short stature original
TRANSCRIPT
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Short Stature
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Definition
Height is >2.5 SD below the mean for age
Height is >2.5 SD below the mean for
that expected based on mid-parental. or:
Height velocity less than 3rdpercentile for
age or less than 4 cm/year at any time
between 5y. and puberty.
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PROCEDURES FOR ACCURATE MEASUREMENT
accurate scale.
Lengthtwo examiners
heightFor older children
Wrong measurements:
Using paper at the foot and head of a supine infant
using a simple wall growth chart with a book or
ruler.
compare with previous, repeat if inconsistent
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Specialized charts
very low birthweight and prematurity
Down Turner
Klinefelter
achondroplasia.
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Z-Score
A Z-score is a measurement of deviation from thenorm.
Its units are standard deviations, so a Z-score of +2
means that the measurement falls two standarddeviations away from the norm.
Anything within 2 standard deviations of the norm
in most scales is fine.
z-scores are a good way to "eyeball" where a givenmeasurement falls.
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Z-Score
68% of the population will fall between +1 and -1 standarddeviation of the average score.
95% will fall between +2 and -2 standard deviations of thescore.
So - if you have a z-score you can estimate your percentilevery roughly as follows:
-3z = 0.1% percentile
-2z = 2.5nd percentile
-1 z = 15th percentile
0 z = 50th percentile
+1z = 84th percentile
+2z = 98th percentile
+3z = 99.9 percentile
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Severity of Malnutrition and Stunting
GRADE OF MALNUTRITION HEIGHT FOR AGE(STUNTING)
0, normal >95
1, mild 9095
2, moderate 8589
3, severe
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Causes of linear growth
problems congenital
constitutional familial
Endocrine
Nutritional
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In endocrine disorders
length or height declines first or at the
same time as weight;
weight for height is normal or elevated.
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In nutritional insufficiency
weight declines before length
weight for height is low (unless there has
been chronic stunting).
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Congenital
In congenital pathologic short stature:
infant is born small and
growth gradually tapers off throughoutinfancy.
Causes include chromosomalabnormalities (Turner syndrome, trisomy
21), perinatal infection (TORCH),teratogens (phenytoin, alcohol), andextreme prematurity.
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constitutional growth delay
1. Slow linear growth during the first three years
2. Normal (but short) growth velocity during pre-
pubertal years
3. Delayed bone age and sexual maturation
4. Normal adult height (but may be below target)
Often family history of late bloomers
Bone age corresponds to height age
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Familial
In familial short stature:
both the infant and the parents are small
growth runs parallel to and just below the
normal curves.1. Similar growth pattern to constitutional delay.
2. Usually have normal birth weights since nutritionand uterine environment determine birth weight
3. Normal onset of puberty4. Bone age c/w chronologic age
5. Final height is short, but appropriate for parentalheight
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Height-for-age curves of the four general causes of proportional
short stature:postnatal onset pathologic short stature, constitutional
growth delay, familial short stature, andprenatal onset short stature.
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OTHER INDICES OF GROWTH
Body proportions follow a predictable sequence ofchanges with development .
The head and trunk are relatively large at birth, with
progressive lengthening of the limbs throughoutdevelopment, particularly during puberty.
The lower body segmentis defined as the lengthfrom the symphysis pubis to the floor, and the upperbody segmentis the height minus the lower bodysegment.
The ratio of upper body segment divided by lowerbody segment (U/L ratio) equals approximately 1.7 atbirth, 1.3 at 3 yr of age, and 1.0 after 7 yr of age.
Higher U/L ratios are characteristic of short-limbdwarfism or bone disorders, such as rickets.
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SKELETAL MATURATION.
In familial short stature, the bone age is
normal (comparable to chronological
age).
In constitutional delay, endocrinologic
short stature, and undernutrition, the
bone age is low and comparable to the
height age.
Skeletal maturation is linked more
closely to sexual maturity rating than to
chronological age.
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Causes of Short Stature
Genetic IS NICE
I= Idiopathic: constitutional= IUGR
S=Skeletal: dysplasia, osteogenesis imperfecta
=Spinal defects: scoliosis, kyphosis.
N=Nutritional: including malabsorption I = Iatrogenic: steroids, radiation
C = Chronic disease: CHD, CRF, CF, IBD
= Chromosomal: Turner, Down, Seckel syndrome
E=Endocrine: GH def., CAH, hypopituitarism, IDDM
pseudohypoparathyroidism.
G = Genetic.
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Short stature
observation and examination1. INTRODUCE SELF
2. GENERAL INSPECTION
Position patient: standing,
fully undressed
Diagnostic facies
Disproportionate stature .
Tanner staging
Nutritional status
Skeletal anomalies
Colour
Tachypnoea
Skin.
Short stat re
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Short stature
observation and examination3. MEASUREMENTS AND
MANOEUVRESSee separate diagram
4. UPPER LIMBS Structure fingertipsNails
Palms
Pulse
JointsBlood pressure
. 5. HEAD AND NECK Head
Hair
Eyes (full examination) Nose
Mouth and chin
EarsHairtine
Neck (thyroid)
6. CHEST Tanner staging Chestdeformity Precordium Lung fields
7. ABDOMEN
Full abdominal examination
8. GENITALIA
Tanner staging
Anomalies
9. GAIT, BACK AND LOWER LIMBS
Inspect lower limbs
Gait (fun examination)
Back
Lower limbs neurologically
10. OTHER
Urinalysis Stool analysis
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History
Maternal pregnancy
Birth history
Growth history
Family history
Dietary history
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Differential
Variants of Normal
Familial short stature
Constitutional delay
idiopathic Pathologic/Growth Failure
Hormonal
Genetic Systemic
Psychologic
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Familial Short Stature
NL history and PE
Birth weight and
length below 3rd
percentile for GA Family history of short
stature
Growth curve thatparallels 3rdpercentile
nL onset of puberty
Bone age appropriate
for chronological age
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Familial Short Stature
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IUGR
20% of short people had IUGR
Small for gestational age at birth
Slow growth from early infancy
Normal bone age Normal sexual development
Normal PE and lab tests
Normal GH levels
Lower intellect
Normal growth pattern in family
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Endocrine Disorders
Very uncommon causes
GH deficiency, hypothyroidism,
panhypopituitarism, glucocorticoid excess
Usually short, fat child
Start growth hormone labs
If nL, do other tests to rule out steroidexcess such as Cushings
May have delayed bone age
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Isolated GH deficiency
hard to differential from constitutional short
stature
Congenital or acquired
2 peaks for diagnosis
IGF-1 and IGFBP-3 are low
GH provocative testing for diagnosis Do MRI
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Chronic illnesses
Renal disease Nephritis, renal tubular acidosis
GI disease
Celiac disease, Crohns, Cystic Fibrosis
Cardiac disease
Pulmonary disease
HIV
Short stature is maltifactorial Decreased or normal wt/ht ratio
Delayed bone age
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Congenital Syndromes Turners
Most common congenital cause of short stature, XO karyotype Short stature 95%, web neck, low hairline, delayed puberty
Noonans Similar features to Turners, nL karyotype
Short stature 80%
Autosomal dominant genetic disorder
Males, females, 1/2500 births
Prader-Willi 1/16000
Obese, feeding problems
Short children, lack of pubertal growth spurt
Downs Special attention to Turners, can present as short stature only
Order karyotype and refer to geneticist
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Turner syndrome
Most common abnormality in earlyabortion
Female, short stature, primary
amenorrhea, sterility, spares hair andunderdeveloped breast
Neonatal: wide spaced nipple,
lymphedema , shield chest, Coarctation of the aorta
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Continue turner syndrome
Normal IQ scale with difficulty in spatial
orientation such as map
Present with short stature or delay sex
maturation
Hormonal therapy
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continue
Mosaisim (15%), remove gonads
Recurrent risk is 1-2%
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Short stature
Congenital lymphedema
Horseshoe kidney
Patella dislocation
Increased carrying angle of elbowMadelung deformity (chondrodysplasia of distal radial
epiphysis)
Congenital hip dislocation
Scoliosis
Widespread nipples
Shield chest
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Redundant nuchal skin (in utero cystic hygroma)
Low posterior hairline
Coarctation of aorta
Bicuspid aortic valve
Cardiac conduction abnormalities
Hypoplastic left heart syndrome?
Gonadal dysgenesis (infertility, primary amenorrhea)
Gonadoblastoma (if Y chromosome material present)
Learning disabilities (nonverbal perceptual motor and
visuospatial skills) [in 70%]
Developmental delay (in 10%)
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Hypothyroidism (acquired in 1530%)
Type 2 diabetes mellitus (insulin resistance)
Strabismus
Cataract
Red-green colorblindness (as in males)Recurrent otitis media
Sensorineural hearing loss
Inflammatory bowel disease
Celiac disease?
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Turners Growth Curve
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Noonan syndrom
AD, fresh mutation
Pulmonary stenosis,
short stature,
microceph,
mental retardation
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Growth parameters
Size at birth is usually within range.
Short stature in 80% of patients
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Short stature
Failure to thrive
Epicanthal folds
Ptosis
Hypertelorism
Low nasal bridge
Downward slanting palpebral fissures
Myopia
Nystagmus
Low-set auricles
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Dental malocclusion
Low posterior hairline
Short webbed neck
Shield chest
Pectus excavatum or carinatum
Scoliosis
Cubitus valgus
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Pulmonary valve stenosis
Hypertrophic cardiomyopathy
Atrial septal defect (ASD)
Tetralogy of Fallot
Cryptorchidism
Small penis
Bleeding disorders, including thrombocytopenia
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Facial features
Triangular-shaped face Hypertelorism
Down-slanting eyes
Ptosis
Strabismus (48%) Amblyopia (33%)
Refractive errors (61%)
Low-set ears with thickened helices
High nasal bridge
Short webbed neck
Pectus carinatumor excavatum
Scoliosis
http://emedicine.medscape.com/article/1003047-overviewhttp://emedicine.medscape.com/article/1004953-overviewhttp://emedicine.medscape.com/article/1004953-overviewhttp://emedicine.medscape.com/article/1003047-overview -
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Prader-willi syndrome
(A fat red faced boy in state ofsomnolency) Charles Diickens
Early hypotonia
Obesity Short stature as adult
Almond shaped blue eyes
Mental retardation (mild tomoderate)
Narrow hands
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Clinical features and signs
PWS affects approximately 1 in 10,000 to
1 in 25,000 newborns
In utero:
Reduced fetal movement
Frequent abnormal fetal position
Occasional polyhydramnios
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At birth
Often breechor C/S
Lethargy
Hypotonia
Feeding difficulties (due to poor muscletone affecting sucking reflex)
Difficulties establishing respiration Hypogonadism
http://en.wikipedia.org/wiki/Breech_birthhttp://en.wikipedia.org/wiki/Lethargyhttp://en.wikipedia.org/wiki/Hypotoniahttp://en.wikipedia.org/wiki/Sucking_reflexhttp://en.wikipedia.org/wiki/Hypogonadismhttp://en.wikipedia.org/wiki/Hypogonadismhttp://en.wikipedia.org/wiki/Sucking_reflexhttp://en.wikipedia.org/wiki/Hypotoniahttp://en.wikipedia.org/wiki/Lethargyhttp://en.wikipedia.org/wiki/Breech_birth -
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Infancy
Failure to thrive(continued feeding
difficulties)
Delayed milestones/intellectual delay
Excessive sleeping
Strabismus Scoliosis(often not detected at birth)
http://en.wikipedia.org/wiki/Failure_to_thrivehttp://en.wikipedia.org/wiki/Hypersomniahttp://en.wikipedia.org/wiki/Strabismushttp://en.wikipedia.org/wiki/Scoliosishttp://en.wikipedia.org/wiki/Scoliosishttp://en.wikipedia.org/wiki/Strabismushttp://en.wikipedia.org/wiki/Hypersomniahttp://en.wikipedia.org/wiki/Failure_to_thrive -
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Childhood
Speech delay
Poor physical coordination
Hyperphagia (over-eating) from age 28 years.Note change from feeding difficulties in infancy
Excessive weight gain
Sleep disorders Scoliosis
Adolescence &
http://en.wikipedia.org/wiki/Speech_delayhttp://en.wikipedia.org/w/index.php?title=Excessive_weight_gain&action=edit&redlink=1http://en.wikipedia.org/wiki/Sleep_disordershttp://en.wikipedia.org/wiki/Scoliosishttp://en.wikipedia.org/wiki/Scoliosishttp://en.wikipedia.org/wiki/Sleep_disordershttp://en.wikipedia.org/w/index.php?title=Excessive_weight_gain&action=edit&redlink=1http://en.wikipedia.org/wiki/Speech_delay -
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Adolescence &
Adulthood
Delayed puberty
Short stature
Obesity
Infertility (males and females) Hypogonadism
Sparse pubic hair
Hypotonia
Learning disabilities/borderline intellectualfunctioning
Prone to diabetes mellitus
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Neuro-cognitive
5%: IQabove 85 (average to low average
intelligence)
27%: IQ 7085 (borderline intellectual
functioning) 39%: IQ 5070 (mild intellectual disability)
27%: IQ 3550 (moderate intellectual disability)
1%: IQ 2035 (severe intellectual disability)
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Treatment
Prader-Willi syndrome has no cure,
During infancy, manage feeding problems. Speech and occupational therapy.
During the school years, children benefit from a highlystructured learning environment.
Treat severe obesity. Prescription of daily recombinant growth hormone.
GH supports linear growth and increased muscle mass,and may lessen food preoccupation and weight gain
Because of severe obesity, obstructive sleep apnea is acommon sequela, and a positive airway pressuremachine is often needed.
http://en.wikipedia.org/wiki/Growth_hormonehttp://en.wikipedia.org/wiki/Positive_airway_pressurehttp://en.wikipedia.org/wiki/Positive_airway_pressurehttp://en.wikipedia.org/wiki/Growth_hormone -
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Angelman syndrome
Sever mental retardation
Inappropriate laughter
Decrease pigmentation of choroid
or iris (pale blue eyes)
Ataxia and jerky eye movement
Sever speech problem
Deletion of b15q11q13, maternalin origin
Paternal uniparental disomy
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Malnourisment
Starvation, nutritional deficiency, DM type
1, anorexia, malabsorption
Decreased wt/ht ratio
Decreased linear growth and sexual
development, preceded by decreased wt
Adequate nutrition catch up growth
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Malnourishment Curve
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Psychosocial
Truly neglected children, psychosocial
dwarfism
GH deficiency-like picture
Abnormal response to provocative testing
normal growth after removed from
environment
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Idiopathic
normal history, normal physical and labs
Controversy on treatment
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GROWTH HORMONE
DEFICIENCY
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Etiology and Epidemiology
Classic: 1 in 4000 to 10,000 children.
hypothalamicdisease:inadequate GRF.
anatomic defects of the pituitarygland.
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Causes of Growth hormone deficiency
CNS malformations (midline defects)
Hydrocephalus
CNS injuries (birth, forceps)
Meningitis, brain edema
Congenital infections
Hypothalamic or hypophyseal tumors
Cranial radiationCongenital, genetic
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Clinical Manifestations
In congenital GH deficiency:
growth rate slowsafter birth, noticedafter age 2 to 3 years.
elevated weight-to-height ratioandappear chubby and short.
Careful measurements in the first yearof life may suggest the diagnosis.
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high-pitched voice.
normal intellectual growth
Male neonates may have a microphallusfasting hypoglycemia.
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GHR Deficiency/Receptor
(Laron Syndrome)
High GH, low IGF-1
Short stature
Hypoglycemia Poor muscle development
Obesity
Osteoporosis
Can be treated with IGF-1 to correct
growth, and certain metabolic changes
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Diagnosis
GH should be tested for children who are:
1. short(3.5 SDsbelow the mean),
2. growing poorly(
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g
secretionPhysiological tests:
One random sample
Physical activity
Continuous overnight sampling
Continuous 24 hours sampling
Stimulation tests (always two tests):
Insulin iv (hypoglycemia)
Arginine iv
Glucagone iv or imClonidine (oral)
GHRH
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1. GH(useless as a randomdetermination except in GH resistanceor in pituitary gigantism
2. Arginine(a weak stimulus)
3. l-Dopa(Useful clinically)
4. Insulin-induced hypoglycemia(a dangerous but accurate test(
5. Clonidine(useful clinically)
6. IGF1 (affected by malnutrition andGH deficiency)
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Indications for Growth hormone treatment
Main indication:
Growth Hormone Deficiency
Other indications:Turner Syndrome
Renal failure
Prader-Willi Syndrome
Small for gestagional age without catch-upgrowth ?
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The recommended dose of hGH is
0.18
0.3mg/kg/wk SC in 6 or 7 divideddoses during childhood.
Higher doseshave been used duringpuberty.
Maximalresponseto GH occurs in the1styearof treatment.
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It should be continued until near final
heightis achieved.
Criteria for stopping treatment;
- becomes tall enough- bone age >14 yr in girls and >16 yr in
boys.
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COMPLICATIONS AND ADVERSE EFFECTS
OF hGH TREATMENT
1. Leukemia.
2. Pseudotumor cerebri,
3. Slipped capital femoral epiphysis, Gynecomastia,
4. Worsening of scoliosis.
5. Increase in total body water
6. It may increase the risk of type 2 diabetes.
7. In the extracted pituitary GH treatment era,patients were at risk for Creutzfeldt-Jakob(CK)
disease8. Hypothyroidism
adrenal insufficiency.
G th h th
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Growth hormone therapy
Available only as injection
Subcutaneous
Administer after 8.00 pm
3 to 7 times a week
0.15 to 0.3 mg/kg/week
Effect is dose-dependent
G th h th
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Growth hormone therapy
Effect reduces with time; esp after 3 years
?Formation of antibodies
?Hypothyroidism
Side effects more common in adults
G th h th
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Growth hormone therapy
Response better ifstarted earlier
Average increment =
10 cm/year Better response in
classic GHD
Higher dose needed
in Turner syndrome
1 D fi iti f h t t t
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1. Definition of short stature:
A. Height is >2.5 SD below the mean forage
B. Height is >2.5 SD below the mean for
that expected based on mid-parental
C. Height velocity less than 3rd
percentile for age
D. All are correct
E. A+B only are correct.
1 D fi iti f h t t t
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1. Definition of short stature:
A. Height is >2.5 SD below the mean forage
B. Height is >2.5 SD below the mean for
that expected based on mid-parental
C. Height velocity less than 3rd
percentile for age
D. All are correct
E. A+B only are correct.
2. All are correct for Z-Score
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2. All are correct for Z Score
Except:
A. 68% of the population will fall between+1 and -1 standard deviation of the
average score.
B. 95% will fall between +2 and -2standard deviations of the score.
C. -3z = 0.1% percentile
D. -2z = 5th percentile
E. +1z = 84th percentile
2. All are correct for Z-Score
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Except:
A. 68% of the population will fall between+1 and -1 standard deviation of the
average score.
B. 95% will fall between +2 and -2standard deviations of the score.
C. -3z = 0.1% percentile
D. -2z = 5th percentile
E. +1z = 84th percentile
3. The following is incorrect for
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g
causes of short stature
A. In endocrine causes weight for heightis normal or elevated
B. In nutritional insufficiency weight for
height is lowC. In constitutional there is normal linear
growth during the first 3 years.
D. In congenital growth gradually tapersoff throughout infancy.
E. all of the above are incorrect.
3. The following is incorrect for
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g
causes of short stature
A. In endocrine causes weight for heightis normal or elevated
B. In nutritional insufficiency weight for
height is lowC. In constitutional there is normal linear
growth during the first 3 years.
D. In congenital growth gradually tapersoff throughout infancy.
E. all of the above are incorrect.
4. Delayed sexual maturation is a
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feature ot the following cause of
short stature:A. constitutional
B. endocrinal
C. congenital
D. familial
E. none of the above
4. Delayed sexual maturation is a
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feature ot the following cause of
short stature:A. constitutional
B. endocrinal
C. congenital
D. familial
E. none of the above
5. The following is incorrect for
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g
familial short stature:
A. similar growth pattern toconstitutional short stature
B. birth weight is usually normal..
C. normal onset of puberty.
D. delayed bone age.
E. short final height.
5. The following is incorrect for
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g
familial short stature:
A. similar growth pattern toconstitutional short stature
B. birth weight is usually normal..
C. normal onset of puberty.
D. delayed bone age.
E. short final height.
6. Bone age is delayed in thefollowing cause/s of short
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following cause/s of short
stature:
A. endocrinal
B. nutritional
C. constitutionalD. all of the above
E. A+C only
6. Bone age is delayed in thefollowing cause/s of short
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following cause/s of short
stature:
A. endocrinal
B. nutritional
C. constitutionalD. all of the above
E. A+C only
7. Limbs and trunk are short in the
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following cause of short stature:
A. achondroplasia.
B. Pseudohypoparathyroidism
C. Mucopolysaccharidosis.
D. All of the above
E. None of the above
7. Limbs and trunk are short in the
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following cause of short stature:
A. achondroplasia.
B. Pseudohypoparathyroidism
C. Mucopolysaccharidosis.
D. All of the above
E. None of the above
Stunting with obesity is found isfound in all of the following
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found in all of the following
disorders except:
A. Lourance-Moon-Biedle syndrome
B. Prader-Willi syndrome
C. HypothyroidismD. Hypochondroplasia
E. Growth hormone deficiency.
Stunting with obesity is found isfound in all of the following
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found in all of the following
disorders except:
A. Lourance-Moon-Biedle syndrome
B. Prader-Willi syndrome
C. HypothyroidismD. Hypochondroplasia
E. Growth hormone deficiency.
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8/21/2019 Short Stature Original
101/101