Haemorrhagic and Haemolytic of Newborn DiseasesNaqib Bajuri
actually for haemorrhagic newborn diseases, mainly focus of vit K def...the other is for revision n more commonly occur in child n adults....for haemolytic newborn disease, mainly focus on Rh disease n ABO incompatibility.....the other when childhoods
This presentation was done by Dr. Julius P. Kessy,MD. An intern Doctor at Dodoma Regional Referral Hospital (DRRH) during pediatrics unit clinical meeting and supervised by Dr. Christina K. Galabawa,MD,Mmed2, Pediatrics and Child Health, University of Dodoma (UDOM) in November, 2017.
Please find the power point on Phototherapy in jaundice . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
Most pictures were taken from Google images
Haemorrhagic and Haemolytic of Newborn DiseasesNaqib Bajuri
actually for haemorrhagic newborn diseases, mainly focus of vit K def...the other is for revision n more commonly occur in child n adults....for haemolytic newborn disease, mainly focus on Rh disease n ABO incompatibility.....the other when childhoods
This presentation was done by Dr. Julius P. Kessy,MD. An intern Doctor at Dodoma Regional Referral Hospital (DRRH) during pediatrics unit clinical meeting and supervised by Dr. Christina K. Galabawa,MD,Mmed2, Pediatrics and Child Health, University of Dodoma (UDOM) in November, 2017.
Please find the power point on Phototherapy in jaundice . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
Most pictures were taken from Google images
This slide contains neonatal jaundice by including real case senario and nursing management through by passing definition, pathophysiology and diagnosis modality
Neonatal jaundice (hyperbilirubinemia) by Rajiv MavachiRajiv Mavachi
Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin.
Jaundice is the yellow color seen in the skin of many newborns. Jaundice happens when a chemical called bilirubin builds up in the baby’s blood. During pregnancy, the mother’s liver removes bilirubin for the baby, but after birth the baby’s liver must remove the bilirubin. In some babies, the liver might not be developed enough to efficiently get rid of bilirubin. When too much bilirubin builds up in a new baby’s body, the skin and whites of the eyes might look yellow. This yellow coloring is called jaundice.
When severe jaundice goes untreated for too long, it can cause a condition called kernicterus. Kernicterus is a type of brain damage that can result from high levels of bilirubin in a baby’s blood. It can cause athetoid cerebral palsy and hearing loss. Kernicterus also causes problems with vision and teeth and sometimes can cause intellectual disabilities. Early detection and management of jaundice can prevent kernicterus.
Centers for Disease Control and Prevention:
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. Neonatal Jaundice
• Objectives:
• Define hyperbilirubinemia.
• Differentiate between physiological and
pathological jaundice.
• Causes of hyperbilirubinemia.
• Discuss the pathophysiology of hyperbilirubinemia.
• Describe the most dangerous complication of
hyperbilirubinemia.
• Therapeutic management.
• Design plan of care for baby has
hyperbilirubinemia.
3. (Hyperbilirubinemia)
• Definition: Hyperbilirubinemia refers to an
excessive level of bilirubin accumulation in the
blood and is characterized by yellowish
discoloration of the skin, sclerae, mucous
membranes and nails.
• Unconjugated bilirubin = Indirect bilirubin.
• Conjugated bilirubin = Direct bilirubin.
5. Neonatal Jaundice
• Visible form of bilirubinemia
–Newborn skin >5 mg / dl
• Occurs in 60% of term and 80% of preterm
neonates
• However, significant jaundice occurs in 6 %
of term babies
• 6-10% require phototherapy/ other
therapeutic options.
6. Bilirubin metabolism
Hb → globin + haem
1g Hb = 34mg bilirubin
Non – heme source
1 mg / kg
Bilirubin
glucuronidase
Bilirubin
Bilirubin
Ligandin
(Y - acceptor)
Bil glucuronide
Intestine
Bil
glucuronide
Stercobilin
bacteria
β glucuronidase
8. Clinical assessment of jaundice
(Kramer’s staging)
Area of body Bilirubin levels
mg/dl (*17=umol)
Face Zone-1: 4-6
Upper trunk Zone-2: 6-8
Lower trunk & thighs 8-16
Arms and lower legs Zone-3: 8-12
Palms & soles Zone-4 :12-14
Zone-5 :>15
9. Causes of jaundice
Appearing within 24 hours of age
• Hemolytic disease of NB : Rh, ABO
• Infections: TORCH, malaria, bacterial
• Red cell enzymes defects like G6PD
deficiency,pyruvate kinase
• Administration of large amount of certain drugs
like vit k, sulfonamides.
• Hereditary spherocytosis.
• Crigler-najjar syndrome,lucey-driscoll syndrome….
10. Causes of jaundice
Appearing between 24-72 hours of life
• Physiological.
• Sepsis.
• Polycythemia.
• Intraventricular hemorrhage.
• Increased entero-hepatic circulation.
• Cretinism,breastfeeding,
11. Causes of jaundice
After 72 hours of age
• Sepsis
• Cephalhaematoma
• Neonatal hepatitis
• Extra-hepatic biliary atresia
• Breast milk jaundice
• Metabolic disorders such as galactosemia,
tyrosinemia,cystic fibrosis,gilbert syndrome.
12. Risk factors for jaundice
JAUNDICE
• J - jaundice within first 24 hrs of life
• A - a sibling who was jaundiced as neonate
• U - unrecognized hemolysis
• N – non-optimal sucking/nursing
• D - deficiency of G6PD
• I - infection
• C – cephalhematoma /bruising
• E - East Asian/North Indian
13. Physiological jaundice
Characteristics:
• Appears after 24-72 hours
• Maximum intensity by 3th-5th day in term &
7th day in preterm
• Serum level less than 15 mg / dl
• Clinically not detectable after 14 days
• Disappears without any treatment
Note: Baby should, however, be watched for worsening
jaundice.
15. “Pathological jaundice”
• Appears within 24 hours of age
• Increase of bilirubin > 5 mg / dl / day
• Serum bilirubin > 15 mg / dl
• Jaundice persisting after 14 days
• Stool clay / white colored
16. Causese of pathological jaundice
• Immaturity
• Hemolytic disease of the new born due to feto maternal
blood group incompatibility.
• Breast milk jaundice
• Hypothyroidism.
• Crigler-najjar syndrome
• Gilbert syndrome
• Malaria,concealed hemorrhage.
NJ - 16
17. Breast milk jaundice
• In 2-4 % EBF babies
• SBr>10mg/dl beyond 3rd
-4th
week
• Should be differentiated from Hemolytic
jaundice, hypothyroidism, G6PD def
• T/t: Some babies may require PT
Continue breast feeding
Usually declines over a period of time
18. Dangers of hyperbilirubinemia
• Jaundice is the medical emergency.
• Uncojugated bilirubin causes bilirubin
encephalopathy or kernicterus.
• c/f of b.encephalopathy lethergy,hypotonia followed
by hypertonia ,refusal of feeds,shrillcry,setting sun
sign,fever,convulsions,coma,retrocollis and
opisthotonus .sluggish moro”s rflex.
NJ - 18
19. Kernicterus pathogenesis
• Conctroversial but interplay between three points
A.unconjugated bilirubin level >20mg/dl.
B.gestational maturity of infants.
C.integrity of blood-brain barrier.
-Cross the blood-brain barrier and gains access into the
neurons located in the basal
ganglia,hippocampus,auditory nuclei.
-serum bilirubin/protein more than 3.5 may be
associated with the brain damage.
NJ - 19
20. INVESTIGATIONS
• HISTORY OF SEVERE JAUNDICE OR EXCHANGE BLOOD
TRANSFUSION OR KERNICTERUS IN A PREVIOUS SIBLING.
• MOTHER O GROUP OR RH-NEGATIVE.
• ONSET OF JAUNDICE WITH IN 24 HOURS OR AFTER 72 HOURS
OF AGE.
• PERSISTENT OF JAUNDIC BEYOND 3 WEEKS.
• JAUNDICED INFANT WITH YELLOW-COLORED URINE OR CLAY
COLORED STOOLS.
21. Therapeutic Management
• AIM OF THERAPY: reduce level of serum bilirubin and
prevent bilirubin toxicity
• EXCHANGE BLOOD TRANSFUSION IS THE SINGLE MOST
EFFECTIVE AND RELIBLE METHOD OF TO LOWER THE
BILIRUBIN WHEN IT APPROCHES CRITICAL LEVELS.
• Supportive and therapeutic measures are useful to
prevent excess rise of serum bilirubin and reduce the
need for EBT
22. “PREDICTION OF HYPERBILIRUBINEMIA IN
HEALTHY NEAR-TERM AND TERM BABIES”
• Identify risk factors for development
hyperbilirubinemia.
• Routine screening for serum bilirubin levels.
• End-tidal corbon monoxide levels.
NJ - 22
23. PREVENTIVE AND SUPPORTIVE
MEASURES
• Adequate feeding.
• Aspiration of cephalhematoma.
• Treatment of sepsis and hepatitis.
• DRUGS:1.phenobarbitone 10mg/kg single
dose intramuscular or 5mg/kg/day in 2
divided doses orally for 3 days,2.clofibrate
50mg/kg single dose orally.
NJ - 23
25. Phototheraphy
• Phototheraphy is a drug.
• Widely accepted and efective method.
• Wave lenth is 425-475nm.
• Photo-oxidation of bilirubin into water slouble
colorless forms of bilirubin like lumirubin.
• AAP recommends that phototheraphy should be
started,if serum bilirubin approaches the level of
18mg/dl.(15mg/dl if baby is having hemolysis or is
sick due to sepsis and perinatal distress factors).
• Phototheraphy is decline TSB@1-2mg/dl per 4-6
hours.
NJ - 25
26. Continue……
• Phototheraphy may be discontnued when TSB falls below
15mg/dl.
• Side effects :
• Passage of loose greeen stools because of lactose intolerance
and irritant effect of photocatabolites.
• Hyperthermia,irritability,and dehydration due to insensible
water loss may occur
• Infants with parenchymal liver disease with biliary obstruction
may develop peculiar bronze discoloration of skin due to
accumulation of one of the photoisomers designated as
lumirubin.
NJ - 26
28. EXCHANGE BLOOD TRANSFUSION
• It is most effective method to reduce bilirubin levels.
• Serum bilirubin level of 20-25mg/dl at the age of 4-5 days.
• Early indications for exchange blood transfusion in infants
with Rh-haemolytic disease of the newborn.
• A.cord Hb% <10g/dl or haematocrit <30%.
• B.cord bilirubin of 5mg/dl or more.
• C.unconjugated serum bilirubin of 10mg/dl with in 24 hours
or 15mg/dl within 48 hours or rate of rise of >0.5 mg/dl /hr.
NJ - 28
29. INDICATIONS FOR EXCHANGE BLOOD
TRANSFUSION IN BABIES
BIRTH WEIGHT (G) TOTAL SERUM BILIRUBIN
(MG/DL)
NARMAL INFANTS HIGH RISK-INFANTS
UP TO 1000 10-12 8-10
1001-1250 12-14 10-12
1251-1500 14-16 12-14
1501-2000 16-18 14-16
2001-2500 18-20 16-18
>2500 20-22 18-20
NJ - 29
30. MANAGEMENT OF IDIOPATHIC HYPERBILIRUBINEMIA
IN HEALTHY TERM INFANTS
TOTAL SERUM
BILIRUBIN
AGE (HOURS) CONSIDER
PHOTOTHERAPHY
PHOTOTHERAPHY EBT
<24 - - -
25-48 >=12 >=15 >=20
49-72 >=15 >=18 >=25
>=72 >=17 >=20 >=25
NJ - 30
33. PERSISTENT NEONATAL JAUNDICE
• PERSISTENCE OF JAUNDICE BEYOND 3 WEEKS MAY OCCUR
DUE TO UNCONJUGATED HYPERBILIRUBINEMIA OR
CHOLESTATIC JAUNDICE.
• DUE TO NON HEMOLYTIC UNCONJUGATED
HYPERBILIRUBINEMIA.
• COMMONEST CAUSE IS BREAST MILK JAUNDICE.
• DOWNS SYNDROME,GILBERTS
SYNDROME,HYPOTHYROIDISM,CRIGLER-NAJJAR SYNDROME,
………….
NJ - 33
34. CONTINUE………………
• Conjugated hyperbilirubinemia during early neonatal period is
rare.
• Occurs after 3weeks of neonatal age.
• Causes of conjugated hyperbilirubinemia.
• Idiopathic neonatal hepatitis.
• Inspissated bile syndrome.
• Infections
• Malformations.
• Metabolic disorders like galactocemia,tryosinemia,cystic
fibrosis…….
• Chromosomal causes and miscellaneous causes……………
NJ - 34
35. Nursing considerations of Hyperbilirubinemia
• Assessment:
observing for evidence of
jaundice at regular intervals.
Jaundice is common in
the first week of life and
may be missed in dark skinned
babies
Blanching the tip
of the nose
36. Approach to jaundiced baby
• Ascertain birth weight, gestation and postnatal age
• Ask when jaundice was first noticed
• Assess clinical condition (well or ill)
• Decide whether jaundice is physiological or
pathological
• Look for evidence of kernicterus* in deeply
jaundiced NB
*Lethargy and poor feeding, poor or absent Moro's, or
convulsions
37. The goals of planning
• Infant will receive appropriate therapy if
needed to reduce serum bilirubin levels.
o Infant will experience no complications from
therapy.
o Family will receive emotional support.