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Module 203 > Failure to Thrive > Flashcards

Failure to Thrive Flashcards

1
Q

What is a general definition of failure to thrive?

A

occurrence of growth faillure in either height or weight in childhood

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2
Q

What are the two causes of failure to thrive?

A

organic vs non organic

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3
Q

What are the percentile cutoffs for failure to thrive?

A

Weight

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4
Q

what % of FTT that is non organic?

A

90%

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5
Q

what % of FTT is organic

A

10%

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6
Q

What causes non organic FTT?

A

complex factors in parent/child relationship (dietary intake, knowledge about feeding, improper mixing of formula, economic factors, feeding environment, child behaviours, hunger/satiety cues, social factors, stress, poverty)

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7
Q

What are the causes of organic FTT

A

Inadequate intake, vomiting, oromotor dysfunction, anorexia, excessive consumption (CHD, CF, hyperthyroidism), abnormal ultilization (inborn error of metabolism), excessive output (IBD, celiac disease, malabsorption)

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8
Q

When a child is not having adequate intake what are the two major causes?

A

Organic illness (inability to suck/swallow, lack of appetite) and nonorganic/psychosocial

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9
Q

When a child has adequate intake what are the two categories of causes?

A

increased demands and inadequate absorption and/or utilization of nutrients

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10
Q

What does the acronym SMALL KID stand for (in relation to the clinical signs of FTT)

A

SQ Fat loss, Muscle atrophy, Alopecia, Lethargy, Laggnig behind normal, Kwashiokor, Infection, Dermatitis

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11
Q

What is the FTT pattern of decreased weight, normal height, normal head circumference suggestive of?

A

Caloric insufficiency, decreased intake, hypermatabolic state, increased losses

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12
Q

What is the FTT pattern of decreased wt, decreased ht, normal HC indicative of?

A

Structual dystrophies, Endocrine disorder, Constitutional growth delay (bone age

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13
Q

What is the FTT pattern of decreased wt, decreased ht and decreased hc indicative of?

A

Intrauterine insult, genetic abnormality

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14
Q

Define maldigestion?

A

inability to break down large molecules in the lumen of the intestine into their component small molecules

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15
Q

Define malabsorption

A

inability to transport molecules across the intestinal mucosa into circulation

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16
Q

Define malassimilation?

A

encompasses both of the above

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17
Q

Where is iron absorbed?

A

duodenum and upper jejunum

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18
Q

where is calcium absorbed?

A

duodenum, upper jejunum (binds ca binding protein in cells; levels increased by Vit D)

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19
Q

Where is folic acid absorbed?

A

jejunum

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20
Q

Where is vitamin B12 absorbed?

A

ileum but causes a big cascade of events before absorption

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21
Q

Where are carbohydrates absorbed?

A

duodenum/ jejunum (have to be broken down into monosaccharides first)

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22
Q

Where are proteins digested and absorbed?

A

digestion at stomach, brush border and inside cell. Absorption in Jejunum

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23
Q

What is needed for the digestion of fats?

A

Lipase, colipase and phospholipase A (pancreatic enzymes), and bile salts needed for digestion of fats

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24
Q

What do products of lipolysis do and aid in?

A

form micelles which solubilize fat and aid in absorption

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25
Q

Where do fatty acids diffuse into?

A

cell cytoplasm

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26
Q

Where do we get Vtiamin A from?

A

milk, eggs, liver, carrots, sweet potatoes

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27
Q

Where do we get vitamin D from?

A

Skin (UV light), diet (eggs, fish oil, fortified milk)

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28
Q

Where do we get vitamin E from?

A

Vegetable oils, nuts, leafy greens

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29
Q

Where do we get Vitamin K from?

A

synthesized by intestinal flora, increased risk of deficiency after prolonged use of broad spectrum Abx or starvation

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30
Q

What are the clinical diseases associated with iron deficiency?

A

hypochromic microcytic anemia, glossitis, kolonychia (spoon nails), pica

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31
Q

What are the clinical diseases assocaiated with calcium deficiency?

A

metabolic bone disease, tetany and paresthesias if serum ca falls

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32
Q

What are the clinical diseases associated with folic acid defiicency?

A

megaloblastic anemia, glossitis, decreased RBC folate

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33
Q

What are the clinical diseases associated with Vitamin B12 deficiency?

A

subacute combined degeneration of the spinal cord, peripheral/optic neuropathy, dementia, megaloblastic anemia, glossitis

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34
Q

What are the clinical diseases associated with carbohydrate deficiency?

A

generalized malnutrition, weight loss, flatus, diarrhea

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35
Q

What are the clinical diseases associated with protein deficiency?

A

general malnutrition, weight loss, amenorrhea and decreased libido if severe

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36
Q

What are the clinical diseases associated with fat deficiency?

A

generalized malnutrition, weight loss, diarrhea, foul smelling feces + gas, steatorrhea

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37
Q

What are the clinical diseases associated with vitamin A deficiency

A

Nigh blindness, dry skin, keratomalacia

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38
Q

What are the clinical diseases associated with Vitamin D deficiency?

A

Osteomalacia in adults, rickets in children

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39
Q

What are the clinical diseases associated with Vitamin E deficiency?

A

retinopathy, neurological patterns

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40
Q

What are the clinical diseases associated with Vitamin K deficiency?

A

prolonged INR causing bleeding

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41
Q

What kind of genetic disorder is CF

A

Autosomal recessive genetic disorder (most lethal genetic disorder in white population?

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42
Q

What does CF Transmembrane regulator dysfunction result from?

A

Single gene mutation. Chloride channel on the apical surface of epithelial cells, results in defective chloride transport and increased Na reabsorption in airway and ductal epithelia, creates thick and viscous secretions in the respiratory, hepatobiliary, GI and reproductive tracts

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43
Q

What are the GI complications of CF?

A

Steatorrhea, pancreatic insufficiency, malabsorption, DM, distal intestinal obstruction, salivary gland inflammation, cholelithiasiss

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44
Q

What is does the acronym C BASE H20 Stand for when assessing severe dehydration?

A

Cap refill. BP. Anterior fontanelle. Skin turgor. Eyes sunken. HR. Oral mucosa. Output of urine.

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45
Q

What % of mother experience postpartum blues?

A

50 - 80%

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46
Q

When does postpartum blues start and how long does it last for?

A

begins 2 - 4 days post partum lasts 48h to 10 days

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47
Q

How many mothers experience post partum depression

A

10%

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48
Q

When does post partum depression start?

A

during pregnancy of within 4 weeks of delivery. Lasts 2 - 6 months, residual sx up to a year

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49
Q

What are the RF for post partum depression?

A

previous mood disorder, stressful life events, unemployment, marital conflict, lack of social support, unwanted pregnancy, colicky or sick infant

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50
Q

What is cerebral palsy?

A

Non progressive central motor impairment syndrome due to insult to or anomaly of the immature CNS. A symptom complex, not a disease.

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51
Q

how many per 1000 live births experience cerebral palsy?

A

1.5 - 2.5 / 1000

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52
Q

What causes Cerebral palsy?

A

10% intrapartum asphyxia, 10% postnatal insult (infections, asphyxia, trauma), associated with SGA babies

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53
Q

What is the clinical presentation of cerebral palsy?

A

delay in motor milestones, developmental delay, learning disabilities, visual/hearing impairment, seizures, micorcephaly, uncoordinated swallow

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54
Q

What are the 4 types of cerebal palsy?

A

Spastic, Athetoid/Dyskinestic, Ataxic, Mixed,

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55
Q

What % of cerebeal palsy cases are spastic?

A

70 - 80%

56
Q

What % of CP cases are athetoid/Dyskinetic?

A

10- 15%

57
Q

What % of CP cases are ataxic?

A
58
Q

What % of CP cases are mixed?

A

10 - 15%

59
Q

What are the characteristics of spastic CP?

A

Truncal hypotonia in first year. Increased tone, increased reflexes, increased clonus. Can affect one limb (monoplegia), one side of the body (hemiplegia), both legs (diplegia) or both arms and legs (quadriplegia)

60
Q

What areas of the brian are involved in spastic CP?

A

UMN of pyramidal tract. Diplegia associated with periventricular luekomalacia in premature babies. Quadriplegia associated with asphyxia (higher incidence of intellectual disability)

61
Q

What are the characteristics of dyskinestic CP?

A

Athetosis (involuntary writhing movements) +/- chorea (involuntary jerky movements). Can involve face, tongue (results in dysarthria)

62
Q

Whar areas of the brain are involved in dyskinetic (athetoid) CP?

A

Basal ganglia (may be associated with kernicterus)

63
Q

What are the characteristics of ataxic CP?

A

poor coordination, poor balance (wide based gait), can have intention tremor)

64
Q

What areas of the brain are involved in ataxic CP?

A

cerebellum

65
Q

Hwo do you investigate CP?

A

metabolic screen, chromosome studies, serology, neuroimaging, opthalmology assessment, audiology assessment

66
Q

How do you treat spasticity in CP?

A

baclofen or botox

67
Q

Define Type I DM?

A

chronic illness characterized by the body’s inability to produce insulin due to the autoimmune destruction of the beta cells in the pancreas?

68
Q

What is the typical age of onset for Type I DM?

A
69
Q

How much of DM does type I account for?

A

5 - 10%

70
Q

What is type I DM associated with geneticallY?

A

HLA class II DR3 and DR4

71
Q

What causes type I DM?

A

autoimmune process believed to be triggered by environmental factors (BOVINE CUM)

72
Q

What happens the pancreatic cells during type I DM?

A

pacreatic cells are infiltrated with lymphocytes

73
Q

how much pancreatic cell mass is destroyed before onset of S&S?

A

80%

74
Q

What are the clinical features of Type I DM?

A

polyuria, polydipsia, polyphagia, fatigue, dehydration, abdo pain, weight loss, wasting, FTT

75
Q

What is hyperthyroidism?

A

increased level of circulating thyroid hormones

76
Q

What are the usual causes of hyperthyroidism?

A

Grave’s Disease, Toxic adenoma, mulinodular goiter, thyroiditis

77
Q

What are two rare causes of hyperthyroidism?

A

excessive ingestion of thyroid hormone, thyroid production from ectopic site (stuma ovarii)

78
Q

What is the etiology of hyperthyroidism in children?

A

Fetuses of women with current or prior graves disease (autoantibodies in the mother cross the placenta, neonatal graves is usually transiet)

79
Q

What causes >90% of infant/child hyperthyroidism?

A

graves dsease

80
Q

What are infant S&S of hyperthyroidism

A

irritability, feeding problems, HTN, tachycardia, exophthalmos, goiter, frontal blossing, microcephaly, FTT, vomiting, diarrhea

81
Q

What are some childhood S&S of hyperthroidism

A

SLEEP DIFFICULTIES, HYPERACTIVITY, EMOTIONAL LIABILITY, DECREASE IN CONCENTRATION, vomiting, diarrhea, irritability, feeding problems, HTN, tachycardia, exophthalmos, goiter, frontal blossing, microcephaly, FTT

82
Q

What are severe complication of hyperthyroidism if not detected until the neonatal period?

A

craniosynostosis, impaired intellect, growth failure, short stature

83
Q

What is the mortality percent of fetal hyperthyroidism isn’t detected until the neonatal period?

A

10 - 15%

84
Q

What is the tx of hyperthyroidism

A

antithyroid meds (methimazole with or without a beta blocker), radiactive iodine, sx

85
Q

What can hypothyroidism cause in infants and children?

A

retardation of growth and development and permanent motor and mental retardation

86
Q

What are some congential causes of hypothyroidism?

A

agenesis, dysgenesis, hypoplastic thyroid, thyroid dyshormogenesis, maternal iodine deficiency, congential pituitary disease

87
Q

What are some acquired causes of hypothyroidism?

A

hashimoto thyroiditis, autoimmune thyroiditis

88
Q

What are clinical features of infants with hypothyroidism?

A

severe growth failure, coarse facial features, intellectual disability, spasticity, low muscle tone, sensorineural hearing loss, prolonged hyperbilirubuinemia, umbilical hernia, resp distress, macroglossia, large fontanelles, poor feeding, hoarse crying

89
Q

How do you dx infant hypothyroidism?

A

routine newborn screening, thyroid functino tests, thyroid US, Radionucleotide scan

90
Q

What is growth hormone deficiency also known as?

A

pituitary dwarfism

91
Q

What can be isolated Growth Hormone Deficiency or Generalized Hypopituitarism?

A

growth hormone deficiency

92
Q

What is the treatment for growth hormone deficiency?

A

recombinant GH supplements

93
Q

Is achondroplasia lethal?

A

no

94
Q

what is the most common type of short limb dwarfism?

A

achondroplasia

95
Q

What causes achondroplasia?

A

mutation in the fibroblast growth facts receptor 3 - gene (FGFR3)

96
Q

What is the neurologic presentation of achondroplasia?

A

hypotonia in infancy, delayed motor milestones, normal intelligence

97
Q

What are the craniofacial presentations of achondroplasia?

A

large calvarial bones compared to small cranial base and facial bones, true megalencephaly (large head) with frontal bossing, midface hypoplasia, dental malocclusion and crowding

98
Q

What are the skeletal presentations of achondroplasia?

A

short stature, normal trunk length, small thoracic cage, shortening of proximal limbs, lumbar kyphosis, genu varum

99
Q

What are the hallmarks of congenital short stature?

A

bone age appropriate for chronological age, normal growth velocity, predicted adult height appropriate to the familial pattern

100
Q

What are the signs of fetal alcohol syndrome at birth?

A

small stature, facial traits (another card re these), abnormal palmar creases, cardiac defects, joint contractures

101
Q

What are the 8 facial traits of fetal alcohol syndrome?

A

microcephaly, micropthalmia, short palpebral fissures, epicanthal folds, small or flat midface, flat elongated philtrum, thin upper lip, small chin

102
Q

What are the S&S of Fetal alcohol syndrome after birth?

A

cognitive deficits

103
Q

What is the most common cause of noninherited intellectual disability?

A

fetal alcohol syndrome

104
Q

What is the incidence of trisomy 21 (down syndrome)

A

1 in 600 - 800 births

105
Q

What is the incidence of trisomy 21 at maternal age 20 years vs maternal age 45 years

A

1 :1500 (20 years)/ 1:20 (45 years)

106
Q

What are the CNS S&S of down syndrome?

A

Mental retardation (IQ 20 - 70), early alzheimer disease, hearing impairment

107
Q

What are the head & neck S&S of down syndrome?

A

upslanting palpebral fissures, epicanthial folds, speckled iris (brushfield spots), flat nasal bridge, open mouth with protruding tongue

108
Q

What are the MSK S&S of down syndrome?

A

hypotonia, atlanto-axial instability, short hands with single transverse palmar crease (simian crease)

109
Q

What are the cardiac S&S of down syndrome

A

endocardial cushion defects (atrioventricular septal defects), VSD, ASD, PDA, ToF

110
Q

What are the GI S&S of down syndrome

A

duodenal atresia or stenosis, annular pancreas, tracheoesophageal distula, hirschsprungs disease, omphalocele, imperforate anus

111
Q

What are the immunologic sx of down syndrome

A

impaired cellular immunity, high incidence of infections and autoimmune disorders and malignancies

112
Q

What are the hematologic sx of down syndrome

A

AML (500x increased risk) and ALL (10 - 20x increased risk)

113
Q

What are the endocrine S&S of down syndrome?

A

Hypothyroidism, hyperthyroidism, Type I DM, infertility in males

114
Q

What is the cause of turner syndrome?

A

absence of one set of genes from the short arm of one X chromosome

115
Q

What are the immunologic sx of down syndrome

A

impaired cellular immunity, high incidence of infections and autoimmune disorders and malignancies

116
Q

What are the hematologic sx of down syndrome

A

AML (500x increased risk) and ALL (10 - 20x increased risk)

117
Q

What are the endocrine S&S of down syndrome?

A

Hypothyroidism, hyperthyroidism, Type I DM, infertility in males

118
Q

What is the cause of turner syndrome?

A

absence of one set of genes from the short arm of one X chromosome

119
Q

What are the features of turner syndrome?

A

short stature, webbed neck, low posterior hairline, wide carrying angle, broad chest, widely spaced nipples, lung hypoplasia, coarctation of the aorta,, renal and CV abnormalities, mild cognitive deficits

120
Q

What is the treatment for turner syndrome?

A

sympotmatic control, GH therapy to help prevent short stature, estrogen replacement for developmental of secondary sexual characteristics

121
Q

What is prematurity defined as?

A

neonates born

122
Q

How do you define late preterm, very preterm and extremely preterm neonates?

A

Late preterm 34 - 37 weeks, very preterm

123
Q

What is low, very low or extremely low birthweight?

A

Low

124
Q

What are the short term complications of prematurity?

A

hypothermia, resp distress syndrome, bronchopulmonary dysplasia, apnea or prematurity, patent ductus arteriosus, hypotension, intraventricular hemorrhage, glucose abnormalities, necrotizing enterocolitis, infections, retinopathy of prematurity

125
Q

What are the long term complications of prematurity

A

Neurodevelopmental outcome, impaired cognitive skills, motor deficits, sensory impairment, behavioural and psychological problems, growth impairment, impaired lung function (asthma).

126
Q

What is pyloric stenosis a result of?

A

hypertrophy and hyperplasia of the muscular layers of the pylorus, causing a functional gastric outlet obstruction

127
Q

What % of live births have pyloric stenosis ?

A

0.03 - 1%

128
Q

What is the M:F ratio of pyloric stenosis?

A

4:1

129
Q

When can pyloric stenosis present? and when does it most commonly present?

A

Can present 1 - 20 weeks of age. Most commonly presents at 6 - 8 weeks

130
Q

What is a risk factor for pyloric stenosis?

A

early erythromycin exposure (

131
Q

What is the pathophysiology behind pyloric stenosis?

A

hypovolemia due to emesis, electrolyte disturbances (hypochloremia, hypokalemia, metabolic acidosis)

132
Q

What are the clinical features of pyloric stenosis?

A

Hungry vomiter, projectile non bilious vomiting (30 - 60 min post feeding), 1 -2cm palpable mass above the umbilicus (olive sign)

133
Q

What is the treatment for pyloric stenosis?

A

treat acute dehydration, electrolyte disturbances, acid base disturbances, pyloromyotomy

134
Q

What is the definition of GERD?

A

condition in which the stomach contents (most characteristically acid) moves backwards from the stomach into the esophagus

135
Q

What is the aetiology of GERD?

A

transient relaxation of LES, Low basal LES tone, Acid hyper secretion: Zollinger Ellison syndrome (gastrin secreting tumour)

136
Q

What investigations do you do with GERD?

A

pharmacotherapy, gastroscopy, 24h pH monitoring

Module 203 (4 decks)

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