You can do this! Flashcards

1
Q

Most common organisms associated with viral gastroenteritis

A
Rotavirus
Adenovirus
Astrovirus
Calicivirus
Coronavirus
Sapovirus
Parvovirus
Top 3-4 are going to be
Rotavirus
Adenovirus
Noravirus
Coronavirus
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2
Q

Organisms associated with bacterial gastroenteritis

A
Staphylococcus
E.Coli
Campyobacter
Salmonella
Shigella
Yersinia
Vibrio Parahaemolyticus
Aeromonas
Bacillus Cereus
Clostridium Perfringens
C.Difficile
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3
Q

Protozoa and parasites associated with gastroenteritis that cause infection resulting in fluid loss and malabsorption

A

Cryptosporidium
Isospora
Cyclospora

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4
Q

Protozoa and parasites associated with gastroenteritis that directly infect the small bowel leading to malabsorption

A

Giardia

Enteromonas hominis

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5
Q

most common 3 symptoms for gastroenteritis

A

fever
vomiting
diarrhea

not all 3 are required to be present

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6
Q

diarrhea definitions

A

1) a normal BM that has increased in frequency and large water content
2) Stool output greater than 3 times per day (24 hours)

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7
Q

days to be acute diarrhea

A

<= 14 days

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8
Q

days to be persistent diarrhea

A

15-29 days

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9
Q

days to be chronic diarrhea

A

> =30 days

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10
Q

bloody diarrhea, vomiting, and periorbital edema or edema of extremities
should make you think about

A

HUS (Hemolytic Uremic syndrome)

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11
Q

Can ear infections be a reason for vomiting and/or diarrhea

A

yes

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12
Q

diarrhea, vomiting and oral lesions may be a sign of

A

IBD

certain viral illnesses

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13
Q

diarrhea, vomiting, fever, and erythema in the oropharynx or malodorous breath may be evidence of

A

sinusitis or pharyngitis

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14
Q

Pain in the RLQ should make you think

A

appendicitis

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15
Q

Pain in the LUQ may be associated with what organs

A

pancreas

Spleen

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16
Q

Pain at the costovertebral angle may indicate

A

kidney infection

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17
Q

Pain at the flank may be related to

A

pylonephritis

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18
Q

localized pain is a red flag that says what about gastroenteritis

A

that there is another cause for the pain other than gastroenteritis

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19
Q

maintenance ORS guidelines

A

Use for maintenance fluids
<10kg- 60mL-120mL for each episode of vomiting or diarrhea
>10kg - 120-240mL for each episode of vomiting or diarrhea
plus regular diet

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20
Q

ORS for mild to moderate dehydration

severe requires IV fluid

A

first replace fluid deficits then maintain
50-100mL/kg over 2-4 hours

An additional
<10kg- 60mL-120mL for each episode of vomiting or diarrhea
>10kg - 120-240mL for each episode of vomiting or diarrhea

start small (5-10 mL) every 5-10 min and increase as tolerated

after replace losses and vomiting stops, resume diet and continue maintenance ORS

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21
Q

Probiotic use in gastroentritis

A

may shorten by 1 day

Lactobacillus rhamnosus GG (LGG) was most effective

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22
Q

Zinc in gastroenteritis

A

Not formally recommended by CDC but research shows potential reduction in diarrhea with improved outcomes

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23
Q

which organisms cultured from stool would a pt need to demonstrate several negative stool cultures before returning to school or daycare

A

Salmonella serotype Typhi
Shiga toxin-producing E.Coli (STEC)
E.Coli 0157:H7
Shigella

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24
Q
In general, other than 
Salmonella serotype Typhi
Shiga toxin-producing E.Coli (STEC) 
E.Coli 0157:H7
Shigella

afebrile pts with gastroenteritis may return to school when?

A

when they have less than 3 episodes of loose stool a day

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25
Q

Which organism does the book point out as the cause for nearly 600,000 visits to HCPs , upwards of 70,000 hospitalizations and 20-70 deaths exceeding 1 billion in care costs

A

Rotavirus

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26
Q

Type of transmission for Gastroenteritis

A

Fecal-oral transmission

person to person…direct…fomites, ect

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27
Q

a right lower quadrant pain elicited by pressure applied on the left lower quadrant

A

Rovsing’s sign

appendicitis

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28
Q

Rovsing’s sign

A

a right lower quadrant pain elicited by pressure applied on the left lower quadrant
appendicitis

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29
Q

the point on the lower right quadrant of the abdomen at which tenderness is maximal

A

McBurney’s point

appendicitis

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30
Q

McBurney’s point

A

the point on the lower right quadrant of the abdomen at which tenderness is maximal
appendicitis

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31
Q

Pain is elicited by having the patient lie on his or her left side while the right thigh is flexed backward

A

Psoas sign

appendicitis

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32
Q

Psoas sign

A

Pain is elicited by having the patient lie on his or her left side while the right thigh is flexed backward
appendicitis

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33
Q

discomfort felt by the subject/patient on the slow internal movement of the hip joint, while the right knee is flexed with lateral movement of flexed knee outward

A

Obturator sign

appendicitis

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34
Q

Obturator sign

A

discomfort felt by the subject/patient on the slow internal movement of the hip joint, while the right knee is flexed with lateral movement of flexed knee outward

appendicitis

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35
Q

What sign?

pain with coughing

A

Dunphy

appendicitis

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36
Q

Dunphy sign

A

pain with coughing

appendicitis

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37
Q

What sign

pain with heel drop

A

Markle sign

appendicitis

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38
Q

Markle sign

A

pain with heel drop

appendicitis

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39
Q

stool that has the appearance and consistency of liquid tar, is black in color and offensive in odor

A

Melena

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40
Q

The vast majority of patients with UGI bleeding have ________ or _____ secondary to _____

A

lesions of the GI mucosa
esophageal varices
liver disease

The vast majority of patients with UGI bleeding have lesions of the GI mucosa or esophageal varices secondary to liver disease

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41
Q

most common cause of colonic bleeding worldwide

A

Infectious colitis

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42
Q

an infant with GI bleeding who is fed cows milk or soy based formula may have

A

allergic collitis

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43
Q

A history of dry heaves followed by hematemesis or melena may suggest

A

Mallory Weiss tear

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44
Q

Recent illness with GI bleeding may lead you to what

A

HUS

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45
Q

Ingestion of ______ can lead to gastritis, duodenitis, or ileal and right colonic lesions

A

NSAIDS

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46
Q

Liver disease may be related to what inherited deficiency

A

Alpha 1 antitrypsin

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47
Q

what disease can be transmitted at birth and affect the liver

A

Hepatitis B

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48
Q

BRUE symptom with GI bleed…think…

A

UGI bleed such as esophagitis, gastritis or ulcer

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49
Q

Urgency to defecate or Tenesmus ( the feeling that you need to pass stools, even though your bowels are already empty) suggests

A

colitis

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50
Q

Delayed passage of meconium or constipation in infancy can be a sign of

A

Hirschsprung disease

Cystic Fibrosis

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51
Q

The presence of spider angiomata, palmar erythema, fetor hepaticus or splenomegaly suggests chronic ______ disease and _____ _____

A

Chronic liver disease

Portal Hypertension

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52
Q

If a pt is on antibiotics and getting no enteral nutrition, what should you be concerned with?

A

Killing the intestinal track’s vitamin K producing bacteria which will cause the patient’s prothrombin time (PT) to rise, resulting in a coagulopathy. Add NG suction to this perfect storm and you have an UGI bleed from the NG tube suction induced mucosal injury

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53
Q

GI bleed patient that you find a palpable moveable rectal mass on might identify _____ as a possible etiology

A

Polyps

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54
Q

what are some things that patients may ingest that can give the appearance of blood in stool

A

commercial dyes (#2 and #3)
Blueberries
Beets
Bismuth

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55
Q

what diagnostic exam is used if you suspect upper GI bleeding

A

upper endoscopy

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56
Q

what diagnostic exam is used if you suspect bright red lower GI bleeding

A

Colonoscopy

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57
Q

what organism is associated with bleeding duodenal or gastric ulcer

A

Helicobacter Pylori

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58
Q

What should occur with bleeding esophageal varices or varices that have recently bled

A

Should be sclerosed or banded to decrease risk of re-bleeding

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59
Q

what medication is used to decrease central venous pressure for management of bleeding esophageal varices before endoscopic intervention

A

Octreotide

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60
Q

In the case of variceal bleeding that is not controlled by endoscopic and/or tamponade intervention, what procedure is warranted

A

emergency transjugular intrahepatic portosystemic shunting (TIPS) or surgical shunting to decrease portal hypertension may be warranted

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61
Q

In patients with significant GI bleeding who the source was not detected by upper endoscopy and colonoscopy, what is next step

A

a nuclear medicine tagged RBC bleeding study to help find source of blood loss

(bleeding will have to be brisk enough to detect with this scan)

If actively bleeding, an angiogram with selective vessel embolization may be required

A single or double balloon enteroscopy may help identify a radiographically silent lesion or one beyond the reach of the conventional upper or lower endoscope

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62
Q

does a negative gastric lavage test with NGT rule out UGI bleed

A

No, bleeding may have stopped or pylorospasm could be preventing blood from a duodenal source from entering the stomach

Not routinely performed for a stable patient with formed brown guiac positive stools

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63
Q

why is continuous suction via NGT controversial in GI bleeds

A

can exacerbate bleeding

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64
Q

Polyps are removed with what during a colonoscopy

A

Electrocautery

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65
Q

When does GI bleeding resolve in Henoch-Schonlein Purpura (HSP) and HUS

A

with resolution of the disorders

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66
Q

UGI bleeds - when can the patient resume their diet

A

within 24 hours

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67
Q

Upper GI bleed discharge meds

A

PPI for gastritis
Beta blocker (propanolol) for esophageal varices
follow up with GI

lower GI bleeds will depend on the etiology of the bleed

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68
Q

upper GI bleeding differentials
infant vs young child vs older child/adolescent

Bolick chart pg 441

A

All ages

  • Hemorrhagic gastritis/gastritis
  • Stress ulcer
  • Reflux esophagitis

Infant only
-Vascular malformation

Young child to adolescent

  • gastric/duodenal ulcer
  • Esophageal varices
  • Epistaxis
  • Mallory-Weiss tear

Young Child

  • Foreign Body
  • Toxic Ingestion
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69
Q

Lower GI bleeding differentials
infant vs young child vs older child/adolescent

Bolick chart pg 441

A

All ages

  • Infectious colitis
  • Anal fissures

Infant only

  • Necrotizing enterocolitis
  • Milk Protein Allergy
  • Hirschsprung disease
  • Lymphonodular hyperplasia

Infant and young child

  • Midgut volvulus
  • Intussusception

young child only

  • Pseudomembranous colitis
  • Ischemic colitis

young child through adolescence

  • Hemorrhoid
  • Ulcers
  • Polyps
  • Juvenile Polyps
  • Hemolytic-uremic syndrome (HUS)
  • Inflammatory bowel disease
  • Henoch-Schonlein purpura (HSP)
  • Meckel Diverticulum
  • Angiodysplasia
  • Graft-vs-host disease

older child through adolescence
-Bacterial enteritis

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70
Q

Pediatric end-stage liver disease scoring formula

A

PELD score = 1 x (0.48 x (bilirubin)) + (1.857 x (INR)) - (0.687 x (albumin)) + listing age factor + growth

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71
Q

Upper GI bleed vs Lower GI bleed is differentiated by the

A

Ligament of Treitz (located between jejunum and duodenum)

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72
Q

hematemesis is associated with upper or lower GI bleeding

A

upper

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73
Q

Hematochezia is associated with upper or lower GI bleeding

A

Lower

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74
Q

Most common intra- abdominal tumors in children

A

neuroblastoma and Wilms tumor

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75
Q

an ischemic and inflammatory disorder of the bowel most prominently seen in the jejunum, ileum, and colon primarily affecting premature infants after then initiation of enteral feeding.

A

Necrotizing enterocolitis (NEC)

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76
Q

What happens in NEC

A

intestinal injury then activates the gut’s inflammatory cascade, causing mucosal damage and allowing invasion of the bowel wall by bacteria

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77
Q

who is at highest risk for NEC

A

preterm infants in the first 6 weeks of life
more than 90% of cases occur in preterm infants born less than 32 weeks PCA and birth weights less than 1500gms

10% of NEC cases occur in term infants with underlying pre-existing illnesses such as congenital heart disease

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78
Q

Maternal risk factors associated with NEC

A

placental insufficiency
gestational hypertension with superimposed pre-eclampsia
maternal smoking
maternal infection/inflammatory conditions

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79
Q

shiga-toxin producing organism strain that causes gastroenteritis

A

E. coli O157:H7

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1222). Wolters Kluwer Health. Kindle Edition.

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80
Q

what organism for bacterial gastroenteritis is antibiotics contraindicated in treating

A

E. coli O157:H7

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81
Q

antidiarrheal medications for gastroenteritis for kids

A

Antidiarrheal medications often contain aspirin, which contributes to Reye syndrome and should be avoided.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1223). Wolters Kluwer Health. Kindle Edition.

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82
Q

causes of inflammatory bowel disease

A

Crohn disease

ulcerative colitis.

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83
Q

Meckel diverticulum (ectopic gastric mucosa) is most common in what age

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1224). Wolters Kluwer Health. Kindle Edition.

A

school aged children

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84
Q

coffee ground emesis….are you thinking upper or lower GI bleed

A

upper

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85
Q

Management of GI bleed, unstable

A
  • Obtain IV access and administer fluid volume.
  • Initial fluids: normal saline, lactated Ringer solution, and/or packed RBCs (PRBCs).
  • NPO.
  • Proton pump inhibitor; intravenously.
  • Consider octreotide for bleeding esophageal varices; may also require banding via upper endoscopy.
  • Consider vitamin K administration if coagulopathy noted.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1225-1226). Wolters Kluwer Health. Kindle Edition.

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86
Q

infant risk factors for NEC

A
gestational age
birth weight less than 1500 gms
nonhuman milk enteral feeding
circulatory instability with associated GI ischemia
Anemia with blood transfusion
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87
Q

clinical presentation of NEC

A
mild to gaseous abd distention
feeding residuals - can be bilious or bloody
vomiting
bloody stools
signs of shock
also can have
lethargy
episodes of apnea
resp distress
bradycardia
desaturations
temp instability
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88
Q

diagnostic for NEC

A

AP or Lat decub of abdomen may show ileus, dilated loops of bowel, pneumatosis intestinalis, ascites, intrahepatic portal venous air, persistent fixed loops of bowel and free air indicative of perforation

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89
Q

lab findings commonly found in NEC

A
metabolic acidosis
thrombocytopenia
neutropenia
coagulopathies
electrolyte disturbances
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90
Q

Management of NEC

A
decompression of bowel
broad spectrum abx coverage for sepsis
supportive care
NPO
collect blood cultures, urine, CSF
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91
Q

pneumatosis intestinalis on x ray

A

NEC

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92
Q

The infant with medical NEC will typically recover after

A

prolonged period of bowel rest (parenteral nutrition support)
empiric treatment for infection (7-10 days)

if they perforate they will need peritoneal drain or laparotomy of diseased segments of bowel

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93
Q

abd mass with weight loss, anorexia, fever, night sweats, and often easy bleeding or bruising

A

think neoplasm

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94
Q

abd mass with hx of bilious emesis or encopresis (fecal incontinence)

A

bowel obstruction

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95
Q

cola- colored urine and acholic stools

A

Urinary excretion of bile salts

associated with renal pathology of abd mass

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96
Q

RUQ masses most often involve

A

liver
gallbladder
biliary tree

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97
Q

Epigastric masses can include both

A

epigastric hernias

Diastasis recti

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98
Q

LUQ masses think

A

spleen
stomach
adrenal gland
kidney

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99
Q

R and LLQ masses may be from

A

ovarian and fallopian processes

or intestines in orgin

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100
Q

suprapubic masses are most commonly ____ in nature

A

genitourinary

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101
Q

mobility or immobility of abd mass suggest

A

degree of attachment or invasion of the retroperitoneum

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102
Q

immobile abd mass

A

invasive tumors or

masses that arise from the retroperitoneal organs

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103
Q

Tenderness to abd mass generally suggests

A

a recent change such as bleeding

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104
Q

Firmness, hardness and irregularity of an abd mass suggest either

A

tumor or

desmoplasia (scar)

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105
Q

smoothness of an abd mass suggests

A

encapsulated mass

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106
Q

Tympany indicates

A

gas such as in a hollow viscus

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107
Q

dullness indicates

A

fluid or solid mass

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108
Q

diagnostic imaging for Hepatobiliary and pancreatic masses

A
Neither US nor CT is effective at imagining the biliary and pancreatic ductal system 
HIDA scan (Hepatobiliary iminodiacetic acid)- traditionally used first now have MRCP (magnetic resonance cholangiopancreatography is now used for hepatobiliary and pancreatic disease
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109
Q

milk allergy typically presents how long after introduction of dairy into diet

A

within a week

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110
Q

types of benign cystic lesions (uncommon in children)- abd masses

A

choledochal cyst
polycystic kidney disease
duplication cyst
cystic teratoma

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111
Q

most common age of presentation of a neuroblastoma

A

18 months with the prevalence greatest in children <4 yrs

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112
Q

Most common renal tumor and 5th most common pediatric malignancy

A

Wilms tumor

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113
Q

Most common age of presentation of Wilms tumor

A

1-5 yrs

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114
Q

most common malignant liver tumor

A

Hepatoblastoma

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115
Q

mean age at diagnosis for hepatoblastoma

A

1 year old

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116
Q

What is hepatoblastoma associated with (increased risk factors)

A
extreme prematurity
very low birth weight
Beckwith-Wiedemann syndrome
Gardner syndrome
Familial Adenomatous Polyposis Disease
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117
Q

what is the preferred diagnostic test for neuroblastoma

A

CT

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118
Q

what race and gender is at highest risk for NEC

A

Black males

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119
Q

prevention for NEC

A

Breastfeeding

preliminary evidence shows probiotics

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120
Q

type of small bowel obstruction….

history of surgery

A

adhesive SBO

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121
Q

type of small bowel obstruction….

with bilious or feculent vomiting and no gas or stool

A

Complete obstruction

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122
Q

type of small bowel obstruction….

decreased stool and almost no gas

A

partial SBO

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123
Q

Bilious vomiting should always suspicious for

A

malrotation with volvulus

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124
Q

why? In pyloric stenosis, their vomitus never contains bile

A

because gastric outlet obstructed proximal to duodenum

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125
Q

Gastric peristaltic waves are often visible in LUQ in

A

pyloric stenosis

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126
Q

“olive” may be palpated

A

pyloric stenosis

Hypertrophied pylorus “olive” may be palpated

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127
Q

lab expectations in pyloric stenosis

A

Hyperchloremic, hypokalemic metabolic alkalosis, elevated BUN secondary to dehydration

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128
Q

xray in pyloric stenosis

A

xray- show huge stomach and diminished or absent gas in intestine

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129
Q

string sign

A

pyloric stenosis

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130
Q

treatment for pyloric stenosis

A

Hydration
electrolyte correction
Surgery - Pyloromyotomy (Ramstedt’s procedure)

Before surgery correct dehydration and hyperchloremic alkalosis
NS bolus followed by infusion of ½ NS containing 5% dextrose and KCl when urine output is observed

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131
Q

classic presentation age for pyloric stenosis

A

3-6 weeks old

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132
Q

Alvardado/MANTRELS rule

A
Appendicitis
1 point for each the following-
-Migration of pain to RLQ
-Anorexia
-N/V
-Rebound pain
-Temp of at least 37.3
-WBC great then 75% neutrophils
2 points for each of 
-tenderness in RLQ and
-leukocytosis greater than 10,000

Children with score of 4 or less- unlikely appy
Score of 7 or greater- increased likelihood

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133
Q

thick-walled appendix with surrounding fluid

Diameter over ___mm considered dx

A

6

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134
Q

most common reason for abd surgery in kids in the US

A

appendicitis

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135
Q

most common age and gender for appendicitis

A

Although it can occur at any age, it is most commonly diagnosed between 10 and 12 years of age and occurs more often in males than females.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1200). Wolters Kluwer Health. Kindle Edition.

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136
Q

a finger-like structure projecting from the cecum,

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1200). Wolters Kluwer Health. Kindle Edition.

A

Appendix

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137
Q

perforated appendicitis treatment

A

• Antibiotic therapy is generally prescribed for 5 to 7 days depending on patient response. Ceftriaxone and Flagyl for perforated appendix have proven to be adequate.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1204). Wolters Kluwer Health. Kindle Edition.

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138
Q

Characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, renal injury

A

HUS

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139
Q

Most common type of HUS

A

prodromal diarrheal illness (D+HUS)
Contaminated meat, fruit, veggie, or water with verotoxin producing E.coli (O157:H7) or Shigella → will have hemorrhagic enterocolitis and progress to HUS

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140
Q
what am I?
presents without prodrome of diarrhea
Can occur at any age 
More severe
Can be secondary to infection (strep pneumo, HIV), genetic, medication, malignancy, SLE, pregnancy
A

Atypical HUS

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141
Q

Entercolitis with bloody stools, followed in 7-10days by weakness, lethargy, anuria/oliguria
Irritable, pallow, petechiae
Dehydration, however some children have volume overload (hypertension may occur)
CNS seizures in 25%, pancreatitis, cardiac dysfunction, colonic perforation

A

D+ HUS

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142
Q

Lab smear: microangiopathic hemolysis
Anemia, thrombocytopenia, schistocytes/helmet/burr cells on smear, incr LDH, incr indirect bili, incr AST, incr reticulocyte
Coombs test is NEGATIVE
Renal injury: elevated Cr, hematuria, proteinuria, pyuria, casts on UA
Leukocytosis, E coli stool culture, shiga toxin, elevated amylase/lipase

A

HUS

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143
Q

Treatment of HUS

A

Volume repletion
Hypertension control
Managing renal insufficiency – dialysis
RBC transfusions
DO NOT GIVE PLATELETS – may add to thrombotic microangiopathy
Only give if active hemorrhage or procedural
NO ABX OR ANTIDIARRHEAL – will make HUS worse

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144
Q

double bubble sign on x ray

A

volvulus

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145
Q

coffee bean sign on x ray

A

volvulus

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146
Q

swirl sign on CT

A

volvulus - diagnostic

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147
Q

an infant with acidosis and abdominal distension is most suspicious for

A

bowel obstruction

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148
Q

infant with aganglionic section of bowel

A

Hirschsprung’s disease

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149
Q

absence or obstruction (due to fibrosis) of the biliary tree, (extrahepatic) leading to intrahepatic bile duct obstruction and proliferation.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1207). Wolters Kluwer Health. Kindle Edition.

A

Biliary atresia

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150
Q

types of Biliary atresia

A

(1) syndromic BA and associated malformations (i.e., BA splenic malformation syndrome, cat-eye) and random malformations (e.g., esophageal atresia (EA), jejunal atresia, malrotation)
(2) cystic BA—cystic change in an obliterated biliary tract
(3) cytomegalovirus-associated BA, in which the infants have positive serology
(4) isolated BA (largest group of infants).

•Proposed nongenetic etiologies: infection, intrauterine infection, toxin exposure.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1207). Wolters Kluwer Health. Kindle Edition.

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151
Q

physical exam findings in biliary atresia

A

jaundice
acholic stools
dark urine

labs
hyperbili
elevated LFT

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152
Q

infectious causes of biliary atresia

A
viral hepatitis
TORCH
Toxoplasmosis
other agents
Rubella
Cytomegalovirus
Herpes simplex
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153
Q

diagnostics for biliary atresia

A

• Radiologic evaluation. • Abdominal ultrasound: gallbladder noted to be absent or small. • Hepatobiliary scintigraphy, in which there is no excretion of the isotope detected in the intestine. • Confirmatory cholangiogram is done at the time of laparotomy/laparoscopy for surgical intervention.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1208). Wolters Kluwer Health. Kindle Edition.

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154
Q

surgical management for biliary atresia

A

• Kasai procedure or portoenterostomy. • Best results in children <2 months of age in experienced hands. •Excision of the extrahepatic biliary tract and anastomosis of a Roux-en-Y limb to the jejunal limb at the porta hepatis. •The goal of the procedure is to reestablish bile flow as evident by pigmented stool in the immediate postoperative period. •Deemed a successful operation if conjugated bilirubin level is <2 mg/dL at 3 months postop; long-term outcome is variable with a small percentage of children achieving lasting drainage that is effective. • Complications: bacterial cholangitis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1208). Wolters Kluwer Health. Kindle Edition.

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155
Q

mutation in CFC1 gene

A

biliary atresia

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156
Q

most common indication for liver transplant

A

biliary atresia

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157
Q

biliary atresia nutritional requirements

A
  • Nutrition. • Require 130% to 150% of the recommended daily allowance, and many require 150 kcal/kg/day to achieve appropriate growth. • May require formulas with increased medium chain triglycerides as they do not require bile acids for digestion (e.g., breastmilk, Pregestimil, or Portagen). • Supplement with fat-soluble vitamins (A, D, E, and K).
  • Supplemental nocturnal feeds with a nasogastric (NG) tube may be necessary for growth failure.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1208-1209). Wolters Kluwer Health. Kindle Edition.

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158
Q

Acute cholecystitis is often attributed to the presence of

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1210). Wolters Kluwer Health. Kindle Edition.

A

Gallstones

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159
Q

Hypoalbuminemia and abdominal mass may suggest

A

nonspecific but indicates significant illness

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160
Q

Uric acid and LDH plus abdominal mass may indicate

A

Solid tumors

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161
Q

Abdominal mass plus BUN and Creatinine may indicate

A

Renal dx

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162
Q

Abdominal mass plus elevated amylase and lipase levels may indicate

A

pancreatic dx

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163
Q

Abdominal mass plus elevated LFTs think

A

Liver dx

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164
Q

2 view abd x ray with abdominal mass will show things such as

A

Intestinal obstruction
fecal impaction
calcifications associated with tumor

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165
Q

US in the setting of abdominal mass may be used to

A

identify origin of the mass
solid vs cystic
can help further lab testing and imaging

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166
Q

CT scan with IV contrast in the setting of abdominal mass may be used to

A
  • evaluate solid abd mass
  • vascular abnormalities
  • associated lymph nodes
  • stage many types of cancers
  • helps with cystic mass to see if there is continuity with bowel or bladder
  • Not helpful if mass of primary bowel or bladder -> Fluoroscopic studies such as UGI series, BE and voiding cystourethrogram
  • Oral contrast will cause artifact to the bowel and bladder
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167
Q

best diagnostic exam for abdominal mass of primary bowel or bladder

A

Fluoroscopic studies such as UGI series, BE and voiding

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168
Q

what diagnostic is used for hepatobiliary and pancreatic masses?

A
  • Neither US nor CT is effective at imagining the biliary and pancreatic ductal system
  • HIDA scan (Hepatobiliary iminodiacetic acid)- traditionally used first now have MRCP (magnetic resonance cholangiopancreatography is now used for hepatobiliary and pancreatic disease
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169
Q

radiograph after standing for 2 minutes has maximum sensitivity for free gas suggesting perforation. (Bowel perforation)

A

Abdominal X-ray- upright chest radiograph

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170
Q

radiograph that has better sensitivity than other radiograph views because gas collects around the liver. Looking for bowel perforation

A

Left lateral decubitus

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171
Q

Radiograph useful for proximal bowel obstruction

A

Upper GI contrast series

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172
Q

imaging Usually appropriate if the abdominal radiograph or physical examination suggests distal bowel obstruction (as might be seen in Hirschsprung disease).

A

contrast enema

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173
Q

imaging used to determine bowel obstruction site

A

CT with IV contrast. Do not use contrast if suspect perforation

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174
Q

on imaging you see numerous air fluid levels, distended bowel normally more central
what does this sound like

A

small bowel obstruction

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175
Q

on imaging you see few to no air fluid levels. Distended bowel normally more peripheral

A

Large bowel obstruction

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176
Q

what type of obstruction?

a small bowel obstruction in a patient who has had surgery or a severe infection of the abdominal cavity

A

Adhesive bowel obstruction

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177
Q

what type of bowel obstruction?

there will be bilious and feculent vomiting with no gas or stool passage per anus

A

Complete bowel obstruction

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178
Q

what type of bowel obstruction??

decreased stool passage and almost no gas passage

A

Partial bowel obstruction

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179
Q

causes of functional bowel obstruction

A
Abd surgery
Peritonitis
Sepsis
Trauma
Medications (opioids, anxiolytics)
Metabolic imbalances (hypokalemia, hyponatremia, hypomagnesemia, acidosis)
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180
Q

causes of mechanical bowel obstruction

A
Postoperative adhesions
Hematoma
Intussusception
Distal intestinal obstruction syndrome
Malrotation with volvulus
Tumors
Bezoar
Congenital abnormalities:
-Duodenal atresia
-Duodenal web
-Annular pancreas
-Jejunoileal atresia
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181
Q

an obstruction caused by a loop in the intestines that twists around itself and surrounding mesentery

A

Volvulus

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182
Q

volvulus that happens in the last part of the large intestines leading to the rectum

A

Sigmoid volvulus

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183
Q

volvulus that happens in the beginning part of the large intestines

A

cecal volvulus

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184
Q

volvulus that happens in the small intestines

A

midgut volvulus

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185
Q

which type of volvulus is the most common type?

A

sigmoid volvulus

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186
Q

occurs when small bowel twists around the superior mesenteric artery, resulting in vascular compromise to large portions of the midgut.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1242). Wolters Kluwer Health. Kindle Edition.

A

Volvulus

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187
Q

______volvulus may lead to widespread intestinal ischemia and progress rapidly to necrosis of the bowel, perforation, shock respiratory failure, and death.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1242). Wolters Kluwer Health. Kindle Edition.

A

Midgut

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188
Q

At approximately the _____week of embryonic life, the gut begins to change from a straight-line structure to an elongated tube herniating into the umbilical cord.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1242). Wolters Kluwer Health. Kindle Edition.

A

4th

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189
Q

Abdominal rotation and attachments are complete by __ months’ gestation.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1243). Wolters Kluwer Health. Kindle Edition.

A

3

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190
Q

______ occurs when the bowel fails to rotate after it returns to the abdominal cavity.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1243). Wolters Kluwer Health. Kindle Edition.

A

Malrotation

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191
Q

Presentation of malrotation is usually when and how does it appear?

Presentation of 
infants
older infants
children
adolescents

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1243). Wolters Kluwer Health. Kindle Edition.

A

in the first year of life with symptoms of acute or chronic bowel obstruction.

Infants present within the first week of life with bilious emesis and acute bowel obstruction.

Older infants present with episodes of recurrent colicky abdominal pain.

Children may present with recurrent episodes of vomiting, abdominal pain, or both.

•Occasionally, patients may present with malabsorption or protein-losing enteropathy associated with bacterial overgrowth. Symptoms are caused by intermittent volvulus or duodenal compression by Ladd bands or other adhesive bands affecting the small and large bowel.

25-50% of adolescents with malrotation are asymptomatic

Symptomatic adolescents present with acute intestinal obstruction of history of recurrent episodes of abdominal pain with less frequent vomiting and diarrhea.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1243). Wolters Kluwer Health. Kindle Edition.

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192
Q

If you suspect malrotation what labs are you ordering?

what is diagnostic?

A

CBC
type and screen
electrolytes (imbalances secondary to vomiting and 3rd spacing fluid into the bowel and abd cavity)

anemia can be caused by pooling of blood intestines

-Flat and upright or lat decub abd x rays - evaluates for intestinal obstruction but cannot diagnose malrotation

Upper GI Series is the preferred study to evaluate the position of the ligament of Trietz
•If malrotation exists, UGI will show abnormal position of the ligament of Trietz, partial obstruction of the duodenum, with a spiral or corkscrew appearance, and proximal jejunum in the right abdomen.
•When volvulus is present, the barium column is noted to end in a peculiar beaking effect and pathognomonic for a volvulus.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1244). Wolters Kluwer Health. Kindle Edition.

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193
Q

management of Malrotation with volvulus

A

emergent LADD procedure

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194
Q

Preop management for Malrotation with volvulus

A

cardiopulmonary and circulatory resuscitation. A gastric decompression tube should be placed, along with the administration of broad-spectrum antibiotics, to cover gut flora.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1244-1245). Wolters Kluwer Health. Kindle Edition.

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195
Q

bilious vomiting in a neonate is highly suspicious for

A

malrotation with volvulus until proven otherwise

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196
Q

cecal volvulus usually occurs in what age group

A

young adults

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197
Q

______ volvulus is most commonly seen in babies and small children

A

midgut volvulus

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198
Q

coffee bean sign on x ray

A

volvulus

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199
Q

birds beak shape on barium enema

A

volvulus

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200
Q

sigmoid volvulus is usually treated with

A

sigmoidoscopy

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201
Q

A _______ may be used to resolve a cecal volvulus

A

Colonoscopy

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202
Q

A colonoscopy cannot be used to treat a _____ volvulus

A

midgut

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203
Q

The most common presenting symptom in Chrohn’s disease

A

is abdominal pain. Pain is commonly crampy, epigastric or periumbilical, and intermittent

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204
Q

increases the risk of IBD

A

smoking
oral contraception
infectious colitis
infectious agents

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205
Q

treatment of Chrohn’s disease

A

Aminosalicylates; oral or IV steroids are more important in reducing remission.

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206
Q

is an umbrella term for Crohn disease and ulcerative colitis, which are inflammatory processes of the GI tract with very similar presentations.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1235). Wolters Kluwer Health. Kindle Edition.

A

Inflammatory Bowel Disease

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207
Q

•The difference between Crohn disease and Ulcerative Colitis is

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1235). Wolters Kluwer Health. Kindle Edition.

A

based on the location and characteristics of the inflammation.

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208
Q

inflammatory process that can affect any portion of the GI tract. Most commonly affects the terminal ileum. The inflammation is in the entire lumen of the intestines.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1235). Wolters Kluwer Health. Kindle Edition.

A

•Crohn Disease:

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1235). Wolters Kluwer Health. Kindle Edition.

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209
Q

inflammatory process that affects the colon and rectum. The inflammation is in the mucosal layer of the intestinal wall.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1235). Wolters Kluwer Health. Kindle Edition.

A

Ulcerative colitis:

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1235). Wolters Kluwer Health. Kindle Edition.

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210
Q

Inflammatory bowel disease is most commonly diagnosed between ____ and ____ age with a second peak between 50-80 yrs of age

A

15 and 30

genetic predisposition that is turned on by environmental factors that causes an excessive immune response that results in chronic intestinal inflammation.

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211
Q

pain, diarrhea, weight loss, perirectal inflammation with fistula.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1236). Wolters Kluwer Health. Kindle Edition.

A

Crohn disease

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212
Q

bloody, watery diarrhea, weight loss, tenesmus, and urgency.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1236). Wolters Kluwer Health. Kindle Edition.

A

Ulcerative colitis

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213
Q

gold standard diagnosis of IBD

A

Endoscopy of the intestinal tract with biopsy and histology

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214
Q

Labs in IBD workup

A
CBC
ESR
CRP
LFT
GGT
IBD serology
Stool studies looking for infectious etiology of diarrhea
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215
Q

induction of remission in IBD

A
  • Corticosteroids are used as first-line therapy for induction and remission after an IBD flare-up. During induction of remission, all maintenance medications are continued because they have the ability to induce remission or help the action of the corticosteroids.
  • Exclusive PN for 8 weeks with bowel rest. This therapy has a similar remission rate as corticosteroids with less side effects.
  • Biologic agents (e.g., Infliximab) are used for severe inflammation or refractory to other treatments to help induce remission.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1236-1237). Wolters Kluwer Health. Kindle Edition.

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216
Q

Maintenance of remission in IBD

A

• Immunosuppressive medications are used to maintain remission because of slow onset of action. • Aminosalicylates (5-ASA) reduce inflammation to maintain remission in mild UC and Crohn disease. • Immunosuppressive therapy should be started while still on steroid treatments; steroids are then tapered. • Supplementary nutrition with any treatment. Probiotics are useful as adjunct therapy. • Antibiotics have a role in treating perirectal fistula or abscess in Crohn disease. •Surgical intervention is appropriate for patients with refractory disease, uncontrolled GI bleeding, bowel perforation, or stricture causing an obstruction, with bowel resection being the last option. •Total colectomy in UC with J-pouch is the surgical treatment of refractory disease, toxic megacolon, perforation, or severe colitis. In UC, a total colectomy can be curative. •Resection of a stricture or area of colitis in Crohn disease is the surgical treatment. In severe cases when the intestines become perforated, an ostomy is required.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1237). Wolters Kluwer Health. Kindle Edition.

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217
Q

Ulcerative colitis is most commonly seen in what age group

A

20-30 yrs old

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218
Q

Ulcerative colitis symptoms

A

Systemic:

  • Fatigue
  • Fever
  • Weight Loss
  • Dyspnea
  • Palpitations (iron def anemia secondary to blood loss)

GI

  • Bloody Diarrhea
  • Colicky Abd pain
  • Tenesmus

Extraintestinal

  • Arthritis
  • Uveitis
  • Episcleritis
  • Skin Lesions (pyoderma gangrenosum & erythema nodosum)
  • Primary sclerosing cholangitis
  • Venous/Arterial Thromboemboli
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219
Q

Acute complications of UC

A
Severe GI bleeding
Fulminant colitis (bleeding with more than 10 stools per day)
Toxic megacolon (nerves and muscles damaged with the colon atonic and dilated) -> can lead to perforation with peritonitis (fevers and severe abd pain)
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220
Q

Long term complications of UC

A
  • increased risk for colorectal cancer

- strictures ->rectosigmoid colon which can lead to bowel obstruction

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221
Q

Chrohns disease symptoms

A

Systemic

  • Fatigue
  • Fever
  • Weight loss

Gastrointestinal

  • Crampy abd pain
  • Watery diarrhea
  • Malabsorption symptoms (Steatorrhea)
  • Fistulas (Communication between 2 epithelial organs)
  • Phlegmon -> abscess
  • oral (ulcers, gingivitis)
  • Gallstones (biliary colic

Extraintestinal

  • Arthritis
  • Uveitis
  • Episcleritis
  • Skin Lesions (pyoderma gangrenosum & erythema nodosum)
  • Primary sclerosing cholangitis
  • Venous/Arterial Thromboemboli
  • Kidney stones
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222
Q

string sign

A

strictures

can be seen in Crohns disease

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223
Q

skip lesions

A

Chrohns disease

not seen in UC

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224
Q

IBD with ileal involvement

A

common in Crohns disease

not seen in UC

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225
Q

IBD with fistulas

A

Common in Chrohns disease

very rare in UC

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226
Q

smoking decreases risk of

A

UC

increases risk of CD

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227
Q

an ilieus is a

A

non-mechanical obstruction of the intestines (caused by a disruption of peristalsis that can be partial or complete resulting in dilation of proximal intestines

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228
Q

Most common cause of an ileus is form

A

manipulation of intestines during surgery

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229
Q

clinical presentation of ilieus

A

Abd distention
absent/hypoactive bowel sounds
pain
vomiting

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230
Q

diagnostic for ileus

A

abd x ray

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231
Q

management of ileus

A

Bowel rest
decompression with NG
Adequate postop pain management w/non-narcotic meds
Routine postop care to include ambulation and time

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232
Q
if an infant doesnt pass meconium within first 48 hrs
abd distension
refuses to feed
bilious vomiting
what should be on your differential
A

Imperforate anus
Meconium ileus
Hirschsprung’s disease

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233
Q

VACTERL Syndrome

A
Vertebral defects
Anal atresia
Cardiac anomalies
Tracheoesophageal fistula
Esophageal atresia
renal anomalies
limb anomalies
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234
Q

meconium ileus is seen with what disease process

A

Cystic fibrosis

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235
Q

what test is for cystic fibrosis if newborn screening test isnt back yet

A

Abnormal sweat chloride test

>60mmol/L

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236
Q

on exam the newborn has a empty rectum with no meconium and with normal sphincter tone

A

Meconium ileus which is a surgical emergency

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237
Q

Abd x ray
Dilated bowel loops
“Soap Bubble”/”Ground Glass” appearance

A

Meconium ileus

238
Q

Squirt sign or blast sign

A

explosive of gas or liquid stool after digital rectal exam (relieves obstruction temporality) in Hirschsprung’s

239
Q

anorectal maonometry will show failure of anal sphincter to relax

A

Hirschsprung’s

240
Q

Disease is due to injury to the mucosa of the small intestine caused by ingestion of gluten (protein component) from wheat, barley, rye, and related gains (causes flattening of the finger-like villi in the small intestine that are used for absorption)

A

Celiac disease

241
Q

celiac disease is associated with what other diseases and syndromes

A

Type I DM
Thyroiditis
Turner’s syndrome
Trisomy 21

242
Q

Diagnostic for Celiac

A

Biopsy diagnostics: villus atrophy; screening with IgA antitissue transglutaminase and antigliadin; resolution of symptoms with gluten elimination and relapse on oral challenge

243
Q

clinical manifestations of celiac disease

A

Chronic diarrhea, irritability, decreased appetite, malabsorption, abdominal distension, flatulence, FTT, weight loss, ascites caused by hypoproteinemia

Other symptoms can include osteopenia, arthritis or arthralgias, ataxia, dental enamel defects, elevated liver enzymes, dermatitis herpetiformis, and erythema nodosum

244
Q

what should be considered in Should be considered in any child with chronic abdominal complaints, short stature, poor weight gain, or delayed puberty

A

Celiac

245
Q

Serological markers for celiac

A

IgA antiendomysial antibody
IgA tissue transglutaminase antibody (ANTI -tTG)

IgA deficient - Use IgG screening test

246
Q

Biopsy for celiac

A

Small bowel biopsy essential to confirm the diagnosis and should be performed while patient still ingesting gluten
Biopsy shows various degrees or villous atrophy (short or absent villi), mucosal inflammation, crypt hyperplasia, and increased numbers of intraepithelial lymphocytes

247
Q

treatment for celiac

A

Elimination of gluten from diet

248
Q

what skin rash can be seen in celiac

A

Dermatitis herpetiformis

249
Q

Celiac disease increases risk of

A

small bowel cancer
T-cell lymphoma
due to chronic inflammation and immune system activation

250
Q

infection responsible for most ulcers in stomach and duodenum in adults; plays a lesser role in childhood ulcer disease

A

H.Pylori

251
Q

What drugs put you at higher risk for Peptic ulcer disease

A

NSAIDS
Tobacco
Bisphosphonates
Potassium supplements

252
Q

other than meds, what other risk factors for PUD

A
Family history
sepsis
head trauma
burn injury
hypotension
253
Q

symptoms of peptic ulcer disease

A
  • “Alarm” symptoms (GI bleeding, weight loss, early satiety, dysphagia or odynophagia, family history of upper GI malignancy, iron deficiency anemia or new upper GI symptoms in patients older than 55)
  • Weight loss, hematemesis, melena (heme-positive stools), chronic vomiting, microcytic anemia, nocturnal pain
254
Q

what type of ulcers?

pain occurs several hours after meals and often awakes patient at night; eating tends to relieve the pain

A

Duodenal ulcers

Gastric and duodenal ulcers heal in 4-8 weeks in 80% patients

255
Q

what type of ulcers?
pain aggravated by eating, resulting in weight loss, GI bleeding can occur; symptom relief with antacids or acid blockers

A

Gastric ulcers

Gastric and duodenal ulcers heal in 4-8 weeks in 80% patients

256
Q

diagnostics for Peptic ulcer disease

A

Endoscopy mandatory with alarm symptoms
Test for H. Pylori
CBC, ESR, amylase, lipase, abd US

-“Alarm” symptoms (GI bleeding, weight loss, early satiety, dysphagia or odynophagia, family history of upper GI malignancy, iron deficiency anemia or new upper GI symptoms in patients older than 55)

257
Q

H-Pylori treatment with ulcers. regimen is twice daily for 1-2 weeks

A
  • Omeprazole (Prilosec)-clarithromycin-metronidazole (flagyl)
  • Omeprazole- amoxicillin- clarithromycin
  • Omeprazole-amoxicillin-metronidazole
  • Other Proton pump inhibitors (PPI) may be substituted when necessary and bismuth compounds may also be considered
  • Tetracycline useful in adults but should be avoided in children less than 8 yo
258
Q

Treatment for PUD with no H. Pylori

A

PPI

259
Q

syndrome that causes a tumor leading to duodenal ulcers

A

Zollinger-Ellison syndrome

260
Q

Risk factors for GERD

A

neurologic impairment, obesity, repaired EA or other congenital esophageal disease, cystic fibrosis, hiatal hernia, repaired achalasia, family history of gastroesophageal reflux disease (GERD).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1218). Wolters Kluwer Health. Kindle Edition.

261
Q

the symptoms or complications of gastroesophageal reflux.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1218). Wolters Kluwer Health. Kindle Edition.

A

GERD

Gastroesophageal reflux: the movement of gastric contents into the esophagus.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1218). Wolters Kluwer Health. Kindle Edition.

262
Q

irritants of peptic ulcers

A

NSAIDS
Alcohol
Tobacco
Caffeine

263
Q

Primary cause is transient relaxation of the lower esophageal sphincter, which allows gastric contents to move into the esophagus.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1218). Wolters Kluwer Health. Kindle Edition.

A

Gastroesophageal reflux

GERD

264
Q

clinical presentation of GERD

A
•   Poor weight gain, feeding aversion. 
•   Unexplained crying, choking, or coughing.
 •   Sleep disturbances.
 •   Gagging. 
•   Regurgitating. 
  Dental erosion (older child).
-Dystonic head positioning (Sandifer syndrome)
-Abdominal or chest pain (older child)

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1219). Wolters Kluwer Health. Kindle Edition.

265
Q

GERD infant managment (non-pharmacologic)

A

• Elevate head of crib 30°; can use reflux wedge, avoidance of overfeeding, upright position for 30 minutes after feeding. • Consider a 1-to-2 week trial of hypoallergenic formula. • Increase caloric density of formula, or consider tube feeding if poor weight gain.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1219-1220). Wolters Kluwer Health. Kindle Edition.

266
Q

GERD child or adolescent non pharmacologic managemment

A
  • Elevated head of bed, left-sided positioning, avoidance of caffeine, chocolate, fatty or spicy foods, carbonated beverages.
  • Small frequent meals, avoid eating 2 to 3 hours before bedtime. • Lose weight if overweight.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1220). Wolters Kluwer Health. Kindle Edition.

267
Q

medication management for GERD

A

• H2 blockers are generally first-line choice, especially for infants. • Proton pump inhibitors; not indicated for infants <1 year of age. • Prokinetic agents can be used to promote stomach emptying.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1220). Wolters Kluwer Health. Kindle Edition.

268
Q

surgical management for GERD

A

•Nissen fundoplication—the fundus of the stomach is wrapped around the lower esophagus to improve function of the lower esophageal sphincter. • Complication rates are higher in neurologically impaired children. •Due to the risk of complications, usually reserved for those children with multiple pneumonia episodes felt to be related to aspiration and those with intractable reflux unresponsive to medical therapy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1220). Wolters Kluwer Health. Kindle Edition.

269
Q

one of the most common causes of vomiting in infant

A

pyloric stenosis

270
Q

Vomiting secondary to gastric outlet obstruction from hypertrophied pyloric muscle and subsequent gastric outlet obstruction.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1252). Wolters Kluwer Health. Kindle Edition.

A

Pyloric stenosis

271
Q

onset of symptoms age for pyloric stenosis

A

2-8 weeks of age with peak at 3-5 weeks

272
Q

common findings on chemistry in pyloric stenosis

A

Hypochloremia
hypokalemia
hyperbilirubinemia

273
Q

•Peristaltic waves may be visualized across the abdomen. •Olive-sized mass may be palpated in right upper quadrant.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1253). Wolters Kluwer Health. Kindle Edition.

A

Pyloric stenosis

274
Q

diagnostic confirmed for Pyloric stenosis with

A

abdominal US

275
Q

How do we fix pyloric stenosis

A

Pyloromyotomy either open or laparoscopically - splits the pyloric muscle to increase diameter and gastric emptying

276
Q

After a pyloromyotomy, when can feedings restart

A

once gastric contents are able to empty into duodenum, usually 6 hours postop

277
Q

Telescoping of segment of proximal bowel into downstool bowel, usually occur between 1-2 yrs old

A

Intussusception

278
Q

symptoms of Intussusception

A

Sudden onset of crampy abdominal pain- infants knees draw up and infant cries out and exhibits pallor with colicky pattern occurring every 15-20 minutes
Feedings are refused
As it progresses and becomes prolonged- bilious vomiting and dilated fatigued intestine generate less pressure and less pain
Currant jelly stools
Lethargy – glassy eyes and groggy infant
Sausage shaped mass palpable in RUQ or epigastrium

279
Q

imaging for Intussusception

A

Abdominal US
Pneumatic or contrast enema under fluoroscopy – can be used to identify and treat intussusception
Air and barium

280
Q

most common cause of intestinal obstruction in infants and children. It can lead to intestinal death and high morbidity if untreated.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1237). Wolters Kluwer Health. Kindle Edition.

A

Intussusception

281
Q

who is Intussusception most commonly seen in

A

slight increase among white males

282
Q

idiopathic Intussusception is most common in what age group

A

infants and young children

283
Q

idiopathic Intussusception - association with what?

A

recent URI or gastroenteritis

284
Q

Lead point intussusception is most common in what age

A

5-14 years

285
Q

Lead point intussusception - increased risk with what

A
Meckel diverticulum
Polyps
cyst
carcinoid tumors
foreign bodies
hemangioma
Non-hodgkins lymphoma
Intestinal hematomas
Henoch-schonlein purpura
286
Q

Postsurgical intussusception is typically seen after

A

abd or chest surgery from decreased motility after anesthesia

287
Q

in babies what is the leading edge most often from that causes intussusception

A

Lymphoid hyperplasia (enlargement of lymph tissue such as peyers patches)

288
Q

sausage like mass in abdomen

A

intussusception

289
Q

intussusception can lead to what complication

A

obstruction and even volvulus

290
Q

Bull’s eye sign

A

intussusception

291
Q

a congenital defect in which there is interruption of the continuity of the esophagus; the esophagus ends in a blind pouch;

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1213). Wolters Kluwer Health. Kindle Edition.

A

Esophageal atresia

292
Q

Esophageal atresia

Type A is

A

EA without fistula

293
Q

Esophageal atresia

Type B is

A

EA with proximal fistula

294
Q

Esophageal atresia

Type C is

A

EA with distal fistula; most common type

295
Q

Esophageal atresia

Type D is

A

EA with proximal and distal fistulas

296
Q

Esophageal atresia

Type E is

A

Tracheoesophageal fistula without atresia

297
Q

•Newborn with excessive oral secretions, drooling, accompanied by coughing, choking, or sneezing. • Feeding can cause cyanosis, choking, and emesis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1214). Wolters Kluwer Health. Kindle Edition.

A

Esophageal atresia

298
Q

diagnostic for Esophageal atresia

A

•Failure to pass NG or orogastric tube into the stomach. •Chest radiograph—anteroposterior and lateral, which demonstrates NG tube coiled in upper esophagus. •Assess for VACTERAL (Vertebral, Anorectal, Cardiac, Tracheoesophageal, Renal, and Limb anomalies) association.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1214). Wolters Kluwer Health. Kindle Edition.

299
Q

Most pt with an esophageal atresia have a

A

Tracheoesophageal fistula

300
Q

In Esophageal atresia The end of the oral gastric tube is typically observed at the ___ to ____ level

A

T2 to T4

301
Q

when air is seen in the stomach and bowel with a esophageal atresia, the presence of what is confirmed

A

distal fistula

However a gasless abdomen on CXR does not negate the presence of a fistula. The TEF can be proximal

302
Q

​​Holiday-Segar Method:

A

1-10 kg= 100 mL/kg/day
10-20 kg= add 1,000 mL + 50 mL/kg/day for every kg greater than 10
> 20 kg= 1,500 mL + 20 mL/kg/day for every kg greater than 20

303
Q

421 method

A

4 mL/kg/hr for 1st 10 kg
Example: a 10kg pt would receive 40 mL/hr
2 mL/kg/hr for next 10 kg
Example: a 20kg pt would receive 60 mL/hr
1 mL/kg/hr thereafter
Example: a 30kg pt would receive 70 mL/hr

304
Q

BSA method

A

Used for pts who are 10 kg or over

1600 mL/m2/day

305
Q

which maintenance fluid calculation method is the most accurate

A

BSA

306
Q

standard formula or breastmilk has how many kcal/oz

A

20 kcal/oz

307
Q

Fortified formula/EBM has how many kcal/oz

A

22-30 kcal/oz

308
Q

Pediasure has how many kcal/oz

A

30kcal/oz

309
Q

If you have 20kcal in 1 oz

how many kcal in 1 mL

A

20 divided by 30

= 0.66Kcal/mL

310
Q

most common type of dehydration, often related to gastroenteritis where losses of water and salt in stool are typically balanced

A

isonatremic

311
Q

type of dehydration?

If patient also has vomiting and more loss of water than salt occurs (most dangerous d/t neurologic damage)

A

Hypernatremic

312
Q

type of dehydration?

Results from loss of fluid, especially salt, in stool or sweat

A

Hyponatremic

313
Q

tachycardia is present in what degree of dehydration

A

moderate and severe

314
Q

Palpable pulses are decreased in what degree of dehydration

A

severe

weak pulses in moderate

315
Q

Orthostatic hypotension is seen in what degree of dehydration

A

moderate

316
Q

Hypotension is seen in what degree of dehydration

A

severe

317
Q

absent tears are seen in what degree of dehydration

A

severe

318
Q

in Hyperchloremic dehydration what is the preferred fluid replacement

A

LR

319
Q

advantage of LR over NS

A

NS will make you more acidotic. pH of NS is 5.7, pH of LR is 6.75

320
Q

what increases insensible losses

A
Fever (12.5% per degree >38 C)
heat
sweating
tachypnea/hyperventilation
vomiting/diarrhea
Hyperosmolar states (dehydration and DKA)
321
Q

what decreases insensible losses

A

Renal failure
Humidity
Hypothermia
Hypometabolic states

322
Q

Standard of care of care for diagnosis of pyloric stenosis and intussusception

A

US

323
Q

Reserved for either treatment or diagnostic uncertainty when US cannot diagnose pyloric stenosis or intussusception

A

Fluoroscopy

324
Q

Excellent for imaging the biliary tree, gallstone dx

A

MRI

325
Q

Diagnosing appendicitis

A

CT

326
Q

diagnosing pancreatitis

A

Acute is a result of inflammation from injury/insult. Diagnosed by having at least 2 of the 3 symptoms=
Abdominal pain (or surrogate symptoms such as irritability or listlessness)
Elevation of serum pancreatic enzymes
Radiological findings

327
Q

what diagnostic test?
•Used to assess colon for etiology of obstruction, some problems include intestinal atresia and Hirschsprung disease.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1255). Wolters Kluwer Health. Kindle Edition.

A

Air or barium enema

328
Q

a plain frontal supine radiograph of the abdomen that visualizes from the diaphragm to the bladder. A KUB will aid in observation of calcifications, gas patterns, feces, or free peritoneal air.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1257). Wolters Kluwer Health. Kindle Edition.

A

KUB

329
Q

•Useful study in detecting GI conditions as well as assessment of indwelling devices (e.g., NG tubes, jejunal tubes).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1257-1258). Wolters Kluwer Health. Kindle Edition.

A

KUB

330
Q

where is olive shaped mass found in pyloric stenosis

A

epigastric

331
Q

Amylase levels are ____ for first 2 months of life

A

low

332
Q

Children up to age ___ have virtually no pancreatic amylase

A

2

333
Q

Adult amylase levels may not be reached until

A

later school-age or adolescent years

334
Q

Kidney insufficiency may lead to hyper/hypo amylasemia

A

hyperamylasemia

335
Q

what labs are elevated in pancreatitis

A

amylase
lipase

other labs affected:
hypocalcemia, transient hypoglycemia, hyperbilirubinemia (d/t possible obstruction of pancreatic duct), increased LFTs, and hypoalbuminemia may be found in conjunction with pancreatitis.

336
Q

imaging of choice for pancreatitis

A

US

337
Q

imaging for chronic pancreatitis

A

ERCP- invasive; sedation is required
Used for chronic pancreatitis to visualize anatomy, perform manometry of sphincter of Oddi, perform therapeutic maneuvers when indicated
Should be avoided during an acute attack of pancreatitis

338
Q

Na level

A

135-145

339
Q

sodium is key in what body functions

A

key to skeletal muscle function, nerve, and myocardial action potentials

340
Q

causes of hyponatremia

A

Hypervolemia -> renal failure, nephrotic syndrome, CHF, and water intox

Hypovolemic - renal losses, diuretic use, diarrhea, vomiting, burns

Normovolemic -> CNS diseases like cerebral salt wasting or meningitis

341
Q

Presentation of hyponatremia

A

nausea, lethargy, seizures, coma

342
Q

Treatment goals for raising sodium in hyponatremia

A

Raise 2-4 mEq/L every 4 hours (10-20 in 24 hours)

If comes in seizing - get to 125 quickly with HTS (3%)
Formula - 0.6x (wt in kg) x (target Na - measured Na)

343
Q

causes of hypernatremia

A
  • Excessive Na intake
  • Inappropriately concentrated formula
  • Excessive free H2O loss→ -breastfeeding failure,
  • –diarrhea,
  • DI
344
Q

presentation of hypernatremia

A

weakness, lethargy, decreased DTR’s, irritability, muscle cramps, renal failure, AMS, seizures

345
Q

diagnostic for hyper/hyponatremia

A

serum Na and osmols

346
Q

treating hypernatremia

A

Avoid decreasing more than 12-15 mEq/L in 24 hours→ risk for cerebral edema

If hypovolemic, calculate free water deficit= 0.6 X kg X (current Na/desired Na) - (0.6 X wt kg)
-This is how much water they’ll need in the next 24 hours. Can give free water PO or via NGT. Be careful if decreasing with IV because D5W will bring level down fast→ check lytes every 2-4 hours. Will typically continue with maintenance of ½ NS or ¼ NS with D5W Y’ed in so that Na level is brought down slower.

347
Q

beta blocker ingestion…looking for

A

bradycardia

hypotension

348
Q

treatment in beta blocker ingestion

A
  • Glucagon IV dosed at 0.05-0.1mg/kg bolus with a maximum of 5mg; may be followed by an ongoing IV infusion or response dose over 1 hour.
  • Improves bradycardia and hypotension via noradrenergic pathway & may cause vomiting & hypokalemia.
  • Nelson says initial bolus is 0.15 mg/kg IV, followed by infusion of 0.05-0.15 mg/kg/hr
349
Q

Calcium channel blocker ingestion

watch for

A

bradycardia

hypotension

350
Q

treatment for CCB ingestion

A
  • Glucagon IV dosed at 0.05-0.1mg/kg bolus with a maximum of 5mg; may be followed by an ongoing IV infusion or response dose over 1 hour.
  • Improves bradycardia and hypotension via noradrenergic pathway & may cause vomiting & hypokalemia.
  • According to Nelson, can also use calcium chloride 10% IV/IO: 20 mg/kg; maximum single dose 2 g; administer slowly
351
Q

Salicylate ingestion….what meds are these?

A

Encompasses a variety of prescription & non-prescription agents with aspirin, also known as salicylic acid (ASA). Other examples include methyl salicylate (oil of wintergreen), trolamine salicylate (muscle rubs), bismuth subsalicylate (GI preparations), salicylic acid (acne preparations, corn & wart removers), and magnesium salicylate (backache and pain relief medication).

352
Q

toxic dose for salicylate ingestion

A

refer to ED for greater than 150mg/kg or 6.5g of ASA equivalent

ingestions of 300-500mg/kg are associated with serious tox

Chronic dose of > 100mg/kg/day for 2 days also will produce tox

353
Q

metabolic derangement seen in salicylate tox

A

wide anion gap metabolic acidosis

resp alkalosis may occur due to direct stim of resp center

354
Q

exposure to _____ can increase risk of pyloric stenosis

A

Erythromycin

355
Q

what medication in maternal while pregnant is associated with pyloric stenosis for neonates

A

fluoroquinolones

-floxacin

356
Q

electrolyte concerns in salicylate toxicity

A

hypoglycemia

hypokalemia (increased renal excretion)

357
Q

symptoms of salicylate tox

A
n/v
hematemesis
gastric pain
tinnitus
impaired hearing
tachypnea
tachycardia
dehydration
diaphoresis
fever

serious tox

  • delirium
  • seizures
  • coma
  • metabolic acidosis
  • rhabdomyolysis
  • noncardiogenic pulmonary edema
  • arrhythmias
  • asystole
358
Q

what syndrome can mimic salicylate tox

A

Reye syndrome

  • vomiting
  • hypoglycemia
  • hepatic dysfunction
  • encephalopathy
359
Q

salicylate tox. How often do you check levels

A

Q2 hours until a peak is determined and Q4 hours thereafter

360
Q

treatment for salicylate tox

A

follow salicylate levels Q2 until peaks then Q4 hours

IV fluids

Wide anion gap metabolic acidosis - correct with IV sodium bicarb at 1-2 meq/kg

correct hypoglycemia with IV dextrose

manage seizures with IV benzos

get x ray and monitor for non-cardiac pulmonary edema - if intubated - important to hyperventilate to maintain a high arterial pH - to prevent salicylates from crossing BBB

Because salicylates become more ionized as the urine pH rises, enhanced urinary excretion of salicylates may be achieved via administration of IV sodium bicarb with potassium chloride, with a goal of alkalinization of the urine to target pH of 7.5-8à known as ion trapping
Obtain arterial blood gases, electrolytes, and urine pH frequently (Q4-6H) to guide therapy.
Urine alkalinization can be terminated when salicylate levels fall below 30mg/dL

Emergent hemodialysis can be necessary to enhance elimination of high salicylate blood levels and correct fluid electrolyte & acid-base abnormalities
Indications of HD include: salicylate levels approaching 100mg/dL in acute ingestions OR 40-60mg/dL in chronic supratherapeutic ingestions, pulmonary edema, CV instability, seizures, AMS, or intractable acidosis or electrolyte abnormalities.

361
Q

what med class?

amitriptyline, clomipramine, desipramine, doxepin, imipramine, and nortriptyline

A

Tricyclics

362
Q

toxic dose of tricyclics

A
  • All TCAs except for desipramine, nortriptyline, trimipramine, and protriptyline were > 5mg/kg.
  • Desipramine, nortriptyline, trimipramine > 2.5mg/kg
  • Protriptyline > 1mg/kg
  • Ingestions of 10-20mg/kg in pediatric patients constitute a serious risk of toxicity.
  • Admission to PICU is advised for any patient demonstrating AMS or CV toxicity until symptoms have resolved.
363
Q

symptoms of TCA tox

A

These are potent CNS and resp depressants and anticholinergic activity with alpha adrenergic blockade

  • Rapid coma and resp failure
  • dry mucous membranes
  • mydriasis
  • Tachycardia
  • agitation
  • delirium
  • hyperthermia
  • decreased GI activity
  • Hypotensive (alpha adrergic)
Sodium blockage in the myocardium -> Wide QRS complex
Prolonged QT
V-Tach
V-Fib
Cardiac arrest

Seizures

364
Q

Treatment for TCA tox

A
  • Consists of appropriate GI decontamination and supportive measures.
  • Patients with rapid obtundation, loss of protective airway reflexes or coma require rapid ETT & ventilatory support.
  • Seizures are managed with benzos and barbiturates for refractory seizures.
  • Cardiac conduction defects noted by a widened QRS complex greater than 110-120 ms may respond to sodium bicarb & serum alkalization (throwing it back to the beginning of the semester)
  • IV sodium bicarb at 1-2meq/kg and hyperventilation in intubated patients with a goal of an arterial pH of 7.45-7.55 can correct many of the wide complex tachydysrhythmias associated with TCA OD.
  • Continuous sodium bicarb is not routinely recommended.
-Hypotension can be managed with IV bolus of sodium bicarb, crystalloid fluids, and administration of pressor agents.
Intralipid emulsion (ILE) can be an alternative treatment for TCA OD with serious effects unresponsive to standard resuscitation measures, but not first line.

-Bolus of 20% of ILE at 1.5ml/kg administered over 2-3 minutes, followed by a repeat bolus or an infusion.

Consultation with a medical toxicologist is advised.

Contraindications:
-physostigmine salicylate is used in the management of anticholinergic poisonings, however in TCA OD, it has been associated with seizures, asystole, and death.

  • Class 1-A & 1-C antidysrythmics such as quinidine, procainamide, disopyramide, flecainide, can WORSEN cardiac conduction & should be avoided.
  • Beta blockers can correct tachycardia but has been linked to severe hypotension and cardiac arrest & should also be avoided.
365
Q

Tylenol OD amount

A

patients should be referred to the ED if the ingested amount is greater than or equal to 200mg/kg in patients <6yrs or 200mg/kg or 10gm (whichever is less) in adults.

For chronic or supratherapeutic ingestions, patients should be referred for emergent eval of pediatric patients younger than 6 years of age ingest–
> 200mg/kg in a 24 hour period
> 150mg/kg per 24-hour period for the preceding 48 hours, OR
> 100mg/kg per 24 hour period for 72 hours or longer

Adults should be referred to ED if a chronic or supratherapeutic ingestion of >10gm or 200mg/kg (whichever is less) per 24 hours, or greater than 6gm or 150mg/kg (whichever is less) per 24 hour period for 48 hours or longer occurs.

366
Q

symptoms tylenol OD

A

Initial symptoms may be nonspecific and include N/V, malaise, and sweating.
Within 24-36 hours following ingestion, elevations of the hepatic enzymes, AST & ALT, begin to occur.
Peak hepatotoxicity occurs at 72-96 hours post ingestion, with possible signs of fulminant hepatic failure, renal failure, coma, encephalitis, and coagulopathy.
At this point patients may begin to recover, require a liver transplant or die.
If recovery occurs, it usually occurs within the first 5-7 days following ingestion.

367
Q

treatment in Tylenol OD

A

Antidote is N-acetylcysteine (NAC)
In the US, an IV preparation, Acetadote, and an oral preparation, Mucomyst, are also available.

-Most effective when initiated within 8 hours post-ingestion but is still effective at any time after a significant OD. Treatment should not be delayed in the absence of rapid blood APAP quantification.

NAC should be initiated in any patient demonstrating abnormal liver function tests thought to be caused by APAP toxicity even if APAP blood level is undetectable.

It possesses hepatoprotective properties by acting as an antioxidant and free radical scavenger & improving blood microcirculation.

2 indications for use of NAC: Patient presenting with a known or suspected toxic blood level of APAP and/or evidence of hepatotoxicity.

2 NAC treatment regimens
72-hour oral course
Considered safe with only minor GI disturbances such as vomiting or diarrhea.
Has an unpleasant sulfur or “rotten egg” taste and odor. Best administered when diluted to a concentration of 5%, mixing it with any soft drink or juice that the patient prefers and served with ice in a covered container.
Any oral dose vomited within an hour of administration should be repeated.

21- hour IV course
Preferred in situations where the patient is unable or is unwilling to take NAC orally in cases where GI bleeding or obstruction is suspected.
Carries greater risk of hypersensitivity reactions such as pruritus and urticaria

368
Q

Criteria for Liver transplantation in Tylenol OD setting

A
  • Acidosis defined as arterial pH <7.3 after adequate fluid resuscitation
  • Coagulopathy, defined as PT > 40 secs at 40 hours OR PT > 100 secs at any time OR rapidly rising PT OR INR greater than 6.5
  • Creatinine greater than 3.3mg/dL
  • Grade III or IV encephalopathy
  • In these patients, NAC is infused continuously at the rate of 100mg/kg/16 hours until the patient improves or undergoes transplant surgery or fails to survive.
369
Q

Digoxin tox symptom

A

bradycardia

370
Q

Treatment for Digoxin OD

A
Digoxin immune fab is the antidote
# vials = digoxin level (ng/mL) x weight (kg) divided by 100
  • This may cause hypokalemia
371
Q

iron tox is due to the effects of _____ iron

A

elemental

372
Q

ferrous sulfate is ___% elemental iron

A

20%

373
Q

ferrous fumarate is ___% elemental iron

A

33%

374
Q

toxic iron dose

A
  • Referral to the ED is recommended in patients with ingestions > 40 mg/kg of elemental iron in the form of adult ferrous salt formulations.
  • Toxicity is likely at > 60mg/kg dose.
  • Ingestion of any quantity of children’s chewable MV with iron, carbonyl iron formulations or polysaccharide iron complexes can be observed at home regardless of the amount ingested.
375
Q

iron tox symptoms

A

Early s&s of iron toxicity within the first 6 hours include N/V, and diarrhea, which can be bloody.
This can be followed by a period of apparent improvement or stability; however some patients may progress to more serious complications, including metabolic acidosis, coma, hypotension, shock, hepatic failure, coagulopathies, seizures, and death.
Late complications can include bowel obstruction or stricture.

376
Q

Iron tox tx

A
Orogastric lavage may be considered in life threatening iron ingestions if It can be performed within an hour however, iron-containing tablets can be large and form concretions, making passage through the lavage tube difficult, especially in young children.
Activated charcoal does not absorb iron and should not be administered.
Iron tablets are radiopaque and can be visualized with abd radiography. If tablets are seen, whole bowel irrigation can be considered.
Supportive measures include: crystalloid fluids & vasopressors for hypotension, IV sodium bicarb for metabolic acidosis, and benzos for seizures.
Deferoxamine methylate (DFO) is a specific antidote for iron poisoning.
DFO acts as a chelating agent that binds to free iron and forms ferrioxamine, a water soluble complex, excreted by the kidneys (can cause “vin rose” or reddish brown urine).
DFO is indicated for patients with severe iron intoxication, presenting with shock, severe acidosis, or serum iron levels greater than 500mg/dL.
End point of therapy is resolution of symptoms.
377
Q

glucagon is tx of choice for what ingestions?

Dosing?

A

B blocker
CCB

This helps bradycardia and hypotension via the noradrenergic pathway

Bolus: 0.05-0.1 mg/kg, max dose 5 mg
Infusion: 0.05-0.15 mg/kg/hr that follows bolus, can also use second dose

378
Q

side effect of glucagon

A

vomiting

hypokalemia

379
Q

hydrocarbon/kerosene abuse includes

A

glue, paint thinners, cleaning products, or spot removers.
Most commonly abused is compressed air computer dusters, typically containing fluorinated hydrocarbons such as difluoroethane.

380
Q

presentation of hydrocarbon/kerosene abuse

A

Generally affects 3 organ systems: CNS, pulmonary, and cardiac.

Upon inhalation, blood levels of most inhalants peak within mins and are rapidly taken up into fat stores.

Patients may present with initial CNS excitation, including euphoria with rapid progression to AMS & CNS depression.

Respiratory tract irritation leading to tachypnea, bronchospasm, hypoxemia, cyanosis, and respiratory distress can occur, especially in patients with asthma or COPD.

Cardiac toxicity is due to myocardial sensitization to endogenous catecholamines and can result in A-fib, v-tach, v-fib, and cardiac arrest.

Cardiac mechanism is unclear but may be due to alterations in potassium channels and delayed calcium release.

Frostbite injury may occur if the product source is compressed gas.

381
Q

tx for hydrocarbon/kerosene abuse

A

Primarily supportive with emphasis on respiratory & circulation.

All symptomatic patients should be placed on cardiac monitors and EKG should be obtained.

Monitor VS & oxygen frequently.

CXR, ABG, and metabolic panel should be obtained.

Avoid catecholamines such as dopamine, epi and norepi unless absolutely necessary for cardiac resuscitation because symptoms may worsen with these agents due to increased cardiac sensitivity.

Phenylephrine is the preferred DOC for hypotension in this patient

Esmolol is preferred for arrhythmias;

Lidocaine can be considered for arrhythmias.

Albuterol sulfate & systemic corticosteroids can be used for respiratory symptoms.

382
Q

ethanol tox presentation

A

Initial stimulation and loss of inhibitions, followed by lethargy, slurred speech, ataxia, stupor, and coma.

Pediatric patients experience facial flushing, vomiting, diaphoresis, respiratory depression, seizures, hypotension, hypothermia, and hypoglycemia.

Ethanol is metabolized in the liver, pediatric patients are at risk of profound hypoglycemia due to impaired hepatic gluconeogenesis. Hypoglycemia may be delayed up to 6 hours after ingestion.

383
Q

ethanol tox tx

A

Can be managed with at home observation and telephone follow-up for exposures of “mouthful” or “taste” ingestions of alcohol.

With more serious ethanol ingestion, no GI decontamination is warranted unless co-ingestants are suspected.

Respiratory, cardiac, blood sugar and electrolytes should all be closely monitored.

Correct hypoglycemia with IV dextrose with the addition of oral caloric intake in an awake and alert patient.

Hemodialysis is indicated in patients with very high blood alcohol levels who do not respond to standard supportive measures.

Hospital admission is advised for any patient demonstrating significant toxicity with signs of marked CNS depression, hypoglycemia, seizures or fluid electrolyte abnormalities.

384
Q

gold standard for ovarian torsion dx

A

color flow doppler US

CT/MRI reserved for pts who have nondefinitive findings or if symptoms are intermittent

385
Q

in ovarian torsion salvage may be possible up to ___ hrs

A

24

386
Q

Twisting of adnexal structures compromising blood flow to the ovary. • Usually associated with a cyst or mass.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1307). Wolters Kluwer Health. Kindle Edition.

A

Ovarian (Adnexal) Torsion

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1307). Wolters Kluwer Health. Kindle Edition.

387
Q

clinical presentation ovarian torsion

A

• Peaks in adolescence.
•Acute onset of abdominal pain caused by ischemia.
• More common on right side.
-N/V

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1307). Wolters Kluwer Health. Kindle Edition.

388
Q

•Twisting of the spermatic cord causing compromised blood flow to testicle.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1305). Wolters Kluwer Health. Kindle Edition.

A

testicular torsion

389
Q

predisposing factors for testicular torsion

A
  • Trauma.
  • Testicular tumor.
  • Testicles lying in horizontal plane.
  • History of cryptorchidism and increasing testicular volume.
  • Occurs in children <3 years of age and after puberty most commonly.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1306). Wolters Kluwer Health. Kindle Edition.

390
Q

clinical symptoms testicular torsion

A
  • Sudden onset of pain involving the testis; usually unrelenting.
  • Testis is enlarged and tender.
  • Absence of cremasteric reflex.
  • Affected testicle higher in the scrotum.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1306). Wolters Kluwer Health. Kindle Edition.

391
Q

procedure to fix testicular torsion is called

A

• Affix testis to scrotal wall to prevent recurrence (orchiopexy).

-Manual detorsion to decrease degree of ischemia prior to surgery → rotate testicle in a medial to lateral direction for 1 or 2 full 360 degree turns

You have 4-8 hours generally before you loose testicle

• If testicle cannot be salvaged, it is removed (orchiectomy).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1306). Wolters Kluwer Health. Kindle Edition.

392
Q

Characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, renal injury

A

HUS

393
Q

types of HUS

A

D+ HUS

Atypical HUS

394
Q

which type of HUS is associated with contaminated meat, fruit, veggie or water with verotoxin producing E.Coli (0157:H7) or shigella

A

D+ HUS

395
Q

Atypical HUS can be secondary to what infections?

A

Strep pneumo
HIV

Can also be genetic
medication
malignancy
SLE
pregnancy
396
Q

HUS typically occurs in children < __ yrs

A

5

397
Q

which type HUS is more severe

A

Atypical HUS

398
Q

Presentation of D+ HUS

A

•Gastroenteritis with fever, vomiting, diarrhea, abdominal pain, and diarrhea that begins as watery but then becomes bloody.

Entercolitis with bloody stools, followed in 7-10days by weakness, lethargy, anuria/oliguria
Irritable, pallow, petechiae
Dehydration, however some children have volume overload (hypertension may occur)
CNS seizures in 25%, pancreatitis, cardiac dysfunction, colonic perforation

•Physical examination: dehydration, edema, petechiae, hepatosplenomegaly, and marked irritability.

399
Q

HUS Triad

A

Triad

1) Microangiopathic Hemolytic anemia (MAHA) -> weakness, fatigue, lethargy, jaundice
2) Thrombocytopenia (easy bruising and purpura) blood clots in brain can cause visual problems, AMS, seizures, stroke, fever
3) Acute renal failure (uremia)

400
Q

D+HUS treatment

A

supportive

Aggressive fluid management with electrolytes and nutrition

shiga like toxin clears in days to weeks
No antibiotics -> dead bacteria release more toxin

For TTP HUS - Plasmapheresis

Volume repletion
Hypertension control
Managing renal insufficiency – dialysis
RBC transfusions
DO NOT GIVE PLATELETS – may add to thrombotic microangiopathy
Only give if active hemorrhage or procedural
NO ABX OR ANTIDIARRHEAL – will make HUS worse

401
Q

Atypical HUS treatment

A

address underlying cause

402
Q

diagnostics for HUS

A

Lab smear: microangiopathic hemolysis
-Anemia (Hgb commonly 5-9), thrombocytopenia, schistocytes/helmet/burr cells and fragmented rbcs on smear, incr LDH, incr indirect bili, incr AST, incr reticulocyte

Coombs test is NEGATIVE

Renal injury: elevated Cr, hematuria, proteinuria, pyuria, casts on UA

Leukocytosis (>300,000)
, E coli stool culture, shiga toxin, elevated amylase/lipase

403
Q

the most common cause of acute renal failure (ARF) in children <4 years of age.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1296). Wolters Kluwer Health. Kindle Edition.

A

HUS

404
Q

•Characterized by the simultaneous occurrence of microangiopathic hemolytic anemia, thrombocytopenia, and uremia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1296). Wolters Kluwer Health. Kindle Edition.

A

HUS

405
Q

pyelonephritis risk factors

A
Female sex
sexual intercourse
indwelling catheter
DM
urinary tract obstruction
Vesicoureteral reflux (VUR)
406
Q

what organism is the most common cause of UTI in children

A

E. Coli

407
Q

upper UTI

A

pyelonephritis

408
Q

for UTI who has the highest incidence in the first 3 months of life

A

uncircumsized males

409
Q

UTI are commonly associated with what organisms

A

gram neg

  • E.Coli
  • Klebsiella species
  • Pseudomonas aeruginosa

gram pos

  • Enterococcus
  • Staph Aureus
  • Group B strep

Also
Candida
Adenovirus
HSV

410
Q

More than ____ colony-forming units/mL of a single organism and pyuria represent UTI in appropriately obtained specimens.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1287). Wolters Kluwer Health. Kindle Edition.

A

50,000

411
Q

when is US indicated for UTI

A

2 mos - 2 yrs of age
Ultrasound: evaluates anatomy, kidney size/shape, and for evidence of hydronephrosis. Can also be used to evaluate for areas of inflammation and signs of pyelonephritis.

412
Q

If renal and bladder US show hydronephrosis, scarring or other evidence of high grade VUR or obstructive uropathy …..what should you order?

A

voiding cystourethrography

413
Q

UTI antibiotics

A

• Trimethoprim–sulfamethoxazole
amoxicillin–clavulanate,
cefixime are acceptable selections for initial oral therapy.

• Ceftriaxone, cefotaxime, gentamicin are acceptable selections for initial parenteral therapy. • In general, oral antibiotics are equally effective as parenteral therapy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1288). Wolters Kluwer Health. Kindle Edition.

414
Q

education on preventing UTI

A

signs of UTI, hygiene, limiting bubble baths, constipation prevention, urination after intercourse if sexually active.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1288). Wolters Kluwer Health. Kindle Edition.

415
Q

•Bacterial infection of the upper urinary tract caused by an ascending infection originated in the lower urinary tract.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1288). Wolters Kluwer Health. Kindle Edition.

A

Pyelonephritis

416
Q

Most common organisms for pyelonephritis

A

• Gram-positive bacteria: Enterococcus spp. and Staph. aureus. •

Gram-negative bacteria: E. coli, Klebsiella spp., Proteus spp.,

• P. aeruginosa, Serratia spp., and Enterobacter aerogenes.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1289). Wolters Kluwer Health. Kindle Edition.

417
Q

symptoms of pyelonephritis

A

• Fever, lethargy. • Tachycardia, tachypnea, dehydration. • Pain (abdominal, suprapubic, flank, and/or costovertebral). • Odorous urine.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1289). Wolters Kluwer Health. Kindle Edition.

418
Q

diagnostic pyelonephritis

A

Urinalysis: detection of leukocyte esterase and nitrites

• Basic metabolic panel: evaluation of kidney function. •CBC with differential: evaluation of WBC count and differential. • Blood culture: Positive culture indicates bacteremia. • C-reactive protein: elevated, indicating an inflammatory process. •Erythrocyte sedimentation rate: elevated, indicating an inflammatory process. •Renal ultrasound for children 2 to 24 months of age.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1289). Wolters Kluwer Health. Kindle Edition.

419
Q

when is VCUG typically done

A

children with recurrent febrile UTIs who have evidence of abnormalities on US

420
Q

Inflammation within the kidney.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1290). Wolters Kluwer Health. Kindle Edition.

A

Nephritis

421
Q

symptoms/clinical presentation of Nephritis

A

Hypertension, gross hematuria, edema = classic triad

  • History of recent throat infection, decreased urine output, dark urine, fatigue, headache.
  • Rash on buttocks and posterior legs, arthralgia, and weight loss (symptoms of secondary GN).
  • Elevated blood pressure.
  • Edema.
  • Other signs of fluid overload/congestive heart failure.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1290). Wolters Kluwer Health. Kindle Edition.

422
Q

diagnostic eval for Nephritis

A
  • Electrolyte panel, creatinine, BUN, CBC with differential, urinalysis with urine culture and sensitivities, and throat culture. •If acute poststreptococcal GN is suspected, a serum antistreptolysin-O (ASO) titer should be checked.
  • To assess for systemic disease, autoimmune panels such as serum complement levels (C3, C4), lupus serologies, anti-DNase B, perinuclear antineutrophil antibody (P-ANCA), cellular antineutrophil cytoplasmic antibody (C-ANCA), and IgA are useful.
  • Low serum C3 levels are indicative of secondary GN.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1290-1291). Wolters Kluwer Health. Kindle Edition.

423
Q

Treatment of nephritis

A
  • Antibiotic: penicillin, first line. - 10 day course (use ceph or macrolide if allergy)
  • Treatment of hypertension or acute renal insufficiency.
  • Judicious fluid management.
  • Sodium-restricted diet.
  • Diuretics.
  • Calcium channel antagonists, vasodilators, or ACE inhibitors.
  • For secondary forms of GN.
  • Corticosteroids and cyclophosphamide to counteract the inflammatory process.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1291). Wolters Kluwer Health. Kindle Edition.

424
Q

pyelonephritis caused by Klebsiella is more common in what gender

A

boys

425
Q

pyelonephritis caused by Enterobacter aerogenes is more common in what gender

A

girls

426
Q
  • Caused by a prior infection with specific nephritogenic strains of a beta-hemolytic streptococcus of the throat or skin.
  • Most common glomerular cause of hematuria.

Commonly follows group A streptococcal pharyngitis during the cold weather months and streptococcal skin infections or pyoderma during warm weather months.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1291). Wolters Kluwer Health. Kindle Edition.

A

Acute poststreptococcal glomerulonephritis

427
Q

clinical symptoms of Acute poststreptococcal glomerulonephritis

A

•Sudden onset of gross hematuria, edema, hypertension, and renal insufficiency.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1292). Wolters Kluwer Health. Kindle Edition.

428
Q

Diagnostics Acute poststreptococcal glomerulonephritis

A

•Urinalysis: red blood cells—often associated with red blood cell casts, proteinuria, and polymorphonuclear leukocytes.
Elevated ASO titer.
•Complement level: C3 level initially decreased; returns to normal 6 to 8 weeks after presentation (sometimes sooner). •Throat culture positive for group A streptococcus can confirm diagnosis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1292). Wolters Kluwer Health. Kindle Edition.

429
Q

mgmt of Acute poststreptococcal glomerulonephritis

A
  • Penicillin: a 10-day course. •Cephalosporins or macrolide antibiotics can be used in patients with penicillin allergy.
  • Acute renal insufficiency: furosemide.
  • Hypertension: antihypertensive agents and sodium restriction.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1292). Wolters Kluwer Health. Kindle Edition.

430
Q

Pyelonephritis complication

A

tubulointerstitial nephritis (TIN): inflammation that affects the interstitium and renal tubules of kidney

Major dysfunction of collecting tubules -> inability to concentrate urine, salt wasting, metabolic acidosis

ONLY DIAGNOSED WITH RENAL BIOPSY – often goes undiagnosed

maculopapular rash, joint pain with flexion and extension, uveitis

431
Q

kidney function is indicated by what

A

GFR

432
Q

•The kidneys of children reach adult GFR at approximately what age

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1281). Wolters Kluwer Health. Kindle Edition.

A

1 year

433
Q

GFR equation

A

•GFR can be estimated (eGFR) with the patient height, serum creatinine, and a constant (Schwartz equation).
eGFR mL/minute/1.73 m2 = (k)(height)/serum creatinine • k = constant of 0.413 for all ages/genders.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1281). Wolters Kluwer Health. Kindle Edition.

434
Q

• Equation used to determine whether kidney dysfunction is only a result of hypoperfusion to kidney.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1281). Wolters Kluwer Health. Kindle Edition.

A

Fractional excretion of sodium

435
Q

normal BUN to creatinine ratio

A

10:1 to 20:1

436
Q

Elevated BUN to creatinine ratios are associated with

A

shock or dehydration with acute kidney failure. Also may result from nephrolithiasis or gastrointestinal or pulmonary hemorrhage.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1282). Wolters Kluwer Health. Kindle Edition.

437
Q

low BUN to creatinine ratios are associated with

A

rhabdomyolysis, syndrome of inappropriate antidiuretic hormone secretion, lung disease, malignancy, low dietary protein intake, or certain medications.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1282). Wolters Kluwer Health. Kindle Edition.

438
Q

Prerenal causes

A

hypovolemia
Distributive volume issues
sepsis
congestive heart failure

439
Q

Intrinsic causes

A
acute tubular necrosis
Glomerulonephritis
Medication induced
Infection (HUS, poststreptococcal GN)
Interstitial nephritis
renal artery or vein thrombosis
vascular lesions
endogenous toxins (Myoglobin)
Exogenous toxins (methanol, ethylene glycol)
Idiopathic
440
Q

postrenal causes

A

obstruction

urolithiasis

441
Q

An abrupt cessation or significant decline in the kidney’s ability to eliminate waste products, regulate acid–base balance, and regulate electrolyte balance.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1282). Wolters Kluwer Health. Kindle Edition.

A

Acute renal failure

442
Q

what type of renal failure is most common

A

Prerenal

443
Q

Genetic conditions associated with acute renal failure

A
Polycystic kidney disease
Alport syndrome
Nephrotic syndrome 
Systemic Lupus erythematosus (SLE)
Diabetes
444
Q

Presenting signs and symptoms of acute renal failure

A
oliguria/anuria
edema
electrolyte abnormalities
decreased appetite
nausea
fatigue
shortness of breath
hypertension
confusion
445
Q

Management of acute renal failure

A

Fluid management: judicious (e.g., restore intravascular volume or diuresis depending on clinical status). Aggressive hydration may result in fluid overload, pulmonary edema, and respiratory compromise.

  • Calculation of fractional excretion of sodium may help guide fluid management.
  • Fluid management with urine output replacement and calculated insensible losses may be warranted.
  • Hyponatremia is common. Risk for seizure activity if serum sodium <125 mEq/L. Treat with hypertonic saline solution (e.g., 3% saline administration).
  • Hyperkalemia may be life-threatening (e.g., ventricular tachycardia, ventricular fibrillation).
  • EKG findings in hyperkalemia may include peaked T waves, prolongation of PR interval, widening of QRS complex, flattening of P waves.
  • Imperative to reduce extracellular potassium level and stabilize the cardiac cell membrane to avoid ventricular tachycardia/fibrillation. Glucose, sodium bicarbonate, insulin, and albuterol shift potassium into the cells.
  • Calcium chloride can stabilize the cardiac cell membrane.
  • Sodium polystyrene can exchange potassium and sodium in the colon. • Emergent dialysis is often indicated for serum potassium levels >7 mEq/L.
  • Hypertension therapy: avoid angiotensin-converting enzyme (ACE) inhibitors. Goal is normal blood pressure for gender and height.
  • Adjust medications that are renally excreted; consult a pharmacist.
  • Renal supportive therapies may be indicated. See more information on renal supportive therapies later in this section.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1283). Wolters Kluwer Health. Kindle Edition.

446
Q

clinical presentation of Renal artery or vein thrombosis

A

• Abrupt onset of hematuria. • Flank mass, unilateral or bilateral. • Flank pain. • Oliguria. • Hypertension.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1293). Wolters Kluwer Health. Kindle Edition.

447
Q

diagnostic for Renal artery or vein thrombosis

A

Doppler US

  • Monitor and maintain fluid and electrolyte balance.
  • Blood pressure monitoring; antihypertensive agents.
  • If refractory to pharmacologic therapy, may require nephrectomy.
  • Treatment with anticoagulants (e.g., heparin) or thrombolytics (e.g., streptokinase, recombinant tissue plasminogen activator) is common, but controversial.
  • Inferior vena cava thrombus may require thrombectomy.
  • Treat underlying disease (e.g., nephrotic syndrome), if indicated.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1294). Wolters Kluwer Health. Kindle Edition.

448
Q

•Result of an inherited or acquired defect that affects the kidneys’ ability to filter bicarbonate or excrete ammonia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1294). Wolters Kluwer Health. Kindle Edition.

A

Renal tubular acidosis

449
Q

what can be a genetic cause of renal tubular acidosis

A

Sickle cell anemia

450
Q

renal tubular acidosis is often associated with the presence of a

A

UTI

451
Q

A relatively uncommon clinical syndrome characterized by defects in the renal tubules as a result of failure to maintain a normal serum bicarbonate level despite the consumption of a regular diet and normal metabolism and acid production.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1294). Wolters Kluwer Health. Kindle Edition.

A

Renal tubular acidosis

452
Q

symptoms of renal tubular acidosis

A
  • Polyuria.
  • Polydipsia.
  • Preference of savory foods.
  • Hypokalemia.
  • Refractory rickets.
  • Metabolic acidosis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1295). Wolters Kluwer Health. Kindle Edition.

453
Q

what type of RTA?
linked to multiple genetic disorders (sensorineural hearing loss and nephrocalcinosis); failure to thrive or short stature, anorexia, vomiting, and dehydration.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1295). Wolters Kluwer Health. Kindle Edition.

A

Type I RTA

454
Q

what type RTA
failure to thrive, hyperchloremic acidosis with hypokalemia, and rarely nephrocalcinosis; rickets or osteomalacia may indicate Fanconi syndrome.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1295). Wolters Kluwer Health. Kindle Edition.

A

Type II

455
Q

what type RTA
no longer used as a classification; now thought to be a combination of types I and II.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1295). Wolters Kluwer Health. Kindle Edition.

A

Type III

456
Q

What type RTA
Hypertension common if child has underlying Gordon syndrome, renal parenchymal disease, or mineralocorticoid dysfunction.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1295). Wolters Kluwer Health. Kindle Edition.

A

Type IV

457
Q

diagnostic eval for RTA

A
  • Serum and urine electrolytes.
  • Fractional excretion of bicarbonate and urine pH.
  • Urine glucose and protein, calcium-to-creatinine ratio.
  • 24-hour urine sample (i.e., citrate, calcium, potassium, and oxalate). •Radiographies of long bone or wrists for evaluation of rickets.
  • Abdominal ultrasound (kidneys).
  • Genetic or chromosomal evaluation.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1295-1296). Wolters Kluwer Health. Kindle Edition.

458
Q

Management of RTA

A
  • Emergency or impatient management for children with hyperchloremic, non–anion gap acidosis requiring bicarbonate replacement intravenously.
  • Slow rehydration and electrolyte replacement, sodium bicarbonate or citrate, diuretic, phosphate replacements in children with rickets.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1296). Wolters Kluwer Health. Kindle Edition.

459
Q

chronic acidity in the blood results in

A

in growth retardation, nephrolithiasis, bone disease, and chronic renal failure.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1296). Wolters Kluwer Health. Kindle Edition.

460
Q

Normal BP

A

Children 1-13 <90%ile

<120/<80 for children >= 13

461
Q

stage 1 HTN

A

old guidelines: 140-159/90-99

new
1-13: >=95%ile to <95%ile + 12 mmHg or 130/80 to 139/89

> = 13 yrs: 130/80 to 139/89

462
Q

Stage 2 HTN

A

old guidelines:
160+/100+

New:
1-13: >=95%ile + 12mmHg or >=140/90mmHg

> = 13 yrs >=140/90

463
Q

key difference from Stage 1 HTN and Stage 2 HTN in approach

A

confirmed stage 1 allows for time for evaluation prior to intervention while stage 2 requires swift eval within 1 week or sooner if symptomatic and intervention.

if symptomatic stage 2. Immediate intervention required with referral to specialist promptly

stage 1 is reevaluated on repeat visits. 3 separate measurements within 1 mth

464
Q

Secondary HTN is more common in ___ than in ____

A

children

adults

465
Q

most common cause of secondary HTN. What are some other causes?

A

Kidney disease

adrenal gland
medications
obstructive sleep apnea
stress
anxiety
coarctation of the aorta
endocrine
pregnancy
metabolic syndrome
466
Q

physical exam clues to HTN

A
  • Tonsillar hypertrophy (sleep-disordered breathing)
  • Papilledema (Intracranial HTN)
  • Acanthosis Nigricans (type 2 DM)
  • Murmur (coarctation of aorta)
  • Abd mass (kidney tumor, hydronephrosis, polycystic kidney disease)
  • Disparate pulses; upper pulses >lower pulses (coarctation of aorta)
  • Elfin or Moon facies (Williams syndrome, cushing syndrome)

Thyroid enlargement (hyperthyroidism)

Muscle weakness (hyperaldosteronism)

Diminished pain response (Familial dysautonomia)

Ambiguous genitalia (Adrenal hyperplasia)

Advanced puberty (intracranial tumor/pathology)

467
Q

labs to order on anyone with stage 1 HTN or higher

A

CBC: Anemia is a classic sign or chronic kidney disease

Renal function panel: looking at BUN/Creatinine and electrolytes. Hyperphosphotemia and hypocalcemia are commonly noted in kidney disease

Urinalysis

Consider Urine protein/creatinine ratio

Lipid panel

Fasting lipid panel and fasting blood glucose measurement on obese patients

468
Q

Other diagnostic studies in HTN

A

Echocardiogram: eval for LV hypertrophy

Renal US: looking for kidney scarring, congenital abnormalities, unequal kidney size

Retinal exam: Eval for retinal vascular changes

469
Q

Nonpharmacy therapy (First line plan in stage 1 HTN)

A

Lifestyle changes:

  • Weight loss
  • exercise
  • dietary mods
  • Reduce salt intake: 2.4g sodium restriction/day
  • Increase fresh fruit and vegetables
  • Increase low-fat dairy products
  • Avoid smoking and alcohol intake

No added salt with preparation
Foods with >200mg Na per serving should be avoided
Limit processed foods, fast foods and fried foods
-consider school meal choices
-no gatorade
-ramen noodles
-Seasonings -Tajin

limit caffeine

  • coffee/tea
  • energy drinks
  • soda
470
Q

Pharm therapy in Stage 2 HTN

A

Pharm treatment is indicated in children with symptomatic HTN, stage 2 without an identified modifiable factor, comorbidities such as DM or CKD or who remain Hypertensive after a tiral of lifestyle mods.

Treatment should be initiated with a single agent at a low dos, with dose adjustments every 2-4 weeks. If BP is not adequately controlled, additional agent(s) can be added. Start with either ACE, ARB, long acting CCB or thiazide diuretic. B blockers are not recommended as initial treatment in children

1) ACE inhibitors (-prils)

or

ARB (-sartan)

or

CCB

Diuretic to decrease blood volume and excrete sodium
-Thiazide-like:

  • Loop
  • Potassium sparing

Vasodilators (hydralazine, minoxidil) -> reserved for patients failing other therapies due to unfavorable side-effect profile.

• Peripheral α1-antagonists and centrally acting α2-agonists.

-B Blockers

471
Q

what does ACE inhibitors do

A

• ACE (angiotensin-converting enzyme) inhibitors (“-prils”): Dilate blood vessels to decrease resistance.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 421). Wolters Kluwer Health. Kindle Edition.

472
Q

common side effects ACE Inhibitors

A
  • Cough.
  • Skin rash (red, itchy).
  • Dizziness/lightheadedness, orthostatic hypotension.
  • Taste impairment (salty or metallic).
  • Edema (lower extremities).
  • Hyperkalemia.
  • Decrease in glomerular filtration rate (GFR).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 421). Wolters Kluwer Health. Kindle Edition.

473
Q

Precautions for ACE inhibitors

A
  • Not to be used in volume-depleted patients.
  • Not to be used in patients with bilateral renovascular hypertension.
  • Avoid salt substitutions as they contain potassium.
  • Avoid nonsteroidal anti-inflammatory (NSAID) medications.
  • Check BP and kidney function regularly.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 421). Wolters Kluwer Health. Kindle Edition.

474
Q

what do ARBS do

A

•ARB (angiotensin II receptor blockers) (“-sartan”): angiotensin II receptor blockers decrease chemicals that cause vasoconstriction; decrease intraglomerular pressure through decreasing efferent arteriolar tone.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 421). Wolters Kluwer Health. Kindle Edition.

475
Q

what med class?
decrease chemicals that cause vasoconstriction; decrease intraglomerular pressure through decreasing efferent arteriolar tone.

A

ARB (angiotensin II receptor blockers) (“-sartan”):

476
Q

what med class?

Dilate blood vessels to decrease resistance.

A

ACE (angiotensin-converting enzyme) inhibitors (“-prils”):

477
Q

side effects for ARBS (-sartan)

A

• Dizziness, orthostatic hypotension (worse with first dose, need to take for a week+ before full effect), muscle cramping, diarrhea.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 422). Wolters Kluwer Health. Kindle Edition.

478
Q

Precaution for ARBS (-sartan)

A

Monitor BP and kidney function

479
Q

what do CCBs do?

A

Calcium channel blockers (“-pine”): dilate blood vessels, decreasing cardiovascular resistance. These agents slow the movement of calcium into cells of the heart and blood vessels. May be the desired class in patients with asthma.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 422). Wolters Kluwer Health. Kindle Edition.

480
Q

preferred antihypertensive in asthma pts

A

CCB

481
Q

what med class?

dilate blood vessels, decreasing cardiovascular resistance. These agents slow the movement of calcium into cells of the heart and blood vessels. May be the desired class in patients with asthma.

A

Calcium channel blockers (“-pine”):

482
Q

side effects for CCBs

A

effects: edema, arrhythmias, fatigue, dizziness.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 422). Wolters Kluwer Health. Kindle Edition.

483
Q

Precautions for CCBS

A

monitor heart rate, avoid grapefruit, avoid alcohol, contraindicated in patients with sick sinus syndrome.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 422). Wolters Kluwer Health. Kindle Edition.

484
Q

How does Thiazide-like diuretics work in anti hypertension treatment

A

decrease blood volume and excrete sodium.

  • Thiazide-like: most effective in lowering BP (metolazone, hydrochlorothiazide).
  • Can be used as primary therapy.
  • Can enhance the effects of other antihypertensive agents.
  • Requires salt restriction as concurrent therapy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 422). Wolters Kluwer Health. Kindle Edition.

485
Q

what med class am I?

Metolazone
Hydrochlorothiazide

A

Thiazide like diuretic

for this ch - used in treating HTN

486
Q

Thiazide like diuretics (metolazone, hydrochlorothiazide) precautions

A
  • Requires salt restriction as concurrent therapy.
  • Can infrequently cause hypokalemia, glucose intolerance, adverse lipid effects.
  • Periodic blood chemistries needed. •

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 422). Wolters Kluwer Health. Kindle Edition.

487
Q

What diuretic can be helpful in Hypertensive emergencies

A

Loop diuretic (lasix)

488
Q

What med class am I?

furosemide
bumetanide
torsemide

A

Loop diuretic

489
Q

which is the more powerful class of diuretics used in treatment for HTN

A

Loop

490
Q

which diuretic can be helpful with CHF

A

potassium sparing

491
Q

which diuretic class is usually used as an adjunct

A

Potassium sparing

492
Q

what med class am I

spironolactone

A

Potassium sparing diuretic

493
Q

side effects of diuretics

A

frequent urination, electrolyte imbalance, fatigue or weakness, muscle cramping, dizziness, dehydration, anorexia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 422). Wolters Kluwer Health. Kindle Edition.

494
Q

what med class am I?

Hydralazine, minoxidil

A

Vasodilators

495
Q

what med class am I?
Doxazosin
Prazosin
Terazosin

A

Alpha 1 antagonists

496
Q

what med class am I?
Clonidine
Guanfacine
tizanidine

A

A2 agonists

497
Q

what med class?
block the effects of sympathetic nervous system (adrenaline) in the heart.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 423). Wolters Kluwer Health. Kindle Edition.

A

B Blockers (-lol)

reduces HR in a reduction of cardiac output

498
Q

Who are BBlockers contraindicated in

A

children with heart block, asthma, or pregnancy. May reduce the ability of a diabetic patient to identify a hypoglycemic event; use with extreme caution in diabetic patients.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 423). Wolters Kluwer Health. Kindle Edition.

499
Q

Hypertensive crisis managment

A
  • Intravenous (IV) form of antihypertensive medications (e.g., esmolol, labetolol, nicardipine, hydralazine).
  • Fluid management and restriction.
  • Goal is NOT to decrease BP to a normal level, but rather to return BP to a safe level.
  • Overcorrection of hypertension may result in hypoperfusion to end-organ and cerebral ischemia.
  • First 6 to 12 hours, reduce BP no more than 25% to 33% of overall goal reduction. Rest of the correction to occur over subsequent 48 to 72 hours.
  • Monitor for hypertensive encephalopathy; can be further exacerbated by antihypertensive pharmacologic therapy.
  • Treat underlying cause (e.g., intracranial hypertension, pheochromocytoma, collagen vascular disease, glomerulonephritis).
  • Evaluate for end-organ damage.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 423). Wolters Kluwer Health. Kindle Edition.

500
Q

complications of HTN

A
  • Kidney disease.
  • Left ventricular hypertrophy (LVH)/CHF.
  • Seizures.
  • Hypertensive encephalopathy.
  • Obstructive sleep apnea.
  • Cerebrovascular accident.
  • Ongoing hypertension into adulthood; increased risk of cerebrovascular accident, myocardial infarction.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 423-424). Wolters Kluwer Health. Kindle Edition.

501
Q

Elevated BP which is the new term for prehypertension

A

> =90%ile to <95%ile or 120/80 to <95%ile

> =13: 120/<80 to 129/<80

502
Q

bladder length of the cuff should be ___ to ____% around arm

A

80-100%

503
Q

preferred medications for antihypertension in the setting of DM, CKD or proteinuria

A

ACE/ARB

504
Q

You should consider a higher inital dosing of ACE or alternative therapies in what race

A

African Americans

505
Q

In HTN treatment….

When do you try other agents other than CCB, ACE, ARB or thiazides

A

reserved for children who do not respond to 2 or more of the preferred agents

506
Q

Antihypertensive pharm treatment goal

A

General population
<=90%ile or 130/80

CKD with HTN
<=50ile 24 hour MAP on ABPM

507
Q

How often do you f/u with HTN patients

A

on pharm treatment
-every 4-6 weeks while titrating meds then every 3-4 months after control is achieved

Lifestyle modifications
-every 3-6 months

508
Q

In a diabetic pt you should treat at what point

A

if BP >= 95%ile or >130/80

509
Q

Hypertension and sports

A

Restricted from competitive sports if

  • LVH beyond what is seen with athletes heart until BP controlled
  • Stage 2 HTN until controlled - particularly high static sports such as weights, boxing, wrestling)
510
Q

CKD classifications

A

1- Kidney damage with a normal or increased GFR (>90)

2 - Mild reduction in GFR
60-89

3-Moderate reduction in GFR
30-59

4- Severe reduction in GFR
15-29

5- Kidney failure
GFR <15 or dialysis

511
Q

GFR equation

A

Modified Schwartz:
eGFR = K (height in cm/serum creatinine)
K=0.413

512
Q

what does this stand for

CAPD

A

Continuous ambulatory peritoneal dialysis

513
Q

what does this stand for

CCPD

A

Continuous cycling peritoneal dialysis

514
Q

considerations for initiating dialysis

A

CKD stage 5 with GFR <15

uremic symptoms

malnutrition/growth

Uncontrolled hypertension

volume overload

metabolic acidosis

515
Q

How does peritoneal dialysis work

A

sterile dialysate introduced into peritoneum through a catheter

Dialysate exchanged at intervals after a prescribed indwelling period.

Particle removal by diffusion

Fluid removed by ultrafiltration (osmotic gradient using dextrose)

516
Q

Peritoneal dialysis fluid is removed by _______

A

ultrafiltration (osmotic gradient using dextrose)

517
Q

differences between hemodialysis and peritoneal dialysis

A

Hemodialysis uses artificial membrane whereas PD uses natural membrane

HD uses continuous dialysate flow so never reaches equilibrium whereas PD stagnate dialysate eventually reaching equilibrium

HD occurs in a center where PD is at home

HD has higher blood flow and PD has higher capillary blood flow

518
Q

typical Peritoneal dialysis prescription

A

Fill 10 minutes, dwell 45 min, drain 5 min = 1 hr exchanges

8-10 hrs each night while sleeping by cycler machine

Caregivers are trained and have RN available for questions. These kids are able to attend school

519
Q

PD catheter exit site instructions

A
  • Away from vesicostomies, G-buttons, ureterostomies
  • Either in lateral of downward facing orientation
  • Prophylactic antibiotic administration at time of placement
  • prevent constipation to prevent catheter malfunction and malposition
  • catheter use delayed for at least 2 weeks for healing
520
Q

contraindications for PD

A

Absolute

  • Omphalocoele or gastrochisis
  • Bladder extrophy
  • Diaphragmatic hernia
  • Peritoneal membrane failure
  • Lack of appropriate caregiver

Relative

  • impending abd surgery
  • impending living related transplant
  • VP shunt
  • Peritoneal leaks
  • Ischemic bowel disease
521
Q

complications of PD

A

exit site infection
tunnel infection
peritonitis
Catheter malfunction

522
Q

Peritonitis symptoms

A
abd pain
fever
cloudy fluid (newspaper test)
nausea
vomiting
523
Q

Diagnostic cell count for peritonitis

A

> 100/mm3 white blood cells

-at least 50% being polymorphonuclear leukocytes (neutrophils)

524
Q

treatment of peritonitis

A

intraperitoneal infusion of antibiotics

-gram positive and gram neg antibiotics given while awaiting culture results

narrow spectrum of antibiotics once results are available

525
Q

co-morbit conditions associated with ESRD

A

Anemia
Cardiovascular complications
growth failure
renal osteodystrophy

526
Q

Patho of anemia secondary to ESRD

A

diminished production of erythropoietin by interstitial cells of the renal cortex

shortened erythrocyte life span in CKD

iron deficiency through diet, GI losses, menses

chronic inflammation - systemic and complement activation from dialysis

Bone marrow suppression- inhibitory factors, hyperparathyroidism, medications

increased red cell turnover - Carnitine deficiency, primary renal disease (HUS)

malnutrition - b12 or folate deficiency

527
Q

Anemia management in ESRD

A

minimize blood draws

Erythropoietin stimulating agent (ESA)

Iron supplements (IV vs PO)

528
Q

_______ disease accounts for most deaths in patients with pediatric onset CKD

A

cardiovascular (almost 1000 times higher than age matched peers)

most common: arrythmias, valvular heart disease, cardiomyopathy, acute cardiac death

529
Q

Cardiovascular disease mgmt in ESRD

A

control risk factors

  • anemia
  • HTN (Left ventricular hypertrophy, volume overload)
  • Hyperlipidemia
530
Q

What is metabolic bone disease

comorbidity of CKD

A

inability of kidneys to excrete phosphorous and synthesize Vit D 1, 25

531
Q

Metabolic bone disease diet restrictions

A

Low phosphorous foods

Foods high in phosphorous content: processed foods, dairy (milk, cheese), dark sodas, beans

532
Q

medications for metabolic bone disease treatment

A

Phosphorous binders (Renvela, PhosLo)

Calcium supplements (Tums, Calcium Carbonate)

Vit D analog (Calcitrol)

533
Q

average height for CKD pt

A

1.5 SD below the mean bc of the protein –calorie malnutrition and growth hormone deficiency

534
Q

co-morbidities of CKD

A

quality of life

neurocognitive

  • impaired memory and executive functioning
  • sleep disturbances

Growth hormone deficiency

Nutrition

  • taste disturbances
  • n/v
  • impaired gastric emptying
  • low nutrition intake
  • limited dietary options

metabolic bone disease

Anemia

Cardiovascular disease

535
Q

Hyperosmolar dialysate solution is infused into the peritoneal cavity to facilitate the removal of electrolytes, toxins, and free water.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1315). Wolters Kluwer Health. Kindle Edition.

A

Peritoneal dialysis

536
Q

Tenckhoff catheter used in

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1315). Wolters Kluwer Health. Kindle Edition.

A

Peritoneal dialysis

537
Q

what type of peritoneal dialysis is used to maximize fluid and toxin removal

A

CAPD - Continuous ambulatory peritoneal dialysis

538
Q

what is kidney biopsy used for

A
  • Diagnostic evaluation of kidney disease.
  • Evaluation of rejection after kidney transplant; guides immunosuppression therapy.
  • Detection of primary or metastatic kidney malignancy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1317). Wolters Kluwer Health. Kindle Edition.

539
Q

most common etiologies for kidney transplant

A

congenital
urologic
inherited disorders

540
Q

when does kidney transplant eval begin

A

When estimated creatinine clearance is <60

transplant prior to dialysis requirement is ideal to avoid associated morbidities

541
Q

what does this look for?

•Anti-human leukocyte antigen antibodies and panel-reactive antibodies:

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1318). Wolters Kluwer Health. Kindle Edition.

A

sensitization to determine which donor antigens should be avoided to prevent rejection

542
Q

Posttransplant care

A

• Maintenance immunosuppression. •Calcineurin inhibitor, usually in conjunction with a second agent such as an antiproliferative agent (e.g., mycophenolate mofetil) or mTOR inhibitor (e.g., rapamune). • Calcineurin inhibitors are nephrotoxic; levels require monitoring.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1319). Wolters Kluwer Health. Kindle Edition.

543
Q

signs of renal transplant rejection

A

hypertension, fever, proteinuria, oliguria, or graft nonfunction.

• Hyperacute: minutes to hours after transplant. • Acute: 3 to 90 days after transplant. • Chronic: >60 days after transplant.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1320). Wolters Kluwer Health. Kindle Edition.

544
Q

Posttransplant education

A

avoid aminoglycosides/nephrotoxic drugs

no live immunizations

545
Q

tumor lysis syndrome lab levels

A
elevated 
-potassium
-uric acid 
-bun 
-creatinine 
-phosphorous
decreased calcium
546
Q

pancreatitis, celiac, short gut and inflammatory bowel disease affects magnesium in what way

A

hypomagnesemia

547
Q

expected

PT/PTT in D+HUS

A

normal

548
Q

Labs for HUS D+

A

Uremia
anemia
thrombocytopenia
reticulocytes

549
Q

clinical presentation of Tylenol overdose

A
  • Initial symptoms, mild.
  • Vomiting.
  • Malaise.
  • > 24 hours, symptoms progress.
  • Increased alanine transaminase (ALT) and aspartate transaminase (AST).
  • > 72 hours, peak toxicity.
  • Coagulopathy.
  • Encephalopathy.
  • Liver failure.
  • Cerebral edema (some cases).
  • Possibly, death.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1098-1099). Wolters Kluwer Health. Kindle Edition.

550
Q

Refer to ER for tylenol ingestion levels of

A

Children <6 years of age.
• >200 mg/kg in children <6 years of age in a 24-hour period.

  • > 150 mg/kg per 24-hour period for the preceding 48 hours.
  • > 100 mg/kg per 24-hour

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1099). Wolters Kluwer Health. Kindle Edition.

551
Q

Tylenol overdose antidote should be started within ___ hours of ingestion for best efficacy

A

8

552
Q
  • The alcohol most commonly recognized; produced by the fermentation of grains, “grain alcohol.”
  • Alcoholic beverages and distilled spirits. • Found in accessible household products—hand sanitizer, mouthwash, colognes, and others.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1103). Wolters Kluwer Health. Kindle Edition.

A

Ethyl alcohol (ethanol)

553
Q
  • Produced from the distillation of wood, “wood alcohol.”
  • Found in industrial solvents, gasoline blends, plastic products, windshield wiper fluid, paint strippers, glass cleaners, hobby and craft adhesives, food warming cans used under chafing dishes (e.g., Sterno), and others.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1103). Wolters Kluwer Health. Kindle Edition.

A

methyl alcohol (methanol)

554
Q
  • Used in various solvents.
  • Primary component of automobile antifreeze.
  • Found in herbicides/pesticides, liquid detergents, paints and paint products, among others.
  • May have a sweet taste and attractive color which can pose a particular danger to children.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1103). Wolters Kluwer Health. Kindle Edition.

A

Ethylene glycol

555
Q

Painless rectal bleeding in preschool or young school age…think

A

Meckels diverticulitis

556
Q

clinical presentation of ethanol ingestion

A
  • Symptoms similar to other sedatives.
  • Vomiting due to GI distress.
  • Slurred speech, ataxia, lethargy, and coma.
  • Respiratory depression.
  • Hypotension.
  • Bradycardia.
  • Facial flushing.
  • Profound hypoglycemia secondary to impaired gluconeogenesis can be problematic, and often is a delayed presentation.
  • An odor to the breath can sometimes be detected.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1104). Wolters Kluwer Health. Kindle Edition.

557
Q

late toxic finding of ethanol ingestion

A

hypoglycemia

558
Q

normal weight gain infant per day

A

20-30 g/day (about an ounce a day)

559
Q

what electrolyte abnormality are you concerned in a jaundice baby receiving phototherapy due to insensible losses

A

hypernatremia

560
Q

electrolyte abnormalities with Amphotericin B

A

Hypokalemia

Hypomagnesemia

561
Q

what electrolyte abnormalities with Tumor lysis syndrome

A

Hyperkalemia
Hyperphosphatemia
Hypocalcemia
High uric acid levels

562
Q

treatment for steroid resistant nephrotic syndrome

A

administer steroids with goal of immunosuppression is recommended

563
Q

treatment for meningococcal meningitis

symptoms?

A

ceftriaxone 100mg/kg/day for 5-7 days

symptoms
rapid onset fever
malaise
vomiting
diarrhea
nuchal rigidity 
maculopapular rash
564
Q

4 wk old infant with projectile vomiting an da palpable olive shaped mass on exam. What are the expected lab findings

A

Hypochloremia
Hypokalemia
Hyperbilirubinemia

565
Q

Phos and Ca have what relationship

A

inverse

566
Q

hallmark sign of necrotizing enterocolitis on x ray is

A

pneumatosis - intestinalis

567
Q

what supplement is often needed with DiGeorge syndrome

A

Calcium

most often hypocalcemic

568
Q

electrolyte derangement expected in massive transfusion

A

Hypocalcemic and hyperkalemic because the calcium citrate binds to the calcium in blood

569
Q

older child with intussusception what are you worried about?

A

usually in younger than 2

older needs workup for oncology

570
Q

what is expected caloric intake for a 3-4 month old or 12kg infant

A

110 calories/kg/day

571
Q

substance ingestion with highest fatality if ingested by a young toddler

A

Calcium Channel Blocker

572
Q

how much breastmilk for 1 month old per day

A

100ml/kg/day

573
Q

how much Na is in NS

A

154

574
Q

organophosphate poisoning

A

atropine for muscarinic symptoms

Pralidoxime

benzos for seizures

575
Q

treatment for nephrotic syndrome

A

high dose steroids (2mg/kg/day) x 6 weeks until in remission which is defined as 3 consecutive days with no protein on urine dipstick

576
Q

KCL dosing

A

0.5-1mEQ/kg over 90 min

577
Q

Type II RTA is associated with what syndrome

A

Fanconi

578
Q

what RTA
FTT
metabolic acidosis and
hypokalemia

A

Type II RTA

579
Q

In RTA what does chloride, bicarb and urine bicarb look like. How to treat?

A

High chloride
low bicarb
high urine bicarb

treat with oral bicarbonate supplements

580
Q

Calcium dosing

A

Ca Chloride - 10mg/kg CVC

or Ca Gluconate 100mg/kg PIV

581
Q

Tests for SLE

A

ANA
Anti-double strand DNA
Anti smith Antibody

582
Q

treat for poststreptococcal GN

A

Penicillin V

583
Q

treat for IgA nephropathy

A

Antihypertensives

584
Q

Treat for PKD

A

Antihypertensives

585
Q

causes of hypermag

A

renal failure
excessive intake
tumor lysis syndrome

586
Q

in DKA treatment what do you expect Mg to do

A

Low Mg

insulin stimulates cell uptake of Mg

587
Q

Serum calcium levels is affected by

A

Albumin levels

588
Q

Low phos causes

A

muscle weakness to include resp muscles

589
Q

High phos causes

A

laryngospasm and tetany

590
Q

Hypochloremia is associated with what syndrome

A

Bartter syndrome

591
Q

Potassium phos is infused over ___ to __ hrs

A

4-6

592
Q

to raise Na levels this should be done

A

2-4 mEQ in 4 hrs or 10-20 meQ in 24 hrs