Diseases Of Infancy & Childhood

DISEASE OF INFANCY & CHILDHOOD Bernadette R. Espiritu, M.D. FPSP. Anatomic & Clinical Pathologist

Neonatal age – 1st 4 weeks Infancy – 1st year Early childhood – 1-4 years Late Childhood – 5-14 years

An unborn child or POC with child parts in the 1st 8 wks after conception EMBRYO

unborn child / POC with child-parts not just placenta, 8 wks after conception to birth ("all-the-way-out with a beating heart”) FETUS

1st 4 weeks of life birth Most hazardous vulnerable period Transition from IUlife Circulation Resp function take over Maintenance of body temp NEONATE

PRE-TERM Born < 37-38 weeks Vital organs are premature

POST-TERM Prolonged pregnancy, Post-dates, Post-maturity pregnancy that lasts > 42 weeks (294 days from the 1st day of LMP) 7 % of all babies - born at 42 wks or later

POST-TERM RISK FOR MOTHERS Longer labors & operative delivery (forceps or vacuum-assisted birth) Vaginal trauma - large baby C/S delivery infection & wound complications & postpartum hge

RISKS OF FETUS & NB: POST-TERM Placenta begins to age Amniotic fluid vol decrease Large baby Meconium aspiration Hypoglycemia

INFANT MORTALITY ,[object Object],10x more in the1st wk of life than in the 2nd wk Born< 34thwk with Wt 1-1500 g : 50%M 90%m Born > 34th wk with Wt of 1-1500 g: 13%M 86%m

CAUSES OF DEATHS 1ST 12 MONTHS: Immaturity RDS Birth trauma, Birth asphyxia Congenital anomalies Complications of Pregnancy Bacterial sepsis, Pneumonia, Meningitis CNS disease Accidents

1st - 4th & 5th -14th y/o ,[object Object], cause of death Natural Diseases: ,[object Object]

LOW BIRTH WEIGHT: “SGA" and "preterm". ,[object Object], <2500 gm ,[object Object], <1500 gm ,[object Object], <1000 gm

SGA: not grow properly in the uterus organs will have problems

SGA CAUSES: 1) FETAL: - reduce growth despite adeq nutrient from mother a. chromosomal disorder b. congenital anomalies c. congenital infections

2) PLACENTAL - 3rd trimester - Uteroplacental insufficiency a. infections b. tumors c. vascular lesions : infarctions

3) MATERNAL - Under nutrition - Narcotic abuse - Alcohol intake - Cigarette smoking - Vascular disease: a. Toxemia b. Chronic c. Hypertension

IMMATURITY OF ORGANS LUNGS - 7th month – alveoli begin to differentiate - epithelial lining-cuboidal not suited in effecting transfer of O2 to blood

...Lungs 26th -32nd wks AOG – cuboidal epith > flat type I alveolar epithelial cells & type II cells that contain lamellar bodies

TYPE I - flattened plate-like pavement covers 95% (membranous) of the alveolar surface TYPE II : rounded or granular which exhibits surface microvilli & contains osmiophilic lamellar bodies

…Type II a. source of pulmonary surfactant b. involved in the repair of the alveolar epithelium after destruction of Type I cells

PULMONARY SURFACTANT : “lecithin”phosphatidylcholine contained in a thin film of phospholipid in the glycoprotein–containing cell coat adjacent to the alveolar cell membrane

SURFACTANT: IMPORTANCE 1) lowers the surf tension of the alveolar lining & maintain the stability of the alveoli 2) synthesized in type II epithelial cells & stored in the osmiophilic lamellar bodies

3) inadequate surfactant activity play a role in RDS of infants & adults

IMMATURE LUNGS: - Unexpanded - red & meaty - alveolar spaces incompletely expanded - contain pink proteinaceous ppt & some squamous cells

PRENATAL RESPIRATORY DISTRESS - large amount of amniotic debris, squames, lanugo hair & mucus

Hyaline membrane dis- Dilatation of the alveolar spaces- Many air spaces- lined by thick hyaline membranes

IMMATURE KIDNEY ,[object Object], incomplete ,[object Object], subcapsular zone ,[object Object], well-formed ,[object Object], 34th wk AOG

Kidneys of FTneonate (37 - 41 wks AOG): full set of nephrons: 850 - 1,200,000 / k

EVENTS: PREGNANCY 1. growth retardation 2. nephrotoxic drugs adm to mothers

BRAIN - Incomplete dev - Surface smooth - delineation of white & gray matter: ill-def ,[object Object], of nerve fiber

BRAIN Vital brain centrs sufficiently dev Homeostasis not perfect Poor vasomotor control Irreg resp Feeble sweating

LIVER Inc size persist EM hematopoiesis Def - bil glucoronyl transferase Def - hydroxylating enzymes Dec- CHON synthetic capacity

APGAR SCORE METHOD: evaluating physiologic condition & responsiveness of NB > chance of survival Evaluation at 1 min or at 5 min 10 – best condition

…APGAR SCORE 0-1 = 50% Mm in 1st mo. 4 = 20% M in 1st mo. 7 or > = 0% M in 1st mo.

BIRTH INJURIES INTRACRANIAL HGE - most common - hge may arise from tears in the dura or rupture of vessels that traverse the brain - subs of the brain may be torn or bruised leading to intraventricular hge into the brain substance

EFFECTS OF INTRACRANIAL HGE Sudden increase in ICP Damage to the brain subs Herniation of medulla into the foramen magnum Serious fatal depression of function of vital medullary centers

CAPUT SUCCEDANEUM: Edema of the scalp head pressed- the cervix prolonged or difficult delivery after ROM - amniotic sac no longer provides protective cushion for baby's head

progressive accumulation - interstitial fluid in the soft tissues of the skull: circ area of edema congestion & swelling assc with PROM or oligohydramnios

SYMPTOMS … CAPUT Soft puffy swelling of scalp Swelling may or may not have discoloration Swelling may extend over the midline of the scalp Seen- head presented 1st Assoc w/ inc molding-head

PROGNOSIS Complete recovery expected Scalp regain normal contour COMPLICATIONS Jaundice - as the bruise breaks down into bilirubin

CEPHALHEMATOMA: Hge under the scalp ("subgaleal hematoma”) No known risks Dark red blood under galea aponeurotica over the cranium fairly common during birth

25%Cephalhematoma ,[object Object],CAUSES: Skull fractures ,[object Object]

Prolonged labor with disproportion between the size of fetal head and birth canal,[object Object]

CONGENITAL MALFORMATIONS Present at birth 3%NBmajor malformation MALFORMATION – intrinsic abnormalities occurring during the developmental process

…Malformation Single body system congenital heart defects anencephaly Multiple body system

CAUSES: Malformation ,[object Object]

deletions of chunks of a chromosome polygenic problems ,[object Object],[object Object]

…Deformation CAUSE: ,[object Object], - fetus grows > the uterus w/ relative dec of the amniotic fluid

Deformation from constraint with oligo-hydramnios in utero(varus deformity) The feet are turned inward CLUB FEET

Maternal Factors: ,[object Object]

LeiomyomasFetal or Placental Factors: ,[object Object]

Abn fetal presentation,[object Object]

Cause: extrinsic or intrinsic factors- vascular insults - Ex: amniotic bands

SEQUENCE: pattern of cascade anom(unrelated) classic exam: POTTER OLIGOHYDRAMNIOS SEQUENCE squashed ("Potter's") face and badly bent limbs

CAUSES: Oligohydramnios Chronic leakage of amn fluid bec of ROM 2. Uteroplacental insuff resulting fr maternal HPN or toxemia of pregnancy 3. Renal agenesis – fetal urine impt constituent of amniotic fluid

Oligo-H SEQUENCE ANENCEPHALY aniridia / WT-1 complex “AGA“ BRACHYDACTYLY (short fingers / toes) BRONCHIECTASIS

ANENCEPHALY Failure of formation of fetal cranial vault Brain not form properly when exposed to amn fluid IUFD-signs of maceration, w/ skin slippage & reddening

absence of cranial vault - anencephaly

EYESappear proptotic with anencephaly - the lack of the skull EAR-low set

NEURAL TUBE DEFECT CAUSE: improper embryonic neural tube closure Most minimal defect: SPINA BIFIDA - with failure of vertebral body to completely form, but the defect is not open

Spina bifida - serious birth abn where the spinal cord is malformed & lacks its usual protective skeletal and soft tissue coverings May appear in the body midline anywhere from the neck to the buttocks

Most severe form- spinalrachischisis: entire spinal canal is open, exposing the spinal cord & nerves More commonly, appears as localized mass - back covered by skin or by the meninges, the three-layered membrane that envelopes the spina cord

Spina bifida - readily apparent at birth because of the malformation of the back and PARALYSIS below the level of the abnormality

FORMS OF SPINA BIFIDA meningomyelocele myelomeningocele spina bifida aperta open spina bifida myelodysplasia spinal dysraphism spinal rachischisis myelocele meningocele

MENINGOCOELE – the spine malform contains only protective covering (meninges) of spinal cord SPINA BIFIDA OCCULTA: one or more of the bony bodies in spine are incompletely hardened, but there is no abn of the spinal cord

CAUSES & SYMPTOMS Spina bifida An isolated abn in the company of other Malform As an isolated abn it is caused by the combination of : genetic factors environ influences

The specific genes & environ influences - not completely known An insuff of Folic Acid Mutations in genes involving metab of folic acid are believed to be signf genetic risk factors

3-5%- Recurrence risk after the birth of infant with isolated spina bifida Specific environ insults : Maternal DM Prenatal exposure to certain anti- convulsant drugs

75% of abn -in the lower back (lumbar) region Rarely- the spinal cord malform occur internally: with connection to the GIT

COMPLICATIONS: Nerves BELOW the level of the abnorm dev in a faulty manner & fail to function= paralysis & loss of sensation: lumbar bowel and bladder: have inadeq nerve connections=inability to control bowel and bladder function

HYDROCEPHALY accum of excess fluid in the four cavities of the brain - At least 1: 7 cases dev ChiariII malform- the lower part of the brain is crowded & forced into the upper part of the spinal cavity

PRENATALDIAGNOSIS UTZ after 12-14 wks AOG Testing mother's blood – level of alpha-fetoprotein at 16 wks AOG - If the spine malform is not skin covered, AFP from the fetus' circ leak to the surrounding amn fluid small portion of which is absorbed in mother‘s bld

DIAGNOSIS: P.E. Paralysis below the level of the abn + fluid on brain (hydrocephaly) Spine abn: cong scoliosis & kyphosis or soft tissue tumors overlying the spine are NOT likely to have these accompanying findings

TREATMENT Surgical & Medical mgt improved the survival & function of infants with spina bifida Initial surgery – 1st days of life, provide protection against injury & infection

Subseq surgery - necess to protect vs excessive curvature of the spine, & with hydrocephaly- place a mechanical shunt to decr the pressure & amt of CSF in the cavities of the brain

Weakness or paralysis below the level of the spine abn - children will require PT bracing & ortho assist to enable them to walk Periodic UB catheter, surgical diversion of urine, and antibiotics - used to protect urinary function

INIENCEPHALYSlight variation of neural tube defect Lack of proper formation of occ bones with short neck & defect of the upper cord Head tilted back

Fetus from a termination of pregnancy via D&C done in the 2nd trimester Note the large neural tube defect in the lower back

ENCEPHALOCELE protruding from the back of the head: merges with the scalp extends down to partially cover a RACHISCHISIS on the back retroflexed head: fr INIENCEPHALY

EXENCEPHALY Cranial vault -not completely present, but brain is present since it was not entirely exposed to amn fluid Very rare Part of craniofacial clefts ass with limb-body wall complex, from Early amnion disruption

RACHISCHISIS in a fetus that also has INIENCEPHALY

Open Neural Tube defects with no skin covering: MENINGOCELE-meninges protrude through the defect MENINGOMYELOCELE- the defect allows meninges and a portion of spinal cord to protrude through the defect Diagnosis: Inc maternal serum alpha-fetoprotein (MSAFP)

MENINGOCOELE ,[object Object],dev NORMALLY but the meninges protrude from a spinal opening ,[object Object],[object Object]

FOLATESUPPLEMENT prior to and during pregnancy reduces the incidence of neural tube defects

SYNDROME: constellation of cong anom that are pathologically related caused by a single etio agent that simultaneously affect different tissues - viral - chromabn

DISEASE: when the underlying cause of the condition becomes known

AGENESIS – complete absence of an organ & its assoc primordium APLASIA – absence due failure of developmental anlage to develop HYPOPLASIA – incompdevt of an organ w/ decr number of cells

ATRESIA: absence opening of hollow visceral organ COLONIC ATRESIA w/ add’nalanom: Persist cloaca: failure of urogenseptum to form R & L testis cryptorchid & absence of penis

HYERPLASIA: overdevt of organ with increase in number of cells HYPERTROPHY: increase in size HYPOTROPHY: decrease in size DYSPLASIA: abnormal organization of cells

CAUSES: MALFORMATION GENETIC - Chromosomal aberration - Mendelian inheritance ENVIRONMENTAL - Maternal/placental infections - Maternal disease states - Drugs & chemicals MULTIFACTORIAL UKNOWN

GENETIC CAUSES "ROCKER BOTTOM" foot with a prominent calcaneus and rounded bottom Chromabn: TRISOMY 18

50% - occur with DOWN SYNDROME UTZ - "double bubble" sign from duodenal enlargement proximal to the atresia Duodenal atresia

MENDELIAN INHERITANCE polydactyly extra fingers/toes syndactyly fused fingers 3rd & 4th fingers fused to 1 large digit; seen w/ triploidy (69 chromosomes)

ARTHROGRYPHOSIS("joint claws") congenital situation with muscle contractures present at birth relatively common non-progressive symptom that can result fr uterine constraint, CNS disease, or failure of certain muscles to develop

Such a stiff fetus freq sustains fractures before or during delivery NB w/ fractured rthumerus

HEMOLYTIC DISEASE OF THE NEWBORN

ERYTHROBLASTOSIS FETALIS Ab from Rh (-) mother enter the blood stream of her unborn Rh (+) infant damaging the RBCs Infant responds by inc RBC prod & sending out immature RBCs that still have nuclei

Normal RBCs, damaged RBCs, & immature RBCs that still contain nuclei

Anemia - dev in unborn infant when maternal Abs attack the RBC of the fetus An IU BT may be indicated

The immune system recognizes Ag & produces Ab that destroy substances containing Ag

HYDROPS FETALIS hydrops, fetal hydrops, universal edema of the NB 1st described by Ballantyne in 1892 serious condition - abn fluid accum in 2 or > fetal compartments: ascites, pleural effusion, pericardial effusion & skin edema

May be assoc with polyhydramnios & placental edema Cause: Rhesus (Rh) blood group iso-immunization of the fetus

Epidemiology 1 : 600 to 1 : 4Kpregnancies Varies accdg to population risk of the conditions known Ex: Thailand - expected freq hydrops fr homozygous α-thalassemia or Bart hydrops is: 1 : 500–1:1,500pregnancies

ETIOLOGY Hematological causes Iso-immunization hemolytic disease of NB Erythroblastosis fetalis Rhesus, Kell, ABO and Duffy incompatibility

Other HEMOLYTIC disorders: Glucose-6-phosphatase Dehydrogenase Def(G6PD) Glucose Phosphateisomerase (GPI) deficiency Pyruvate kinase (PK) Def

ETIO: RBC PRODUCTION Disorders Congenital dys-erythropoietic anemia Diamond-Blackfan syndrome Lethal hereditary spherocytosis Congenital erythropieticporphyria(Günther's disease) α-thalassemia (Bart's hemoglobinopathy)

ETIO: Fetal HEMORRHAGE intracranial or intraventricular hge hepatic laceration subcapsular hepatic laceration feto-maternal hemorrhage twin-to-twin transfusion

ETIO: CARDIAC causes Abnormalities of Lt Vent outflow Aortic valvularstenosis or atresia Coarctation of the aorta Truncus arteriosus Hypoplastic left heart Endocardialfibroelastosis

ETIO: Abn of Rt Vent outflow Pulmonary ValvularAtresia or insufficiency Ebstein's anomaly AV-Malforamation ,[object Object],[object Object]

…ETIO: Congenital heart block - 66-75% in pregnancies complicated by maternal collagen disease Prenatal closure of the foramen ovale or ductus arteriosus Myocarditis Idiopathic arterial calcification Hypercalcemia

ETIO: INFECTIVE causes Parvovirus B19-slapped cheek syndrome PCR testing demonstrated that 20% fetal hydrops is assoc with: CMV SY HERPES SIMPLEX

…INFECTIVE Causes Toxoplasmosis Hepatitis B Adenovirus Coxsackie virus type B Listeriamonocytogenes Ureaplasmaurealyticum

ETIO: METABOLICand other causes -inborn errors of metabolism Glycogen-storage disease type IV Lysosomal storage dis Hypothyroidism Hyperthyroidism

ETIO: CHROMOSOMAL SYNDROMES: Trisomies 10,13,15,18 Trisomy 21(Down's syndrome) Turner's syndrome (45, X) other autosomal recessive genetic disorders

ETIO: Tumours Sacrococcygeal Teratoma

PROGNOSIS Spontaneous remission: CAUSES: Cardiac arrhythmias Twin-to-twin transfx syndrome Cystic hygroma Parvovirus & CMV infections Idiopathic ascites or pleural effusions

HYPOSPADIAS Urinary tract opening or urethral meatus opens the underside of the penis or on the perineum

ETIOLOGY Abnormal Devt of penis Various problems w/ male hormone action Genetic

DIAGNOSIS: P.E. - urethral opening in a wrong position combined with other symptoms : Foreskin incompletely dev resulting in a dorsal hood (tip of the penis exposed) penis curvature (chordee) undescended tested

Untreated HYPOSPADIAS Abn direction of urine flow Abn appearance of penis Infertility Inability of sexual intercourse

Treatment SURGERY - create a normal straight penis with a urinary channel - tip of the head

If the opening is proximal, treatment with ♂hormone TESTOSTERONE prior to surgery recommended Hypospadias located within or near the scrotum should have a voiding cystogram to R/O add’l urinary tract anomalies

Recommended age of surg repair: between 4-12 mo. - size of the penis - slow rate of growth of the penis Children should not be circumcised: foreskin is essential in repair surgery

Very few children experience post-op complications: wound infections unexpected opening near the repair site

HYDROCEPHALUS ,[object Object],the cranium > vent to dilate ,[object Object],early adulthood ,[object Object], brain tumors, infection, trauma, or devt’lanom

PRIMARY ROUTES: Trans-cervically – Ascending - Herpes Simplex II - inhalation of amniotic fluid pneumonia sepsis most common sequelae meningitis

2. TRANSPLACENTALLY – Hematologic via the chorionic villi PARASITIC VIRAL HIV Parvovirus B19 – 5th disease BACTERIA Listeria Treponema TORCH INFECTIONS

CONGENITAL SYPHILLIS Early evidence: osteochondritisof femur & tibia early evidence of infection: bullae and vesicular rash

Later evidence saber shins later evidence saddle nose Later evidence - Hutchinson's teeth

PRIMARY SY SECONDARY SY TERTIARY SY TERTIARY SY – trophic degeneration

CONGENITAL SYPHILIS granulomatous process : "gumma“ Gumma- located in the heart of a fetus Syphilis acquired IU in the 3rd trimester.

Spirochetes - T. pallidum, the causative agent

CONGENITAL RUBELLA SYNDROME Rubellacause: Togavirus genus Rubivirus Child: Few/no symptoms Adults:1-5 day prodrome LG fever, headache, malaise, coryza, & conjunctivitis Arthralgia/arthritis: 70%adult ♀

1st trim- CRS can cause Abortions Miscarriages Stillbirths Severe birth defects

The most common CRS Congenital defects are: Cataracts Heart disease Sensorineural deafness Mental retardation

HERPES VIRUS HSV-type 1: oral herpes fever blisters: mouth/ face HSV-type2: Genital Herpes

Both viral types can: Inactive/'silent‘: no symptom cause 'outbreaks' of blisters and ulcers People can remain infected for life after the 1st episode

TRANSMISSION: Direct contact ,[object Object]

Skin-to-skin contact,[object Object]

HSV-2 Mild to no symptoms Recurrent painful genital ulcers Severe with suppressed immune systems

Severe genital herpes - psychological & emotional stress Pregnants- fatal infections in infants C/S delivery - with active genital herpes

EARLY SYMPTOMS : ,[object Object]

painful urination,[object Object]

CYTOMEGALOVIRUS Cause: DNA, ether sensitive virus of the herpes family Occurs worldwide Transmission: HUMAN CONTACT – harbors infection for mos. or yrs. About 4 / 5 people > 35 y/o - been infected with CMV in childhood or early adulthood Most cases - mild

CMV – pregnancy hazardous to the fetus: brain damage neonatal illness other birth defects stillbirth CMVfound in: Blood / breast milk / cervical secretions Feces / saliva / semen / urine/ vaginal secretions

RISK GROUPS : Immunodeficient patients AIDS patients Who received transplanted organs those receiving immunosuppressives - dev pneumonia / other secondary infections Recipients of BT from donors with + CMV Abs

CMV - spread through the body in lymphocytes or monos to the lungs, liver, and CNS where it produces inflammatory reactions self-limiting

Tubular epithelium of fetal kidney - many large violet INCs Inclusions may appear in the urine

NEONATAL RESPIRATORY DISTRESS SYNDROME Cause: inadeq prod surfactant Surfactant - prod by type II pneumocytes with property of decreasing surface tension Alveolar surfactant - prod after 30 wks AOG

Inadeqsurfactant - causes air sacs to collapse on expiration & greatly increasethe energy req for breathing Interstitial edema makes the lung even less compliant – leads to O2 & retention of CO2

The immature lungs: cannot retain air the air spaces empty completely and collapse after the 1st exhalation Plasma leaks out of the lung tissue and coats the air spaces with a pink coating that is glassy or hyaline in appearance

RISK FACTORS Premature delivery C/S without maternal labor Male infants Hypothermia Perinatal asphyxia Maternal DM Multiple pregnancy Family history of RDS

PRESENTATION preterm delivery - with RD: tachypnea & expiratory grunting subcostal and intercostal retractions diminished breath sounds cyanosis nasal flaring & fatigue apnea and hypoxia

SUDDEN INFANT DEATH SYNDROME SIDS is the unexpected, sudden death of a child under age 1 in which an autopsy does not show an explainable cause of death.

Causes Unknown Problems w/ sleep arousal Inability to sense a build-up of CO2 in the blood

occur w/o any warning or symptoms when the infant sleeping SIDS is most likely to occur betwn 2 - 4 mos & 90% occur by 6 mos occurs more often wet months, with the peak in January

Factors: risk of SIDS Babies who sleep on their stomachs Babies who are around cigarette smoke while in the womb or after being born

Babies who sleep in the same bed as their parents Babies who have soft bedding in the crib Multiple birth babies (being a twin, triplet, etc.) Premature babies

Babies who have a brother or sister who had SIDS Mothers who smoke or use illegal drugs Teen mothers Short time period between pregnancies Late or no prenatal care Situations of poverty

Symptoms no symptoms Babies who die of SIDS do not appear to suffer or struggle Exams and Tests Autopsy - not able to confirm a cause of death

Beneath the skin surface are many dilated vascular channels filled with many red blood cells

LYMPHANGIOMA There is a large mass involving the left upper arm and left chest of this fetus.

Large lymphatic spaces lined by a thin endothelium Adjacent stroma w/ lymphoid nodules Tend to involve head, neck, & chest

Enlarged lymphatic spaces lined by a thin endothelium – HPO Poorly circumscribed & extend widely to surrounding soft tissues surgical removal difficult

FIBROMATOSIS Fibromatoses: Rare soft tissue disease characterized by fibroblastic proliferation

CLASSIFICATION Fibroblastic fibromatoses DesmoidFibromatosis (desmoid tumor, aggressive fibromatosis) Fibromatosiscolli

….Classification Digital infantile fibromatosis Aponeuroticfibromatosis ,[object Object]

penile fibromatosis,[object Object]

….. Classification: Myofibroblastic fibromatoses(myofibromatoses) Infantile myofibromatosis (infantile myofibroma)

According to the LOCALIZATION Superficial Deep

A 45 days old female infant was brought to the hospital with swelling in the right thigh Noticed swelling - 11 days old, No hx fever, pain / birth trauma, Swelling diffuse from lower end of femur > mid shaft, Margins indistinct but well defined on palpation, Temp normal, No tenderness, Shape fusiform, firm hard in consistency, Non-mobile, overlying skin & surr muscles - free

LNs in drainage area - not palpable, Distal neuro-vascular status - N° x-ray 11 days old did not show any abnormality

On the 45th day of life, - a circumferential overgrowth of radio opaque tissue which covered the normal bone like a shell. Cortices of underlying bone were intact FNAC and Tissue Biopsy - CMF suggestive of fibromatosis

TERATOMA Large nasopharyngeal teratoma that is protruding from the oral cavity

Benign 3 embryologic germ layers : Skin (ECTODERM) Cartilage (MESODERM) Colonic gland (ENDODERM)

CYSTIC FIBROSIS : PANCREAS Ducts - dilated &plugged w/ eosinophilic mucus Acini of exocrine glands - atrophic & replaced by fibrous tissue

Diseases Of Infancy & Childhood

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