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EOR- PEDS > GI > Flashcards

GI Flashcards

1
Q

Obstruction of the lumen of the appendix, resulting in inflammation & bacterial overgrowth

A

Appendicitis

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2
Q

MCC of appendicitis

A

Lymphoid hyperplasia due to infection = MCC in children

Fecalith & lymphoid hyperplasia most common, inflammation, malignancy or foreign body

MC age 10-30, MCC of acute abdomen in children 12-18, perforation rate highest in young children

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3
Q

Sx of appendicitis

A

anorexia & periumbilical or epigastric pain followed by RLQ abdominal pain (12-18 hours), N & V

(vomiting usually occurs after the pain)

Pts w/ a retrocecal appendix may have an atypical pattern (diarrhea), & (+) rectal/gyn exam – appendix may also be pelvic

Appendiceal inflammation stimulates nerve fibers around T8-T10, causing vague periumbilical pain

• Once the parietal peritoneum becomes irritated, it radiates to right lower quadrant

Rebound tenderness, rigidity & guarding – retrocecal appendix may have atypical findings

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4
Q

What are the 4 tests for appendicits

A

Rovsing sign: RLQ pain w/ LLQ palpation

Obturator sign: RLQ pain with internal & external hip rotation with flexed knee

Psoas sign: RLQ pain with right hip flexion/extension (raise leg against resistance)

McBurney’s point tenderness: point 1/3 the distance from the anterior sup. iliac spine & navel

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5
Q

Frequent complex of paroxysmal abdominal pain & severe crying

A

Colic

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6
Q

Colic sx

A

Sudden onset of loud crying (paroxysms may persist for several hours) with facial flushing & circumoral pallor

Abdomen is distended, tense – legs drawn up

Temporary relief with passage of feces or flatus

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7
Q

Complete absence or closure of a portion of the duodenum, leading to a gastric outlet obstruction

A

Duodenal atresia

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8
Q

Abdominal XR: double bubble sign

A

Seen with duodenal atresia

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9
Q

Sx of duodenal atresia

A

Neonatal intestinal obstruction: shortly after birth (within 1st 24-48 hours of

life) with bilious vomiting (may be nonbilious), abdominal distention

Associated anomalies include: malrotation, esophageal atresia, congenital heart disease

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10
Q

Tx of duodenal atresia

A

Decompression of the GI tract, electrolyte and fluid replacement

Duodenoduodenostomy = definitive management

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11
Q

Tx of foreign body in esophagus

A

Observe for 24 h w/ serial XR & remove endoscopically if object doesn’t pass distally within that time-frame

If the object causes symptoms or time-point of ingestion is unknown attempt immediate endoscopic removal

If the ingested item appears relatively benign & has already progressed inferior to the diaphragm on imaging, observe and wait for spontaneous passage

If the ingested object is sharp then remove immediately with endoscopy

Batteries in esophagus have the potential to cause severe tissue damage & should be removed immediately withendoscopy

Consider using a Foley catheter to remove retrograde from esophagus or bougienage to pass the object distally into the stomach

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12
Q

Tx of foreign body distal to esophagus (Stomach = MC)

A

Symptomatic: remove immediately w/ endoscopy Asymptomatic:

  • *Small blunt object** - follow with serial XR; remove endoscopically if it doesn’t advance past pylorus in 3-4 w Large object (> 3 cm) - beyond pylorus? monitor with serial imaging; in stomach? remove endoscopically
  • *Sharp object** - before pylorus? remove endoscopically; beyond pylorus? monitor with serial imaging & remove if no progress for 3 days
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13
Q

Most common overall cause of gastroenteritis in adults in N. America & MC cause of viral GE worldwide

A

Norovirus gastroenteritis

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14
Q

Sx of norovirus

A

24-48 hour incubation period, symptoms last 2-3 days

Vomiting predominant symptom – nausea, non-bloody diarrhea that lacks mucus & fecal leukocytes (noninvasive), generalized symptoms

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15
Q

Most common gastroenteritis in young unimmunized children between 6 months – 2 years of age

A

Rotavirus

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16
Q

MCC of diarrhea breakout in daycare

A

Rotavirus

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17
Q

Gastritis due to infection from heat-stable enterotoxin B, IP within 6 hours

A

Staph aureus gastroenteritis

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18
Q

Diarrhea after a picnic w/ egg salad

A

Staphylococcus aureus gastroenteritis

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19
Q

Enterotoxin that can survive reheating, IP within 6 hours (mc from fried rice)

A

Bacillus Cereus Gastroenteritis

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20
Q

MCC of travelers diarrhea

A

Enterotoxin E. Coli Gastroenteritis

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21
Q

Gram (-), comma-shaped rod transmitted via contaminated food & water – ** shellfish

Outbreaks may occur during poor sanitation & overcrowding conditions (especially abroad)

A

Vibrio cholerae gastroenteritis

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22
Q

copious watery diarrhea = “rice water stools” (gray with flecks of

mucus & has a “fishy odor” but no fecal odor, blood or pus)

A

Vibrio cholerae gastro

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23
Q

Gram-negative rods transmitted via raw or undercooked shellfish consumption and seawater (direct contact of water with wounds or shucking oysters), especially during warm summer months

A

Vibrio Parahaemolyticus & Vulnificus

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24
Q

Spore-forming, toxin-producing gram-positive anaerobic bacterium

A

C.diff

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25
Q

RF for c.diff

A

Recent antibiotic use (Clindamycin), advanced age, gastric suppression therapy (PPI, H2 blockers)

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26
Q

Dx of c.diff

A

C. difficile toxin (stool) – initial test of choice

Leukocytosis

Sigmoidoscopy in select patients: pseudomembranous

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27
Q

Tx of C.diff

A

Contact precautions & hand hygiene (NO sanitizer – hands are resistant to killing by alcohol)

Oral Vancomycin or oral Fidaxomicin = 1st line agents, Metronidazole = alternative

2nd recurrent CDI episode: pulse-tapered oral Vancomycin or Fidaxomicin

Recurrent disease treated with metronidazole: oral Vancomycin

Frequently recurrent disease (at least 3 recurrences) – fecal microbiota transplant

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28
Q

What invasive infectious enteritis is this:

Fever, abdominal pain mimics acute appendicitis (can cause mesenteric lymphadenitis, producing abdominal tenderness or guarding)

A

Yersinia Enterocolitica = Gram-negative coccobacillus with bipolar staining (“safety pin” appearance)

Sources: contaminated port MC in the US, milk, water, & tofu

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29
Q

MCC of bacterial enteritis in the US, MC antecedent event in post-infectious Guillain-Barre syndrome

A

Campylobacter Enteritis

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30
Q

What type of invasive infectious gastroenteritis is this:

Contaminated food – raw or undercooked poultry most common, raw milk, contaminated water, dairy cattle – puppies important source in children

A

Campylobacter Enteritis

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31
Q

Ingestion of undercooked beef, unpasteurized milk or apple cider, day care centers & contaminated water

A

E.coli

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32
Q

Watery diarrhea early on before becoming bloody, crampy abdominal pain, vomiting, fever usually absent/low-grade

A

E.coli sx

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33
Q

Diarrheal illness most caused by the gram-negative rod Salmonella typhi and paratyphi

More common in children & young adults – IP 5-21 day

A

Typhoid (enteric) Fever

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34
Q

Sx of typhoid “enteric” fever

A

Headache, intractable fever, chills, abdominal pain, constipation initially followed by non-bloody diarrhea (may be “pea-soup” green in color), malaise & anorexia

Fever with relative bradycardia (classic but rare)

Rose spots (faint pink or salmon-colored macular rash that spreads from trunk to extremities) occurs in 2nd week, abdominal tenderness

Hepatosplenomegaly, GI bleeding, signs of dehydration, & delirium may be seen in later stages

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35
Q

Tx of Typhoid (Enteric Fever)

A

Oral rehydration & electrolyte replacement first-line management, antibiotics often given→

Antibiotics: Fluoroquinolones first-line (Ciprofloxacin, Ofloxacin), macrolides, ceftriaxone

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36
Q

One of the MCC of foodborne disease in US (**poultry and pork, eggs, milk products, fresh produce) & contacts w/ reptiles

Incubation period 8-72 hours

A

Nontyphoid salmonella

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37
Q

Lower abdominal pain, abdominal cramps, high fever, tenesmus, explosive watery diarrhea that progresses to mucoid & bloody diarrhea

Neurologic manifestations especially in young children (febrile seizures)

A

Shigellosis

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38
Q

Dx of Shigella

A

Stool cultures, positive fecal WBCs & RBCs

CBC: Leukemoid reaction (WBC 50,000+)

Sigmoidoscopy: punctate areas of ulceration

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39
Q

Tx of Shigella

A

Oral rehydration & electrolyte replacement therapy mainstay of treatment,

In general, anti-motility drugs should be avoided (can worsen the illness d/t retained toxins)

Antibiotics indicated if severe: Fluoroquinolones, 3rd gen cephalosporins, azithromycin, Bactrim are options

40
Q

Why are antimotility drugs not used in bloody diarrhea?

A

↑ likelihood of hemolytic uremic syndrome

41
Q

Diarrhea in poorly canned home foods, think

A

C. perfringens

42
Q

Diarrhea after drinking fresh mountain stream water:

A

Giardia lamblia – incubates for 1-3 weeks, causes foul-smelling bulky stool that may wax and wane over weeks before resolving

43
Q

Idiopathic chronic inflammation of the liver d/t circulating autoantibodies, MC in young women

A

Autoimmune hepatitis

44
Q

Dx of autoimmune hepatitis

A

Autoantibodies: Type I: positive ANA, smooth muscle antibodies, Type II: anti-liver/kidney microsomal antibodies, increased IgG

45
Q

Tx of autoimmune hepatitis

A

Corticosteroids, CS + Azathioprine, or 6-Mercaptopurine

46
Q

Acute viral hepatitis sx

A

Prodromal phase: malaise, arthralgia, fatigue, URI symptoms, anorexia, decreased desire to smoke, N/V, abdominal pain, loss of appetite, alcoholic stools; Hepatitis A is associated with a spiking fever

Icteric phase: jaundice (most don’t develop this time), if present, jaundice usually develops once the fever subsides

Fulminant: encephalopathy, coagulopathy, hepatomegaly, jaundice, edema, ascites, asterixis, hyperreflexia

47
Q

a clinical syndrome of severe liver function impairment, which causes hepatic coma and the decrease in synthesizing capacity of liver, and develops within eight weeks of the onset of hepatitis

A

Fulimant hepatitis

48
Q

3 causes of fulimant hepatitis

A

Acetaminophen toxicity most common in the US

Viral hepatitis, autoimmune hepatitis, drug reactions (Tolcapone), sepsis

Reye Syndrome: fulminant hepatitis in children given ASA after a viral infection

49
Q

Fulimant hepatitis sx

A

Encephalopathy: vomiting, coma, AMS, seizures, asterixis (flapping tremor of the hand with wrist extension), hyperreflexia, cerebral edema, increased ICP

Coagulopathy: increased PT, INR 1.5+, & eventually increased PTT d/t ↓ hepatic production of coagulation factors

Hepatomegaly, jaundice (not usually seen in Reye syndrome)

Reye Syndrome: may develop rash (hands & feet), intractable vomiting, liver damage, encephalopathy, dilated pupils with minimal response to light & multi-organ failure

50
Q

Tx of fulimant hepatitis

A

Supportive: IV fluids, electrolyte repletion, Mannitol if ICP elevation, PPI stress ulcer prophylaxis

Active bleeding coagulopathy? Blood products of platelets or cryoprecipitate

Definitive: liver transplant

51
Q

Acute viral infection of the liver, usually a mild acute illness w/ recovery in a few weeks

A

Hep A

52
Q

Sx of Hep A

A

Most patients asyx or mildly syx – may be associated with spiking fever

Malaise, anorexia, nausea, vomiting, abdominal pain – RUQ

53
Q

Dx of Hep A

A

LFT: elevated AST, ALT, bilirubin

Acute: IgM anti-HA V

Past exposure: IgG HAV Av with negative IgM

54
Q

Fecal-oral (similar to HAV) – fecal contaminated food & water, blood transfusions, mother-to-child transmission

A

Hep E

Highest mortality due to fulimant hepatitis during pregnancy

55
Q

Hep C dx

A

anti-HCV antibodies usually becomes (+) within 6 weeks, does NOT imply recovery (may become negative after recovery), increased LFTs

Confirmatory: HCV RNA quant more sensitive than HCV antibody (may be (+) in pts with negative ab testing) – HCV RNA best way to determine viral replication activity

56
Q

Hep B Dx

A

HBcAb = Exposure

HBsAG = Infection

HBsAb = Immunity

57
Q

Congenital megacolon d/t absence of ganglion cells, leading to a functional obstruction

A

Hirschsprung dz

58
Q

Hirschsprung is MC where?

A

MC in the distal colon & rectum;

M>F 4:1, Down syndrome, Chagas disease, MEN II

59
Q

Pathophys of Hirschsprungs

A

Failure of complete neural crest migration leads to an absence of enteric ganglion cells (Auerbach & Meissner plexuses)

which leads to failure of relaxation of the aganglionic segment & subsequent functional obstruction

60
Q

Neonatal intestinal obstruction: meconium ileus (failure of meconium passage 48+ hours) in a full-term infant

Bilious vomiting, abdominal distention, no stool in rectal vault, failure to thrive

A

Hirschsprungs sx

61
Q

Dx of Hirschsprungs

A

Contrast enema: transition zone (caliber change) between normal & affected bowel, also helpful for sx planning

Anorectal manometry: as a screening test (measures anal sphincter pressure); increased anal sphincter pressure & lack of relaxation of the internal sphincter with balloon rectal distention

Rectal biopsy: definitive, rectal suction biopsy usually performed with full thickness biopsy (need submucosa)

Abdominal XR: decreased or absence of air in rectum + dilated bowel loops

62
Q

Tx of Hirschsprungs

A

Resection of the affected bowel segment

63
Q

Nonobstructive, extreme colon dilation >6cm + signs of systemic toxicity

A

Toxicmegacolon

64
Q

Sx of Toxic megacolon

A

Profound bloody diarrhea, abdominal pain & distention, N/V, tenesmus

Lower abdominal tenderness & distention

Signs of toxicity: AMS, tachycardia, hypotension, dehydration, & may have signs of peritonitis (rigidity, guarding, rebound tenderness)

65
Q

Dx of Toxic megacolon

A

Initial imaging of choice: Abd XR = evidence of colon 6cm+, can use CT to assess complications • 3 or more of the following:

Fever 38C+, Pulse 120+, Neutrophilic leukocytosis 10,500+/Ul, Anemia

Plus at least one: hypotension, dehydration, electrolyte abnormalities, AMS

66
Q

Type of inguinal hernia with bowel protrusion through the *internal inguinal ring down the inguinal canal (may pass into the scrotum)

A

Indirect Hernia = GOES IN!

67
Q

Indirect lateral or medial to inferior epigastric artery?

A

The origin of the sac is LATERAL to the inferior epigastric artery

68
Q

MC type of hernia in both sexes (M>F), young children & young adults

A

Indirect

69
Q

Where is direct hernia located?

A

origin of the sac is MEDIAL to the inferior epigastric artery within Hesselbach’s triangle

70
Q

Hesselbach’s triangle (RIP)

A

Rectus abdominis @ Medial border,

*Inferior epigastric vessels @ lateral border,

*Poupart’s (inguinal) ligament @ inferior border

71
Q

Telescoping (invagination) of a proximal intestinal segment into adjoining distal lumen→bowel obstruction

A

Intussusception

72
Q

MC location of intussusception

A

MC occurrence @ the ileocolic junction

MCC of bowel obstruction in children 6 months→4 years of age

73
Q

MCC of bowel obstruction in children 6 months→4 years of age

A

Intussusception

74
Q

vomiting + abdominal pain + passage of blood per rectum – “currant jelly” stools (stool mixed with blood + mucus), abdominal pain is colicky in nature occurring every 15-20 minutes

A

Intussusception

75
Q

sausage-shaped mass in the right upper quadrant or hypochondrium + emptiness in the right lower quadrant (Dance’s sign) due to telescoping of the bowel

A

Intussusception

76
Q

Intussusception Dx

A

Ultrasound: best initial test – donut or target sign

Abdominal radiograph: lack of gas in the bowels, “Crescent sign”/“Bull’s eye/target sign/coiled spring lesion” representing layers of the intestine within the abdomen.

Air or contrast enema: both diagnostic & therapeutic, air enema more commonly used than barium, especially if peritonitis is present – water-soluble contrast preferred over barium

77
Q

MCC of neonatal jaundice

A

Breastfeeding failure – caused by insufficient breast milk consumption (inadequate amounts of bowel movements to excrete bilirubin from the body)

Breast milk jaundice – infant liver is not mature enough to process lipids, occurs around 4th and 7th day of life (mom should keep breastfeeding)

Pathologic: Crigler-Najjar syndrome, Gilbert syndrome, cretinism, hemolytic anemia, Dubin-Johnson syndrome

78
Q

Kernicterus

A

cerebral dysfunction and encephalopathy due to bilirubin deposition in brain tissue – can manifest as seizures, lethargy, irritability, hearing loss, mental developmental delays – associated with bilirubin levels 20 mg/dL+

79
Q

Tx of neonatal jaundice

A

No management needed in physiologic jaundice

Phototherapy = initial management of choice of all types

  • For term infants without risk factors: phototherapy is initiated based on total bilirubin: 24 hours of age 12+, 48 hours 15+ or 72 hours of age 18+ – values lower can be used in preterm or at-risk infants
  • Exchange transfusion in severe cases (hemolysis, ABO incompatibility, Rh isoimmunization), IV immunoglobulin may be needed with iso-immune hemolysis
80
Q

Hereditary conjugated (direct) hyperbilirubinemia d/t decreased hepatocyte excretion of conjugated bilirubin d/t gene mutation MRP2

A

Dubin-Johnson Syndrome

81
Q

3 D’s in Dubin Johnson

A

Think Ds: Dubin, Direct bilirubinemia, Dark liver

82
Q

Dx of Dubin Johnson

A

Mild, isolated conjugated (direct) hyperbilirubinemia (often between 2-5 mg/dL) but can increase with concurrent illness, pregnancy or OCPs

Biopsy: grossly black liver, & dark granular pigment in the hepatocytes

83
Q

Hereditary unconjugated (indirect) hyperbilirubinemia

A

Crigler-Najjar Syndrome

84
Q

2 types of Crigler-Najjar

A

Type I: no UGT activity, autosomal recessive…!!!

Type II (Arias Syndrome)

85
Q

Dx of Crigler-Najjar

A

Mild, isolated conjugated (direct) hyperbilirubinemia (often between 2-5 mg/dL) but can increase with concurrent illness, pregnancy or OCPs

Biopsy: grossly black liver, & dark granular pigment in the hepatocytes

86
Q

Dx of lactose intolerance

A

Clinical diagnosis – symptom improvement after a trial of a lactose-free diet

Hydrogen breath test: test of choice, hydrogen produced when colonic bacteria ferment the undigested lactose – usually performed after a trial of a lactose free diet if the diagnosis is uncertain

87
Q

Hypertrophy & hyperplasia of the pyloric muscles causing a functional gastric outlet obstruction

A

Pyloric Stenosis

88
Q

Nonbilious, projectile vomiting (after feeding)

A

Pyloric stenosis

89
Q

PE findings of pyloric stenosis

A

palpable pylorus (“olive-shaped” nontender, mobile hard mass on right of epigastrium)

esp. after emesis, hyperperistalsis, succession splash on auscultation

90
Q

Dx of pyloric stenosis

A

Initial test of choice: Abdominal U/S – elongated, thickened pylorus (more sensitive test) – will see “double-track”
Barium upper GI series:

String sign (thin column of barium through narrow pyloric channel), delayed gastric emptying

Railroad track sign: excess mucosa in the pyloric lumen → 2 columns of barium Labs: hypokalemia & hypochloremic metabolic alkalosis from vomiting

91
Q

MCC of intestinal obstruction in infancy

A

Pyloric stenosis

92
Q

Tx of pyloric stenosis

A

Initial: Rehydration (IV fluids) & electrolyte repletion (eg, potassium replacement)

Definitive: Pyloromyotomy [surgical incision of the hypertrophied pyloric muscle – Ramstedt procedure]

93
Q

Sx of pellearain Niacin deficiency

A

Pellagra (3Ds): dermatitis, diarrhea, & dementia

94
Q
  • The prevalence of ________ deficiency is approximately 30 percent among children under age five worldwide and nearly 50 percent in young children in South Asia and sub-Saharan Africa
A

vitamin A

95
Q

Swollen gums, bruising, petechiae, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, and corkscrew hair

A

Sx of Scruvy

96
Q

How does vitamin D def present in kids

A

Disease in children = Rickets & osteomalacia, Adults = osteomalacia

EOR- PEDS (9 decks)

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