Neonatal Jaundice Flashcards

0
Q

What is kernicterus?

A

A histology cal finding if uncongugated bili getting deposited in basal ganglia and brainstem nuclei.
Un conjugated bili>exceeds bili binding capacity of albumin>crosses bbb as it fat soluble>deposit in basal ganglia and cr nerve nuclei> encephalopathy

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1
Q

Why NJ is important

A
  1. Another disorder

2. kernicterus

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2
Q

Clinically jaundice visible at what level if bili?

A

80-120 micrmls/l

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3
Q

When do u say its conjugated bilirubinimea

A

When conjugated bili is >20% of total or

>2mg/dl

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4
Q

Divide jaundice according or age of onset

A

3weeks

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5
Q

Causes for NJ <24 hrs

A
Haemolitic anaemia
 ABO incomp
 Rh incomp 
 G6PD def
 Pryuvate kinase def
 Spherocytosis
 Eleptocytosis

Cong infections

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6
Q

Causes for 24hrs to 3 weeks

A
In 1st week-
Physiol J
Breast feeding J
Infections-UTI
Haemoly Anaemia
Polycythemia 
Bruising
Crigler najjar syn
After 1st week-
Phy
B milk j
Infections
Non immune ahem anaemia 
Hepatitis 
B atresia  
hypothyroid
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7
Q

Causes for J >3 weeks

A
Conjugated-
N hepatitis
Biliary atresia
Choledochal cyst
Paucity if bile ducts
Cystic f
Insipissted bil sy
Conge infection
Galactosemai
Uncongu-
BM j
Phys J
Infections
Hypothyroidism 
Haemolitic an
Downs
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8
Q

Rh incompatibility pathophysiology

A

Rh -v mom has Rh +v baby> fetal blood goes to mom>mom produce anti Rh AB>IgM crossing the placenta is less >1st baby less affected
IgG later crosses affect next baby if Rh pos>severe anaemia >HF with increase hydrostatic pressure and liver failure by extram hematopoietic and low protein with increase cap permiabilt >fluid in cavities
liver and spleen erythroposis>hepatospleenagaly>hydrops fetal us and death

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9
Q

ABO incompat pathophysiology

Dct usually wat

A

O mother affect A>B baby
Less effect as most AB are IgM
Some produce IgG anti A haemolysin o B haemolysin

Less severe anaemia,
no organomegaly
DCT pos but usually neg

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10
Q

Congenital infections get which bilirubinarmia

A

Conjugated

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11
Q

2causes for physiological jaundice

A
1. Increase bili load-
Incr Hb
Red life span
2- Reduce excretion
Red ligandin
Enz immatinc enterohepatic cir
Slow gut motility
Incr B glycuronydase 
Red bacteria in gut
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12
Q

Breast feeding-jaundice pathophysiology
Appear when
Mx

A

Poor BF and dehydration
Poor BF >increase enterohepatic circulation of bile>

1st week

Promote BF,EBM,FF

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13
Q

Infection cause which bilirubinemia and why

A
Both uncongugated and conjugated 
Uncongugated- 
 Dehyd
 enterohepatic circ >
 Haemolysis
 Impaired liver
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14
Q

Main 2 symptoms of conjugated bili

A

Pale stools
Dark urine
Hepatomeg

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15
Q

Progression if jaundice spreading and resolving

A

Head to toe

Toe to head

16
Q

Rate of change if jaundice

A

Inear rise and a plateau

17
Q

Why preterm at high risk

A

Low albumin

Immature liver

18
Q

Relationship BW jaundice and clinical status

A

Severely ill child more susceptible for

Damage from jaundice

19
Q

2 main treatment modalities for NJ

A

Phototherapy

Exchange transfusion

20
Q

Phototherapy light range?
Types 2
Complications 4

A

Blue 450 nm
Single &double
Dehydr,temperature instability ,
Rash and bronzed decouloration of eyes

21
Q

ET done via and how,

How much

A

Umbilical vein
Withdrow 10-20ml blood and replace with donor blood
Twice the baby’s blood vol(80ml/kg*2)

22
Q

Other new treatment methods for NJ

A

Immunoglobulins for baby

Albumin if low to baby

23
Q

Explain Hb catabolism

A

In RES
Hb>heme+globin
Heme by heme oxygenase>fe,bili verdin ,CO
BIliverdin by biliverdine reductase>bilirubin
Binds to albumin and transported to liver.

In LIVER
Taken by ligand into cells.
Conjugated with 2UDP molec by UDP glycuronyl transferase
Excreted via bile.some goes to kidney via blood

In TERMINAL ILEUM
Deconj by B glycuronydase >reabsorption >enterohepatic cir to liver

In COLON
Bacterial action>urobilinogen>reabsorption >enterohepatic cir to liver(95%)
Rest converted to stercobilinogen>stercobilin>stool
Urobilinogen > urobilin>stools

In KIDNEY
Urobilinogen >urobilin >urine

23
Q

How’s bili excreted in fetus

A

Unconjugated form via placenta

23
Q

What other substance make bili

A

Myoglobin

Cytochrome

24
Q

What are the physiological causes for jaundice with ex 5

A

1.^ bili -hemolysis,polycythemia ,haemorrages,^enterh cir
2.<uptake -
Premature ,genes
3. Absent o reduce enz amnt-
Gene Criggler najjar
4.reduce activity of enz-
Hypoxia,infection ,drugs,premature ,hypothyroid
5.obstruction -hepatitis,bili atresia

25
Q

Risk factors for jaundice

A

J-Jaundice f

E-extravasated blood,enterohep cir

26
Q

Symptoms if jaundice

A
Icterus
Lethargy
Poor feeding
Seizure
Anemia
Hepatospleenagaly 
Pale stool
Dark urine
27
Q

Causes for congenital hyperbilirubinimi 5

A

Criggler najjar 1&2
Gilbert’s
Dubin Johnson
Rotors

28
Q

Ix for jaundice

Early and late

A
SBR
BLood Grp 
Rh
DAT
Hb
Retic count
Blood picture 
Septic screen
Late onset
Above and
Septic screen
TFT
LFT
Urine for reducing subs
Galactosemia screen
Uss and
HIDA scan to check bili syst 
TORCHS screen
29
Q

Transc bili measurement
Use
Relationship to SBR
can’t use when

A

To screen
Parallel
To asses progress

30
Q

CO measuring test

Use

A

ETCO-end tidal CO level

Ti asses bili production

31
Q

Pys J appear ,peak,disappear when and adult level when

A

2-3d
2-4d
5-7d
19-14d

32
Q

In preterms phy j rises how

A

Slow and prolonged

33
Q

What factors exclude phy J

A

J5mg/dl
Term >12 preterm>14
Direct>2
Prolonged j

34
Q
What's breast milk J
Present when
If BF continues what happens 
If stopped what happens
Mx
A
Some milk has b glycuronydase  which increase enterohepatic cir
After 1 wk
Slowly Reduse 
Rapidly drops 
Withhold BF for 1-2days and give FF
PT