Danil hammoudi.md

Sinoe medical association

EMBRYOLOGY:

FETAL AND NEONATAL CIRCULATION:

THREE STRUCTURES: ***FORAMEN OVALE

***DUCTUS ARTERIOSUS

***DUCTUS VENOSUS

=CARDIOVASCULAR ANATOMY OF THE FETUS

1/ FETAL CIRCULATION:

-OXYGENATION: PLACENTA AND THEN ENTER THE UMBILICAL VEIN

-ONE PORTION OF THE O2 BLOOD PERFUSES THE LIVER AND PROCEEDS TO THE INFERIOR VENA CAVA VIA THE HEPATIC VEINS

-ANOTHER PORTION ENTERS THE DUCTUS VENOSUS, WHICH EMPTIES DIRECTLY INTO THE INFERIOR VENA CAVA.

-THE BLOOD FLOWS INTO THE RIGHT ATRIUM: ***2/3 SHUNTED, VIA THE FORAMEN OVALE

LEFT ATRIUM

LEFT VENTRICLE

ASCENDING AORTA

-THE REMAINDER JOINS THE VENOUS RETURN FROM THE UPPER PART OF THE BODY AND ENTERS THE RIGHT VENTRICLE AND PULMONARY ARTERY.

10% ENTER THE LUNGS

THE REMAINDER, BECAUSE THE HIGH PULMONARY VASCULAR RESISTANCE AND LOW SYSTEMIC VASCULAR RESISTANCE , CROSSES THE DUCTUS ARTERIOSUS TO THE DESCENDING AORTA.

***AT BIRTH WITH THE FIRST BREATHING : CLOSING THE FORAMEN OVALE

CLOSURE OF THE DUCTUS ARTERIOSUS, FONCTIONALLY FIRST AND ANATOMICALLY THEN.

***IN THE FETUS, HIGH PULMONARY VASCULAR RESISTANCE IS MAINTAINED BY CONSTRICTION OF THE MUSCULAR TUNICA MEDIA OF THESE ARTERIOLES.

THE ARTERIOLES START TO DILATE AFTER BIRTH, AND THE TUNICA MEDIA GRADUALLY ATROPHIES.

ABNORMALITIES OF THE PULMONARY CIRCULATION:

1/ PERSISTANCE OF FETAL CIRCULATION

2/ANATOMY CHANGES

3/PHYSIOLOGIC CHANGES

1/ PERSISTENCE OF THE FETAL CIRCULATION:

PULMONARY VASCULAR RESISTANCE CAN REMAIN HIGH AFTER BIRTH IF CONSTRICTION OF THE ARTERIOLAR LUMINA BY A PATHOLOGIC PROCESS OCCURS :

***HYPOXEMIA

***ACIDOSIS

***UNIDENTIFIED FACTOR

RESULT: PULMONARY HYPERTENSION LEADS TO RIGHT TO LEFT SHUNTING AT THE DUCTUS OR FORAMEN OVALE.

2/ ANATOMIC CHANGES:

IF STIMULI TO PULMONARY ARTERIOLAR CONSTRICTION: +++PULMONARY HYPERTENSION

+++VENOUS HYPERTENSION

CONTINUE INTO INFANCY, THE MEDIA REMAINS THICKENED INSTEAD OF ATROPHYING WITH AGE.

PATHOLOGIES OCCURING : CELLULAR INTIMAL PROLIFERATION

FIBROSIS OF THE INTIMA AND MEDIA

ANGIOMA FORMATION

ARTERIOLITIS

3/PHYSIOLOGICAL CHANGES:

EISENMENGER REACTION: COMBINATION OF AN IRRESIBILITY HIGH PULMONARY VASCULAR RESISTANCE [CULMINATING IN PULMONARY VASCULAR OBSTRUCTIVE DISEASE] AND A RIGHT TO LEFT SHUNT.

***HEPATOBILIARY SYSTEM: Prenatally, bilirubin conjugation in the liver is suppressed.

IN THE FIRST DAY OF LIFE, INCREASED GLUCURONYL TRANSFERASE ACTIVITY RESULTS IN CONJUGATION AND ILIMINATION OF BILIRUBIN , VIA REDUCTION PRODUCTS, IN THE STOOL.

***FACTORS THAT ADVERSALLY AFFECT HYPERPLASTIC GROWTH OF THE FETUS:

+++CONGENITAL INFECTION

+++CHROMOSOMAL DEFECT

+++NONCHROMOSOMAL CONGENITAL SYNDROME

+++CELL TOXINS [ ALCOHOL, NARCOTICS]

***ABERRATIONS IN FETAL NUTRITION IN THE LAST STAGE OF PREGNANCY INHIBIT NORMAL CELL GROWTH AND MAY RESULT IN ASYMETRIC GROWTH RETARDATION.

BODY WEIGHT IS PRIMARILY AFFECTED , WITH PRESERVATION OF BRAIN GROWTH.

***FACTORS THAT ADVERSALY AFFECT FETAL NUTRITION :

+++MATERNAL MALNUTRITION

+++PLACENTAL ABNORMALITIES OR ABNORMAL CORD INSERTION

+++PREECLAMPSIA

+++MULTIPLE GESTATION

+++MATERNAL USE OF CIGARETTES

INFANT LARGE FOR GESTATIONAL AGE IN : +++MATERNAL DIABETES

+++BECKWITH-WIEDEMANN SYNDROME

+++GENETIC PREDISPOSITION [MATERNAL HISTORY OF LARGE INFANT]

+++HYDROPS FETALIS

PRENATAL RISK FACTORS FOR ASPHYXIA:

***EXTREME MATERNAL AGE <20 > 35

***PLACENTA ABRUPTION

***PLACENTA PRAEVIA

***PREECLAMPSIA

***PRETERM GESTATION

***POST TERM GESTATION

***MECONIUM STAINED AMNIOTIC FLUID

***FETAL BRADYCARDIA

***MALPRESENTATION

***MULTIPLE GESTATION

***PROLONGED RUPTURE OF THE FETAL MEMBRANES

***MATERNAL DIABETES

***MATERNAL USE OF ILLICIT DRUGS.

SIGNS OF SEVERE ASPHYXIA :+HEART===>HYPOXIC CARDIOMYOPATHY: ***HYPOTENSION

***POOR MYOCARDIAL CONTRACTILITY

***CARDIOMEGALY

***CONGESTIVE HEART FAILURE

+KIDNEY:===>ACUTE TUBULAR NECROSIS BY DECREASED RENAL BLOOD FLOW

+GI===> ILEUS

NECROTIZING ENTEROCOLITIS

+BLOOD: CIVD

THROMBOCYTOPENIA

PROLONGED PROTHROMBIN TIME [PT]

THROMBOPLASTIN TIME [PTT]

BLEEDING

FACTORS ASSOCIATED WITH HIGH RISK PREGANCIES DELIVRIES:

MATERNAL DIABETES

MATERNAL ANTIBODIES SENSITIZATION [RH, ABO]

PRETERM GESTATION [DELIVRY AT <38 WEEKS]

POST TERM GESTATION [DELIVRY AT >42 WEEKS]

MULTIPLE GESTATION

MATERNAL BLEEDING [PLACENTA ABRUPTION, PLACENTA PRAEVIA ]

SEVERE PREECLAMPSIA

INTRAUTERINE GROWTH RETARDATION

MATERNAL NARCOTIC ADDICTION

KNOWN FETAL ANOMALIES

BREECH PRESENTATION

CESAREAN DELIVRY

FETAL DISTRESS

APGAR EVALUATION OF THE NEW BORN

SCORE

SIGN 0 1 2

HEART RATE ABSENT <100 BEATS/MIN >100 BEATS/MIN

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RESPIRATORY EFFORT ABSENT WEAK,IRREGULAR STRONG,REGULAR

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MUSCLE TONE FLACCID SOME FLEXION WELL FLEXED

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REFLEX IRRITABILITY NO RESPONSE GRIMACE COUGH OR SNEEZE

RESPONSE TO CATHETER

IN NOSTRIL

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SKIN COLOR BLUE PALE BODY PINK, ENTIRE BODY PINK

EXTREMITIES BLUE

APGAR EVALUATION IS PERFORMED AT 1 AND 5 MIN AFTER BIRTH.

A SCORE OF 8-10 REFLETS GOOD OXYGENATION AND VENTILATION AND INDICATES NO NEED FOR VOGOROUS RESUCITATION

A SCORE OF 5-7 INDICTES A NEED FOR STIMULATION AND SUPPLEMENTAL OXYGEN

A SCORE LESS THAN 5 INDICATES A NEED FOR ASSISTED VENTILATION AND POSSIBLE CARDIAC SUPPORT.

ANOMALIES IN DVLPMT OF THE GI TRACT :

***ESOPHAGUS: +++ESOPHAGEAL ATRESIA

+++TRACHEOESOPHAGEAL FISTULA

***INTESTINES: +++SMALL BOWEL ATRESIA [FROM VASCULAR ACCIDENT DURING ROTATION]

+++MALROTATION ===> VOLVULUS

+++OMPHALOCELE = HERNIATION OF INTRA-ABDOMINAL VISCERA INTO THE UMBILICAL CORD.

+++GASTROSCHISIS: DEFECT IN THE CLOSURE OF THE ABDOMINAL WALL , PORTION OF THE INTESTINE PROTRUSE.

***COLON : +++IMPERFORATE ANUS

+++HIRSHPRUNG'S DISEASE