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Pediatric Anesthesia > PEDs Exam 2 > Flashcards

PEDs Exam 2 Flashcards

1
Q

what makes up hemoglobin A

A

two polypeptide alpha chains
two polypeptide beta chains

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2
Q

what makes up hemoglobin F

A

two alpha chains
two gamma chains

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3
Q

where is the binding site for 2,3-DPG

A

on the beta chain which is absent in fetal hemoglobin

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4
Q

what is the hgb of term neonate

A

17g/dL

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5
Q

HgbF replaced with Hgb A

A

8-12 weks
10g/dL

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6
Q

what ps P50 at term

A

19mmhg

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7
Q

what is P50 at 6 months

A

27mmhg

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8
Q

infants with RDS ____with adult blood transfusion

A

improve

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9
Q

hgb begins to increase at

A

around 4 months

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10
Q

neonate has physiological anemia due to what

A

decrease in erythropoietin

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11
Q

signs of anemia of prematurity

A

tachycardia
bradycardia
apnea
delayed growth
poor weight gain
prolonged anemia

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12
Q

where is ABO locus encoded

A

chromosome 9

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13
Q

what is the most important Rh antigen

A

D

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14
Q

individuals with Rh D antigen are considered

A

Rh positive

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15
Q

what happens when you give Rh- Rh+ blood

A

produce IgG antibodies against D antigen

hemolysis of transfused RBC

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16
Q

Rh is autosomal

A

dominant

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17
Q

when do Rh - mothers get the RhoGAM shot

A

26-28 weeks
also within 72 hrs after delivery

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18
Q

maternal IgG is present in infants less than

A

4 months

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19
Q

what type of blood do you transfused for all newborns

A

type O-
or
utilize ABO and RH D compatible blood

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20
Q

what should you test infant serum for

A

maternal anti A and Ant B alloantibodies

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21
Q

what clotting factors are in FFP

A

2
7
8
9
10
11

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22
Q

what clotting factors are in PCC

A

2 7 9 10 12
protein C
protein S

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23
Q

what factors are in cryo

A

fibrinogen
vWF

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24
Q

Whole blood is best, BUT:

A

Stored blood: Factors 5 and 8 depleted and PLT lose shape
Fresh whole blood is best

Use whole blood for exchange transfusion, after CPB, ECMO, massive transfusion

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25
Q

10 mL/kg of pRBCs in CPDA-1 increases the hemoglobin

A

by 3g/dl

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26
Q

PRBC characteristics

A

Stores with CPDA-1 or Adsol (AS)

250-300ml

60% Hct

Storage 35-42 days Days

10 mL/kg of pRBCs in CPDA-1 increases the hemoglobin by 3 g/dL

15 mL/kg is required to attain the same increment in hemoglobin when using pRBCs stored in AS

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27
Q

3 Accepted Indications for PRBC

A

To increase oxygen-carrying capacity

To avoid an impending inadequate oxygen-carrying state

Suppress the production or dilute the amount of endogenous hemoglobin in selected patients with thalassemia or sickle cell disease

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28
Q

guidelines for transfusion less than 4 months

A
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29
Q

when are transfusions rarely and almost always indicated

A

rarely hgb>10g/Dl
almost always Hgb <6

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30
Q

allowable blood loss calculation

A

Hi = Pt’s Initial Hematocrit
Hp = Minimal accepted Hct (depends on condition) Average ~ 24%
Hav = Average of Hi & Hp

Allowable blood loss = EBV × (Hi – Hp)/Hav

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31
Q

estimated blood volume for premature infants

A

90-100 ml/kg

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32
Q

estimated blood volume for term newborns

A

80-90 ml/kg

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33
Q

estimated blood volume for infants <1 year old

A

75-80 ml/kg

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34
Q

estimated blood volume for older children

A

70-75ml/kg

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35
Q

whats the equation for volume of PRBC to administer

A
36
Q

what are characteristics of cyanotic congenital heart disease

A

Require a higher oxygen-carrying capacity

Polycythemia develops

Historically – maintain Hgb of 13 to 18 g/dL

37
Q

list transfusion complications

A

viral infections (HIV HCV, fatal hemolysis)

bacterial infections

hyperkalemia

TRALI

38
Q

what decreases risk of TRALI

A

male only FFP donors

39
Q

S/S of TRALI

A

ARDS – dyspnea, hypoxia, pulmonary edema, onset 4-6 hours after transfusion

40
Q

what is treatment for TRALI

A

supportive care

41
Q

what qualifies as a massive transfusion

A

more than one blood volume in a 24 hr period

50% blood volume in 3 hrs

10% of blood volume every 10 min

42
Q

massive transfusion complication chart

A
43
Q

what are some techniques to reduce blood transfusions

A

Autologous blood transfusion
Acute Normovolemic Hemodilution
Deliberate Hypotension
TXA

44
Q

which hemostatic factors are decreased in neonates

A

2,7,9,10,11,12,
plasminogen,
TFPI
AT
PC
PS

45
Q

which hemostatic factors are increased in neonates

A

increased vWF, 8 alpha2m,

46
Q

what does vWF do

A

platelet adhesion to injured blood vessels by bridging exposed collagen to activated platelets

Aids platelet aggregation in conjunction with fibrinogen through interactions with platelet GPIIb/IIIa surface receptor

Carrier protein for Factor 8 (protects it from activated protein C)

47
Q

what are S/S of Von Willebrand disease

A

easy bruising
petechia
nose bleeds
low factor 8

48
Q

type 1 Von Willebrand disease

A

mild-mod Quantitative decrease

TX: DDAVP – stimulates release of vWF from storage sites

Repeated use  tachyphylaxis, hyponatremia, volume overload

49
Q

type 2 von willebrand disease

A

qualitative abnormal vWF (20% of cases)

50
Q

type 3 von willebrand disease

A

severe Quantitative decrease

TX: increase levels of vWF & factor 8

Virally inactivated plasma-derived vWF concentrates (with or without FVIII) or recombinant vWF may be required.

51
Q

what do labs look like for hemophilia

A

Isolated prolongation of the aPTT,
normal PT, thrombin time, platelet count, and bleeding time

52
Q

treatment for hemophilia

A

raise F8 or F9 with concentrated factors

DDAVP for F8 short term

53
Q

what is the most common reason for thrombocytopenia in childhood

A

idiopathic thrombocytopenia purpura (ITP)

54
Q

lifespan of ITP platelets

A

few hrs

55
Q

how do you treat ITP

A

observation alone in children presenting with no bleeding or mild bleeding w/ vigilance

for severe bleeding
Severe bleeding: emergent transfusion, possible splenectomy

56
Q

diagnosis of ITP

A

platelet count of less than 100 × 109/L without concurrent leukopenia or anemia.

57
Q

what is Glucose-6-Phosphate Dehydrogenase Deficiency

A

Most common human enzyme deficiency

Causes acute hemolysis in the presence of various oxidative stressors

Fava beans, methylene blue, nitrofurantoin

Forms Heinz bodies -> lysis of RBC -> jaundice and anemia

58
Q

what is the gold standard test for Glucose-6-Phosphate Dehydrogenase Deficiency

A

quantitative spectrophotometric assay of G6PD activity

Don’t test during acute hemolysis episode – test 2 months later

59
Q

how do you treat patients with G6PD

A

Avoidance of the agents known to trigger hemolysis is of paramount importance like:
Hydralazine, Procainamide, Methylene blue, ASA, Sulfa drugs

Fortunately, narcotics, benzodiazepines, propofol, and ketamine are safe to use in these patients

60
Q

s/s of G6PD

A

neonatal jaundice,
acute hemolytic anemia,
chronic nonspherocytic
hemolytic anemia

61
Q

alpha thalassemia

A

Alpha-trait (2 genes) – asymptomatic with mild microcytic, hypochromic anemia

alpha thalassemia intermedia ( 3 genes affected) & Major (4 genes)

Bart’s hemoglobin – 4 gamma chains (high affinity for O2)
->hydrops fetalis and intrauterine death

62
Q

beta thalassemia

A

One Gene = silent carrier

beta thalassemia intermedia = mild to moderate reduction in beta globin chain

beta thalassemia major, or “Cooley’s anemia” – SEVERE reduction beta globin chain

Presents between 6 and 24 months of life with pallor, jaundice, growth retardation, and hepatosplenomegaly and can be fatal if untreated

Bony deformities in the face 2/2 ineffective erythropoiesis

63
Q

what is the anesthesia management for thalassemia

A

Consider face deformities
Osteoporosis
Hyperdynamic circulation
Cardiac dysfunction
Hepatic disease
Pulmonary hypertension
Thrombosis risk (anticoagulants precribed?)

64
Q

what is the most coomon inherited RBC disorder

A

sickle cell anemia

65
Q

sickle cell anemia traits

A

HbS results from substitution of valine for glutamic acid at the 6th position

Sickle Cell Anemia = Homozygous = produce only HbS

66
Q

s/s of sickle cell anemia

A

Hemolysis and recurrent vasoocclusive episodes that cause severe pain (“crises”) and lead to progressive organ dysfunction

Emotional stress, pain, infection, surgical stress ->increased vasocclusive disease, constriction, RBC trapping -> Ischemia/Infection

67
Q

lifespan of Sickle cell anemia RBC

A

10-12 days which results in anemia

68
Q

what procedure does sickle cell patients often need

A

lap chole

69
Q

sickle cell acute splenic sequestration

A

Age 1 – 4
Traps RBC in splenic sinusoids ->severe anemia, hypovolemia, shock

Tx: aggressive fluids, RBC, splenectomy

Splenic involution is complete by 5 years of age

70
Q

what is the leading complications in SCD

A

Pulmonary and neurologic complications are the leading causes of morbidity and mortality in individuals with SCD

71
Q

acute chest syndrome

A

New pulmonary infiltrate involving at least one complete lung segment on chest x-ray and is the leading cause of death in patients with SCD

72
Q

acute chest syndrome triggers

A

infection, fat embolism from bone marrow infarction, pulmonary infarction, and surgery-induced stress

73
Q

s/s of acute chest syndrome

A

Chest pain, fever, tachypnea, wheezing, coughing, and hypoxemia
Tx: broad-spectrum antibiotics, supplemental oxygen, adequate analgesia, bronchodilators, and incentive spirometry

74
Q

treatment for acute chest syndrome

A

APAP
NSAIDS
steroids
opioids
psychotropics
regional anesthesia

75
Q

indications for SCD transfusion

A

correction of a preexisting anemia
dilution of hemoglobin S concentration (to less than 30%)

76
Q

Intraoperative Management of Coagulopathies

A

Whole blood
PRBC
FFP
Cryoprecipitate
Concentrated factors
Others: TXA

77
Q

FFP facts

A

Must be frozen within 8 hours of collection to preserve labile coagulation factors V and VIII
Must be transfused within 24 hours after thawing
20 mL/kg of FFP will replace approximately 50% of most coagulation factors

78
Q

what is in FFP

A

Contain all of the clotting factors, fibrinogen (400 to 900 mg/unit), plasma proteins (particularly albumin), electrolytes, physiological anticoagulants (protein C, protein S, antithrombin, tissue factor pathway inhibitor) and added anticoagulants

79
Q

cryo facts

A

controlled thawing of FFP to 1° to 6° C to precipitate and extract the high molecular weight proteins

Each unit of cryoprecipitate has a minimum of 80 IU of FVIII activity and 15 g/L of fibrinogen

One unit of cryoprecipitate is transfused per 5 kilograms of weight and should increase a child’s fibrinogen by approximately 100 mg/dL

80
Q

One platelet concentrate per 10 kg of body weight will increase the platelet count by

A

approximately 50 × 109/L.

81
Q

random donor platelet replacement for neonates

A

5-10 ml/kg

82
Q

random donor platelet replacement for older infants

A

0.1-0.2 units/kg

83
Q

single donor platelet replacement for neonates

A

10ml/kg

84
Q

single donor platelet replacement for children

A

less than 15kg= 1/4 unit

15-30kg =1/2 unit

over 30kg = whole unit

85
Q

DDAVP facts

A

Synthetic analogue of the posterior pituitary hormone – AVP

Little effect on blood pressure (unlike vasopressin)

Does NOT stimulate ACTH release like AVP

Acts primarily at the renal collecting duct to limit the amount of water eliminated in the urine

Preferred treatment for patients with type 1 von Willebrand disease.

Increases circulating levels of procoagulant factor VIII : C and vWF

86
Q
A

Pediatric Anesthesia (5 decks)

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