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Families > PEDS- Exam 3 > Flashcards

PEDS- Exam 3 Flashcards

1
Q

Diabetes mellitus is what

A

a metabolic deficiency of insulin

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2
Q

Type 1 diabetes is characterized by

A

destruction of pancreatic beta cells

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3
Q

Type 2 diabetes is characterized by

A

it is a chronic condition characterized by insulin resistance and/ or insufficient insulin production

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4
Q

What is a type 1 diabetic dependent on

A

insulin because they will not be able to produce their own

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5
Q

Risk factors for type 1 diabetes

A

genetic predisposition, autoimmune factors, environmental triggers

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6
Q

Expected findings of diabetes type 1

A

hypoglycemia ( cold and clammy you need some candy), hyperglycemia (high and dry sugar high)

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7
Q

Tell me the findings for hypoglycemia

A

blood glucose less than 60
hunger, lightheaded, cool skin, diaphoresis (cool skin)
tachy.

neuro
headache
difficulty in thinking
slurred speech

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8
Q

tell me the findings for hyperglycemia

A

blood glucose greater than 250
thirst
polyuria
n/v
dry mucous
weak pulse
warm dry

neuro
confusion
weakness
diminished reflexes

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9
Q

telltale sign of type 1 in DKA

A

fruity breath

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10
Q

Diagnostic test for diabetes type 1

A

fasting blood glucose ( 126 or more after an 8-hour fast)
oral glucose tolerance test (200 mg or more in the 2-hour sample)
Random blood glucose ( 200 mg or more with symptoms of diabetes

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11
Q

education for fasting blood glucose

A

ensure an 8-hour fast (only water), postpone antidiabetic medications until after the test

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12
Q

education for oral glucose tolerance test

A

balanced diet for 3 days before fasting for 8 hours
initial fasting blood glucose drawn
consume specified glucose, blood glucose levels drawn every 30 min for 2 hours
monitor for hypoglycemia

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13
Q

Diabetes type 1 treatment

A

only treatment is insulin
insulin pump, insulin injections

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13
Q

Diabetes type 1 nursing education

A

-rotate injection sites, which helps maintain a consistent absorption rate
-inject at 90-degree pinch
- when mixing insulin draw short insulin first followed by long-acting

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14
Q

Diabetes type 1 complication

A

DKA - ketone accumulation in the blood urine and lungs
-Hyperglycemia >330
-glycosuria glucose in urine
-acidosis
- fruity breath

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14
Q

diabetes type 1 nursing consideration

A

-provide isotonic fluid
-blood glucose approaches 250 add glucose to IV fluids to maintain levels between 120-240
-MMonitor glucose and potassium
-administer sodium bicarbonate for acidosis
-maybe provide oxygen

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15
Q

Growth hormone disorder deficiency

A

not enough GH -> slowed growth in children ->metabolic effects in adults

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16
Q

growth hormones deficiency risk factors

A

structural factors (tumors, traumas)
heredity disorders
deficiencies of TSH or ACTH
most often idiopathic

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16
Q

Growth hormone excess

A

too much can lead to gigantism or acromegaly in adults

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17
Q

GH deficiency expected findings

A

-short stature but proportional height and weight
- delayed closure of growth plates
- delayed teeth/ underdeveloped jaw
-increased insulin sensitivity
-standard deviation might have growth rate slower than whats expected

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17
Q

GH excess expected findings

A

before closing of epiphyseal plate
-excessive height and rapid growth
-longer limbs due to continued growth of limbs
-larger heads and feet
-prominent forehead and jaw

after closing the epiphyseal plate
-thickened skin
-deep voice
-excessive sweating and body odor
-headaches and vision problems
-sleep apnea also due to enlarged organs

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17
Q

labs and diagnostic for GH deficiency

A

plasma insulin, gh stimulation, skeletal survey

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18
Q

labs and diagnostic for GH excess

A

elevated IGF-1 levels are a key indication of GH excess
oral glucose tolerance test (gold standard!! Normally GH levels lower after glucose but in excess they remain elevated)
prolactin levels
MRI

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19
Q

Nursing care for both GH-deficient and excess

A

-Height ! and weight tracked
-measure every 6 months under 3 and yearly over 3
-address psychosocial concerns
-encourage realistic age-appropriate goals

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20
Q

Patient education for both GH-deficient and excess

A

-minimal side effects of meds with proper dosing
- supports muscle growth and self-esteem
-injection teaches subcutaneous
- frequency 6-7 times a week
- important to adhere
-reassess need in early adulthood

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21
Q

What is the medication used for GH

A

somatropin
administered via subcutaneous
use cautiously in children receiving insulin

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22
Q

Tay Sachs + risk + findings

A

rare genetic disorder
caused by a deficiency of enzyme Hex-A

Risk
autosomal recessive
Ashkenazi jew descent

Findings
developmental delays
muscle weakness
increased startle reflex
cherry spot on the retina
seizures
vision/hearing loss

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23
Q

Phenylketonuria

A

inherited disorder newborn lacks enzyme phenylalanine hydroxylase cant convert into tyrosine leads to accumulation causing cognitive impairment

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24
Q

Phenylketonuria risk factor and expected findings

A

risk: pku inherited as an autosomal recessive trait
finding
-growth failure
-frequent vomiting
-irritability
-musty odor to urine
-microcephaly
-heart defects
- blue eyes, fair skin, blonde hair

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25
Q

Labs for tay sachs

A

genetic testing for mutations in the HEXA gene, enzyme activity assays to check hex-a levels in blood or tissue, prenatal testing for at risk families

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26
Q

Labs for PKU

A

Newborn metabolic screen: blood spot analysis after the newborn has ingested a source of protein (2 days of birth)
Guthrie test: confirms dx. when blood spot analysis is positive

27
Q

Tay sachs nurisng care

A

no cure for tay sachs, manage symptoms, provide supportive care
care teams

28
Q

PKU nursing care

A

dietary: low phenylalanine formula start restrictions 7-10 days of birth
limit intake: 20-30 mg/kg of body weight
-check levels regularly aim for 2-88 mg levels

29
Q

Complications for Tay Sachs

A

no cure
blindness, paralysis, cachexia, seizure death (3-5)

30
Q

complications for PKU

A

cognitive impairment, hyperactivity, bizarre behavior, head-banging, seizures

31
Q

Galactosemia

A

rare- affects the body’s ability to metabolize galactose (sugar in milk)
inherited autosomal recessive

treatment - dietary management
early diagnosis an dietary management can prevent severe complications

32
Q

Maple Syrup Urine Disease

A

autosomal recessive, enzyme cant metabolize BCCA
treatment for MSUD - dietary low protein, some cases a liver transplant
early diagnosis and effective dietary management can lead to healthy lives

33
Q

Celiac disease

A

the autoimmune disorder affects the small intestine, triggered by the consumption of gluten, protein in wheat barley, and rye. damages lining of small intestines

34
Q

Celiac disease risk factors

A

genetics, autoimmune, down syndrome, turner syndrome, infections, environment

35
Q

Celiac Disease expected findings

A

digestive issues, growth problems (short)
unexplained weight loss
fatigue
skin issues
behavioral changes

36
Q

celiac disease labs

A

ttg-iga
egd
biopsy

37
Q

Celiac disease nursing considerations

A

GI issues, dietary guidance, label reading, education on nutrition and cross contamination, possible emotional support

38
Q

Hypertrophic pyloric stenosis and risk factors

A

thickening of the pyloric sphincter creates an obstruction. typically happens in the first few weeks of life, blocks food causes vomiting
findings: dehydration, failure to gain weight, projectile vomiting/blood-tinged vomiting - treatment surgery

risk factor: genetics

39
Q

Hypertrophic pyloric stenosis labs and diagnostics + therapeutic procedure

A

blood testing, ultrasound
treatment: pyloromyotomy

40
Q

Hypertrophic pyloric stenosis
nursing considerations pre-op and post-op

A

Pre
-IV fluids for dehydration, NG for decompression, NPO, I&O, Daily Weight
Post
- vital signs, Iv fluids, monitor daily weights and I&O, pain meds, observe for infection, clear liquids 4-6hr after surgery, 24 hours after advance to breast miilk as tolerated

41
Q

Hirschsprung’s disease

A

a birth defect where certain segments of colon lack nerve cells
risk factors: genetic predisposition

42
Q

Hirschsprung’s disease findings

A
  • blocked colon, can lead to megacolon
    newborn- failure to pass meconium , vomiting bile, abdominal distention
    infant- failure to thrive, constipation
    child-undernourished, anemic appearance, abdominal distention, foul smelling ribbonlike stool , visible peristalsis
43
Q

Hirschsprung’s disease labs & diagnostic

A

blood electrolytes, CBC, Rectal biopsy to confirm no ganglion cells

44
Q

Hirschsprung’s disease pre and post op consideration

A

pre
improve nutritional status until surgery, high protein, high calorie, low fiber
provide electrolyte and fluid replacement
post
usual plus possible ostomy care

45
Q

Complication of Hirschsprung’s disease

A

Enterocolitis :inflammation of the bowel,

46
Q

Nursing actions for Hirschsprung’s disease

A

monitor vitals, assess abdominal girth, monitor for manifestations of sepsis, peritonitis, shock, manage fluids
measuring abdomen: level of umbilicus at widest point of abdomen

47
Q

Intussusception

A

proximal segment of bowle telescopes into more distal segment, results in lymphatic and venous obstruction causes edema in area

  • common in ages 3 months to 6 years . with progression increased mucus into intestine will occur

Dx. ultrasound

48
Q

Intussusception expected findings

A

-abdominal pain, screaming with drawing knees to chest , *stools mixed with blood and mucus that resemble red currant jellly!

49
Q

Intussusception nursing consideration

A

-Enema, iv fluids correct and prevent dehydration, ng tube
goal to create pressure in intestine and pushes bowel into normal position

50
Q

Cleft lip/ palate Pathology

A

cleft lip- incomplete fusion of the oral cavity during intrauterine life `
cleft palate- incomplete fusion of palates during intrauterine life

51
Q

Cleft lip/ palate risk factors

A

family hx. ,genetic, maternal health (diabetes), ! folate deficiency during pregnancy! exposure to alcohols, cigarette smoke, anticonvulsant, retinoids

52
Q

Expected findings cleft lip/ palate

A

cleft lip is visible separation from upper lip toward nose
cleft palate visible or palpable opening of the palate connecting the mouth and the nasal cavity

53
Q

procedures for repair cleft lip/palate done at what age

A

cleft lip: repair typically done between 2 to 3 months of age, revisions are usually required in severe defects
cleft palate: repair is typically done between 6-12 months most require second surgery

54
Q

Cleft post op

A

position on back or upright or on side to protect repair possible elbow restraint. Make sure we check for gag reflex before eating. if they need oxygen make sure its mask and not nasal cannula

55
Q

complications of cleft lip/palate

A

ear infection, feed in upright position, monitor temperature

more common with cleft palate
-dental problems, possible speech therapist, seek early dental care

56
Q

Appendicitis

A

inflammation of the vermiform appendix caused from obstruction of lumen, average client is 10 years old

if they refuse to jump they most likely have appendicitis. *pain in RLQ (McBurney’s point)

57
Q

Expected findings appendicitis

A

Rigid board like abdomen , decreased or absent bowels , fever, abdominal pain rlq McBurney’s point

58
Q

Appendicitis Labs and considerations

A

CBC, Urinalysis, WBC elevated
-prepare child and family for surgery using developmentally appropriate techniques
-do not apply heat
-avoid laxatives and enemas

59
Q

Appendicitis non ruptured procedure

A

laparoscopic surgery
pre - antibiotics, iv fluids
post- asses resp status, assess bowel sounds and bowel function

60
Q

Appendicitis ruptured procedure

A

laparoscopic or open surgery
Pre- IV fluids, NG tube, Iv antibiotics
Post- ABC’s. low suction NG tube , maintain NPO, assess for peritonitis

61
Q

Appendicitis complications peritonitis expected findings

A

fever, sudden relief from pai after perforation, *followed by a diffuse increase in pain

62
Q

Peritonitis complication of appendicitis Nursing Care

A

-give pain meds, manage Iv fluids, psychosocial support

63
Q

Acute GI Infection -Acute diarrhea

A

Occurs suddenly and is caused by infections (viral bacterial or parasitic) antibiotic use, or laxative use. Typically resolves within 14 days if dehydration doesn’t occur

64
Q

Acute GI Infection Chronic Diarrhea

A

longer than 14 days
conditions like, malabsorption, food allergies, or inflammatory bowel disease

65
Q

expected findings for acute GI infection

A

fatigue, malaise, change in stool pattern, weight loss, thirsty, dark urine, poor appetite

66
Q

Acute Gi Infection Viral vs. Bacterial

A

Viral: rotavirus
Bacterial: C.Diff, E.Coli

67
Q

Acute Gi infection Dx. and medications

A

stool sample
medications - metronidazole: C.Diff
Tinidazole

68
Q

Nursing Consideration and education for Acute GI infection

A

no rectal temperature, baseline height and weight, alert school and keep kiddo home

education: Avoid juices, sodas, gelatin, broth, caffeine, skin care, immunization

69
Q

Isotonic

A

Stays where you put it

70
Q

Hypotonic

A

Cell swells as water is pulled in (Hippo) more water than salt ( extracellular to intracellular outside cell to inside cell)
*Hyponatremia

71
Q

Hypertonic

A

cells shrink as water is pushed out (think thin) more salt than water (intracellular to extracellular inside cell to outside cell)
*Hypernatremia

72
Q

Dehydration differences

A

due to body surface area and age there will be differences in how quickly the child will be and what the expected findings will be we want to catch it when its mild not severe

Families (5 decks)

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