anus are associated with other anomalies

A 
50%
Vertebral anomalies
Anal anomalies
Cardiac
TEF
E
Radial displasia, renal anomalies
Limb abnormalities
86
Q

4 causes of rectal prolapse

A

usually idiopathic
can be associated with:
infections, malnutrition, IBD, chronic constipation
usually painless until chronic and/or ulcerated
treatment: correct underlying cause, reduce it and cauterization

87
Q

A patient with RLQ pain and history and physical suggestive of appendicitis has a positive urinalysis, what is the problem?

A

in fact, it is likely still appendicitis - when appendix is inflamed and presses on the bladder, the bladder can get inflamed too - don’t get fooled

88
Q

How does Hirschprung present n an older chip?

A

with long-standing and/or refractory constipation

most common presentation is in the neonatal period with failure to pass meconium

89
Q

What is Rovsing sign

A

press on LLQ leads to pain in RLQ

90
Q

Psoas sign

A

pain on extension of the right hip

91
Q

Obturator sign

A

pain on internal rotation of the right hip - inflamed appendix in the pelvis

92
Q

Treatment for already perforated appendix in stable patient

A

IV abx, drainage of abscess if present (debate about interval appendectomy)

93
Q

What is annular pancreas

A

it is due to incomplete rotation of the ventral pancreatic bud
associated with :
polyhydramnios, Down syndrome, intestinal atresia, imperforate anus and malrotation
Presents as bowel obstruction, pancreatitis or biliary colic

94
Q

most specific test for pancreatitis?

A

lipase >3 x normal

treatment is NPO and IvF and IV analgesics, slowly reintroduce diet

95
Q

Recurrent pancreatitis - what investigations should you do?

A

lipid
calcium, phosphorus, bili
can consider imaging - US CT MRCP/ERCP

96
Q

Medications which can cause pancreatitis

A

acetaminophen, alcohol, steroids, valproic acid, lasix

97
Q

viruses which cause pancreatitis

A

enterovirus, EBV, hepatitis A/B, influenza, mycoplasma, mumps

98
Q

Anatomical problems that cause pancreatitis

A

panceatic divisum (common)
annular pancreas
biliary tract malformations
gallstones

99
Q

Systemic disease that cause pancreatitis

A

CF, DM, organic academia, SLE, hyperlipidemia

100
Q

2 disease with pancreatic insufficiency

A
  1. Schwachman-Diamond - AR, pancratic insufficiency, neutropenia, metaphyseal dystosis, FTT, shot stature
  2. CF - 85% -90% have insufficiency by age 1 year
101
Q

Pancreatic tumours in children - common or rare?

A

very rare
remember VIPoma - non alpha cel pancreatic tumours, secret VIP
watery diarrhea, hypokalemic metabolic acidosis
lab: increased VIP in blood
resection and octreotide

102
Q

Complications of pancreatitis

A

hemorrhage
pseudocysts
U/S for diagnosis

103
Q

Which vitamin K dependant factor is the most specific for liver injury?

A

factor VII - shortest half life

because the liver needs to make the clotting factors

104
Q

Markers of hepatic synthetic dysfunction

A

prolonged PT/INR
hypoalbuminemia
hypoglycemia

105
Q

Marker of hepatic clearance dysfunction

A

hyperammonemia

106
Q

Ture or false- all patients with autoimmune hepatitis have autoantibodies on presentation

A

false - 20-30% don’t have autoantibodies on presentation
can present insidious or acute hepatic failure
2 types

107
Q

What are some disorders associated with type I autoimmune hepatitis

A

tyroiditis, IBD, arthritis, rash, hemolytic anemia

Gastroenterology (5 decks)

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