Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/47

Click to flip

47 Cards in this Set

  • Front
  • Back
Newborn platelet values compared to adults?
150K to 450K x 10ˆ9/L

Mean platelet volume (MPV) is 7-9FI

**same across all ages
Newborn platelet survival compared to adults?
7-10 days

**same across all ages
Newborn platelet structure compared to adults?
Same number granules

Serotonin and ADP content is ~50% that of adults
Newborn platelet adhesion compared to adults?
1. ↑ as measured by ↓ bleeding time
-- ↑vWF + large RBCs + ↑Hct

2. ↑ agglutination of cord platelets at birth
-- ↑vWF + ↑ high molec wt VW multimers

3. ↑↑agglutination to ristocetin
Newborn platelet aggregation compared to adults?
1. ↓ aggregation to epi
-- ↓ number of α-adrenergic receptors

2. variable aggregation to ADP, collagen, and arachidonic acid
Newborn platelet activation/secretion compared to adults?
No specific abnormalities, however:

Platelets are activated at birth as manifested by elevation of
-- Thromboxane β2
-- β-Thrombomodulin
-- PF4
-- decreased granular content of cord platelets
-- decreased level of epi receptor availability

Activation is multifactorial as thermal changes, hypoxia, acidosis, adrenergic stimulation, and exposure to amniotic fluid are all likely to occur at birth
Vessel wall (endothelium) fxns in a newborn?
1. Antithrombosis
-- production of prostacyclin via liopoxygenase and cyclooxygenase mediated pathway of unsaturated fatty acids
-- promotion of ATIII neutralization of thrombin by cell surface proteoglycans
-- production of NO --> vascular relaxing factor, inhibitor of platelet activation and platelet adhesion to damaged vessel walls

2. Hemostasis
-- promotes formation of fibrin when injured
What is the key step in homostasis?
Thrombin formation
-- significantly decreased in newborns --> similar to adult receiving therapeutic doses of anticoagulant
Why is thrombin decreased in newborns?
Result of:
-- decreased factor and inhibitor production
-- increased clearance
-- increased consumption from activation of the coagulation cascade at birth
Coagulation factors in the fetus?
Do NOT cross the placenta

Measurable by 10wks of gestational age and continue to increase thereafter
Vitamin K factors in the newborn?
II, VII, IX, and X

DECREASE at birth and are directly involved in the hemorrhagic disease of the newborn
Contact Phase factors in the newborn?
XI, XII, Prekallikrein and HMW Kininogen

Decrease at birth and directly responsible for the ↑↑APTT
Other coagulation factors in the newborn?
Fibrinogen, V, VIII, XIII, and vWF

-- NOT decreased at birth
List inhibitors of coagulation.
Direct inhibitors
Protein C/Protein S system
Tissue Factor Pathway Inhibitor (TFPI)
Regulation of thrombin by fibrin
What are the direct inhibitors of coagulation in a newborn?
1. C1 esterase inhibitor
-- increased at birth
2. α2 macroglobulin
-- increased at birth
3. Heparin cofactor II
4. Antithrombin III
5. Fetal anticoagulant (acts via heparin cofactor II)
Explain the Protein C/Protein S system and their levels in the newborn.
1. Thrombomodulin
-- ↑↑↑ at birth until early childhood

2. Protein C
-- ↓↓↓ at birth until 6mos of age
-- fetal form has excess of single chain protein
-- adult levels reached by early childhood

Protein S
-- ↓ at birth but fxnal activity similar to that of adult

STEP 1: binding of thrombin to thrombomodulin

STEP 2: interruption of fibrinogen, factor V and factor VIII cleavage as well as platelet activation

STEP 3: activation of Protein C in the presence of Protein S and inactivation of Va and VIIIa by proteolytic degradation
What does the Tissue Factor Pathway Inhibitor (TFPI) do?
STEP 1: TFPI/Xa complex binds to VIIa and inactivates VIIa

STEP 2: prevents further generation of thrombin
What are the components of the fibrinolytic system in a newborn?
1. t-PA and PAI are ↑↑ in the newborn but ↓↓ in the cord blood at birth

2. α2-antiplasmin: 80% adult level

3. Plasminogen: 50% of adult level

The fibrinolytic system is activated by the birth process
What are the common chief complaints that might indicate a hemostatic disorder in a newborn?
1. oozing from unbilicus
2. bleeding into the scalp
3. large cephalhematoma
4. bleeding after circumcision
5. bleeding at venipuncture sites
6. intracranial hemorrhage
7. sites of invasive procedures (mucous mbrn, bladder, etc)
8. joint bleeding is rare
What are the most common causes of bleeding in healthy infants?
immune mediated thrombocytopenia

Vitamin K deficiency

congenital factor deficiency
What is the most common hemostatic abnormality in newborns?
thrombocytopenia
-- indicative of an underlying pathologic process
Thrombocytopenia incidence in newborns?
-- approx 22% of all newborns admitted into NICU

-- about 50% of affected infants have counts <100 x 10ˆ9/L
-- 20% have counts <50 x 10ˆ9/L

In 75% of sick newborns, thrombocytopenia is present by day 2 of life, reaches its nadir by day 4, and recovers to >150 x 10ˆ9/L by day 10 in 86% of affected infants
What is the risk for serious bleeding in a newborn w/ thrombocytopenia?
Depends on:
-- platelet count (<50 x 10ˆ9/L)
-- presence of a platelet fxn defect
-- maturity of infant (highest risk in premature)
What processes are implicated in the development of thrombocytopenia?
1. decreased production
-- rare, responsible for less than 5% of thromboctopenia in newborns

2. increased destruction
-- directly implicated in the majority of infants

3. increased pooling in the spleen
How do we manage thrombocytopenia?
Depends on underlying disorder and may require combination of modalities

PLATELET TRANSFUSION
-- indicated in bleeding infant, regardless of cause
-- 10-20ml/kg concentrate

IVIG
-- for infants w/ thrombocytopenia induced by placental passage of autoAb
-- indicated to block trapping of platelets by the splenic RES system
Other qualitative platelet disorders in a newborn?
PREVENT NORMAL AGGREGATION:
-- salicylates
-- indomethacin
-- nitric oxide

INCREASED PLATELET AGGREGATION
-- maternal diabetes
-- diet deficient in essential fatty acids and vitamin E
-- perinatal aspiration of aamniotic fluid
Congenital factor deficiencies in the newborn and bleeding incidence?
Usually only severe deficiencies are associated w/ signif bleeding in the newborn
-- do not bleed perinatally unless hemostatically challenged
Factor dificiencies in the newborn?
1. Factor VII and IX
-- two sex-linked d/o's
-- also known as hemophilia A and B
-- most frequent

2. Deficiencies of factors II, V, VII, XI, XII, prekallikrein or HMWK
-- rare, autosomal recessive
-- normally seen in families w/ hx of consanguinuity
-- deficiencies of XII , prekallikrein, and HMWK do not result in hemorrhagic complications
How do we diagnose factor deficiencies in the newborn?
Measurement of plasma concentration of coagulatoin proteins

Use molecular techniques prenatally

Evaluate the parents
What are the most frequent sites of bleeding?
penis (circumcision)

umbilicus

intracranial hemorrhage
-- rare in full tern newborns w/o signif primary promblems
-- should raise possibility of primary hemostatic disorders
What is the usuall treatment of choice for congenital factor deficiencies?
Usually NOT plasma or FFP

Several specific concentrates produced by either recombinant techniques or highly purified and treated against infectious organisms are now available for the majority of congenital deficiencies.
List acquired hemostatic disorders possible in a newborn.
1. DIC
2. Liver disease
3. Vitamin K deficiency
4. Other
Describe DIC in the newborn.
Clinical spectrum continually changing due to improved perinatal care

Accumulation of several factors, those most important being:
-- intensity/duration of activation of the hemostatic system
-- degree of assoc blood flow impairment
-- extent of liver fxn or dysfxn
How do we diagnose DIC in the newborn?
Since the coag system is activated at birth, certain markers like ATII/thrombin complex determination CANNOT be used

Decreased factor V, VII, and fibrinogen are more likely diagnostic since their conc is similar to adults

NO Dx test can confirm or exclude DIC in the neonatal period.
DIC treatment in the newborn?
Control underlying disorder

Factor replacement not indicated unless there is evidence of bleeding

Maintain:
-- platelet count >50K/mm3
-- fibrinogen >1g/L
-- PT values at levels normal for postnatal and gestational age
Liver disease in the newborn?
Coagulopathies encountered are due to failure of hepatic synthetic fxns superimposed to:

-- physiologic immaturity
-- activation of coag and fibrinolysis
-- poor clearance of activated coag factors
-- loss of hemostatic proteins into the ascitic fluid
-- thrombocytopenia (↓platelet production + splenic sequestration + ↑ clearance)

**Increased PT and decreased Plasma proteins commonly found
Common causes of liver disease in newborns?
ciral hepatitis
hypoxia
total parenteral nutrition
shock
fetal hydrops
Treatment for liver disease-induced hemostatic disorders in the newborn?
FFP
cryoprecipitate
exchange transfusion for clinical bleeding

Pts w/ persistent liver failure: liver transplant
What occurs in the absence of Vitamin K?
1. Decreased prothrombin activity
2. Increased PT on day 2 to 4 of life
3. Return to normal by day 5-7

Admin of vitamin K soon after birth prevents the decrease in PT activity during the first 3-4 days of life
VitK deficiency lab test in the newborn?
Screening
-- PT
-- APTT

Factor assays

Decarboxylated forms of VK-dependent factors

Protein induced by VK antagonists (PIVKA)

Direct measurement of VK
Forms of vitamin K?
VK1: phytonadione
-- green leafy vegetables

VK2: metaquinanone
-- produced by intestinal flora

VK3: menadione
-- synthetic water soluble
Vitamin K prophylaxis recommendations for newborns?
Single dose of 0.5 to 1mg IM at birth

OR

Oral dose of 2-4mg at birth w/ subsequent dosing for breast-fed infants
How do we treat Vitamin K deficiency?
VK should be admin SQ or IV but not IM to avoid hematoma formation at the site of injection

Plasma should be admin to infants w/ serious bleeding manifestations
Describe classic Vitamin K dependent bleeding (VKDB).
INCIDENCE
-- 1/10k births

TIMING
-- Day 2 to 7 of life

CAUSES
-- poor placental transfer of VK
-- marginal VK in breast milk
-- inadequate milk intake
-- sterile gut (rare in formula fed infants)

BLEEDING (in order)
1. ICH
2. GI
3. umbilicus
4. ENT region
5. Injection sites
6. Circumcision
Describe early VKDB.
INCIDENCE
-- very rare

TIMING
-- first 24 hours of life

CAUSES
-- maternal use Rx interfering w/ VK metabolism

BLEEDING (in order)
1. ICH
2. GI
3. Umbilicus
4. intra-abdominal
5. Cephalhematoma
Describe late VKDB.
INCIDENCE
-- 4-10/10k births

TIMING
-- weeks 2 to 8

CAUSES
-- disorders interfering with VK supply

BLEEDING (in order)
1. ICH (>50%)
2. GI
3. skin
4. ENT region
5. injection sites
6. urogenital tract
7. intrathoracic
Other causes of aberrant coagulation system activation?
Activation w/ or w/o consumption of platelets has been observed in:
-- respiratory distress syndrome
-- use of extracorporeal mbrn oxygenation (ECMO)