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OB Final Exam > Module 7: Part 3 (71-104) > Flashcards

Module 7: Part 3 (71-104) Flashcards

1
Q

New acute lung injury/acute respiratory distress syndrome that occurs within __ hours of transfusion

A

6

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2
Q

Etiology of TRALI

A
  • host neutrophil activation in the recipient’s lung from donor factors
  • ie: anti-human leukocyte antigen (HLA) antibodies
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3
Q

T/F Is TRALI More common in multiparous donors

A

True
(more likely to carry the offending antibodies)

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4
Q

Neutrophil activation results in

A

an inflammatory pulmonary edema

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5
Q

TRALI manifests as:

A
  • Acute respiratory distress/hypoxemia
  • B/L pulmonary infiltrates/edema
  • fever (1-2oC)
  • hypotension
  • cyanosis
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6
Q

No evidence of Left Atrial hypertension (circulatory overload) with?

A

TRALI

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7
Q

Patient Factors associated with Higher TRALI incidence:

A
  • Liver surgery
  • chronic ETOH
  • higher peak airway pressures during mechanical ventilation
  • current smoker
  • positive fluid balance
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8
Q

Leading cause of transfusion-related death?

A

TRALI

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9
Q

Treatment for TRALI?

A

Stop the transfusion, Respiratory distress - O2 and ventilatory support, Hypotension - Vasopressors

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10
Q

Transfusion-associated Circulatory Overload (TACO):

A
  • Occurs in 1-8% of transfusion
  • Hydrostatic pulmonary edema d/t transfusion
  • 1 RBC is sufficient to trigger the reaction
  • may be fluid overloaded before transfusion
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11
Q

2nd most common cause of transfusion associated death?

A

TACO

Number 1: TRALI

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12
Q

TACO: Circulatory system becomes overwhelmed by:

A

High volume transfusion or a high transfusion rate

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13
Q

Signs of TACO:

A
  • Sudden dyspnea
  • orthopnea
  • Tachycardia
  • wide pulse pressure
  • Hypoxemia
  • often hypertension

If progresses to cardiac collapse → hypotension

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14
Q

TRALI vs. TACO:

A

TACO: S/S Central Venous Overload (elevated jugular venous pulse); respond well to diuretics & oxygen (Unlike TRALI)

TRALI: lung injury with is a/w antibodies directed against the lung parenchyma

TRALI: hypovolemic state
TACO: hypervolemic state

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15
Q

Treatment of Massive Blood Loss:

A
  • Blood products
  • Antifibrinolytic therapy (Tranexamic Acid-TXA)
  • Recombinant activated factor VII
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16
Q

Antifibrinolytic therapy (Tranexamic Acid-TXA):

A
  • Synthetic derivative of lysine
  • inhibits fibrinolysis & anti-inflammatory
  • high affinity for lysine binding sites of plasminogen
  • Blocks the interaction of plasminogen w/ lysine residues of fibrin
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17
Q

Antifibrinolytic therapy (Tranexamic Acid-TXA): Decreases? May attenuate?

A

Blood loss, elevation in D-Dimer and plasmin-antiplasmin complexes (markers of fibrinolysis)

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18
Q

Tranexamic Acid-TXA dosing:

A
  • Loading dose: 1 g in 100 ml IV over 10 mins
  • Second dose: in 30 min if bleeding persists
  • Early administration within 3 hours
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19
Q

Hypertension in pregnancy affects ______ % of pregnancies and is the leading cause of?

A

6-10%, maternal mortality

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20
Q

What are the classifications of hypertension in pregnancy as defined by ACOG?

A
  • Gestational Hypertension
  • Preeclampsia with/without severe features
  • Chronic hypertension
  • Chronic hypertension with superimposed preeclampsia
  • Possibly Postpartum Hypertension
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21
Q

What is the most common cause of hypertension during pregnancy?

A

Gestational hypertension

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22
Q

what is gestational hypertension?

A

New-onset elevations in BP after 20 weeks of gestation

This is w/out proteinuria and in absence of chronic HTN or systemic signs of preeclampsia

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23
Q

Gestational hypertension may be a sign of future…

A

Chronic hypertension

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24
Q

what is chronic HTN in pregnancy?

A

Essential hypertension, BP > 140/90 before pregnancy OR before 20 weeks OR fails to resolve after delivery

No thrombocytopenia or hepatic dysfunction

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25
Q

Women with chronic hypertension are at risk for developing what?

A

Superimposed preeclampsia (new onset of proteinuria or sudden increase in proteinuria or HTN, or both)

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26
Q

What are some other diseases that my exist with chronic hypertension in pregnancy?

A

Lupus, scleroderma, renal disease

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27
Q

It may be impossible to differentiate someone with preeclampsia and what disease?

A

Preexisting renal disease in chronic hypertension

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28
Q

Preeclampsia is a multi-organ disease characterized by what?

A

New onset of hypertension and proteinuria after the 20th week of gestation.

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29
Q

Preeclampsia is rarely diagnosed when?

A

Rarely before 20 weeks except in gestational trophoblastic neoplasia

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30
Q

How is preeclampsia typically diagnosed?

A

Using blood pressure increase after 20 weeks and the presence of proteinuria

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31
Q

What is the early vs late form of Preeclampsia?

A

Early form (type I): from 20 wk point to 34 wks gestation, this has high rate of reoccurrence and strong genetic component, commonly seen younger than 18 years and older than 35

Late form (type II): after 34 weeks, usually from long standing HTN, Diabetes, obesity

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32
Q

What is a disorder of unknown etiology affecting approx. 3 to 10% of all pregnancies w/most cases occurring during a woman’s first pregnancy?

A

Preeclampsia

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33
Q

What is the diagnostic criteria for pre-eclampsia without severe features?

A
  • BP > 140/90 after 20 weeks
  • 300+ mg protein in 24-hour urine
  • protein:creatinine ratio 0.3+
  • 1+ on urine dipstick specimen
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34
Q

Edema and diagnostic criteria for preE?

A

No longer a diagnostic criteria because it is not specific enough, a lot of moms are edematous

35
Q

What are classic clinical manifestations of preeclampsia with severe features: (BP, PLT, Cr, UOP)

A
  • Blood pressure > 160 /110 mm Hg
  • Thrombocytopenia < 100,000/mm3
  • Creatinine > 1.1 mg/dL (or AST & ALT >2X the baseline)
  • Oliguria (urine output < 500 ml/24 hours) or small gestation
  • Pulmonary edema
  • Persistent right upper quadrant pain
  • Visual disturbances
36
Q

T/F: preeclampsia can only be diagnosed with both hypertension and proteinuria.

A

False, can now be diagnosed if they have other symptoms with no other causes even if they do not have proteinuria

37
Q

Central nervous system involvement is the determining diagnostic factor for what?

A

Eclampsia, only happens to about 0.6% of moms with preeclampsia with severe features

38
Q

How would we diagnose a new onset of seizures or unexpected coma during pregnancy or the postpartum period in pre-eclamptics moms without a preexisting neurologic disorder?

A

Eclampsia

39
Q

When do most seizures occur with eclampsia?

A

Intrapartum or within the first 48 hours after delivery

40
Q

How long after delivery can late eclampsia happen?

A

From 48 hours after delivery to 6 weeks postpartum

41
Q

Eclampsia has a high rate of ________ and is associated with what?

A

Perinatal death
Associated with placental abruption, fetal growth restriction, & extreme prematurity

42
Q

What is a primary sign of eclampsia present in 80% of patients?

A

80% have headache and visual disturbances

Can also have: photophobia, epigastric or RUQ pain, hyper-reflexia, altered mental status either before or after seizures (photophobia is hard to distinguish from PDPH)

43
Q

What are the immediate OB goals for a mom with eclampsia?

A

Stop seizures, blood pressure control, patent airway, and deliver the baby

44
Q

What are the anesthetic goals for eclampsia?

A
  • Assess seizure and neurologic function
  • Airway
  • Fluid balance (restrict to decrease cerebral edema)
  • BP control
  • Monitor and follow labs
45
Q

HELLP is considered a subtype of what syndrome?

A

Severe Preeclampsia, but not everyone with severe preeclampsia has help, so it is not the same thing

46
Q

What are the AST, ALT & platelet counts seen with HELLP?

A

AST > or = 70 IU/L
ALT elevated
Platelets usually < 100,000 per mm3

47
Q

What are the blood pressure and proteinuria levels seen in HELLP?

A

Blood pressure can be normal in 15% of the cases, and may not have proteinuria

48
Q

HELLP is associated with what complications?

A

DIC
placental abruption
pulmonary edema
acute renal failure
liver hemorrhage/failure
ARDS
sepsis
stroke
death

49
Q

What does HELLP stand for?

A

Hemolysis, Elevated Liver enzymes, Low Platelets

50
Q

What is the hallmark sign of HELLP?

A

Presence of microangiopathic hemolytic anemia (a subset of anemia caused by destruction of RBC caused by factors in the small blood vessels)

51
Q

Hemolysis in HELLP a/w what bilirubin/LDH levels?

A

Increased bilirubin > 1.2 mg/dl and increased LDH > 600 IU/L

52
Q

What are some maternal symptoms of HELLP?

A
  • RUQ pain
  • N/V
  • headache
  • hypertension
  • proteinuria
53
Q

When do we want to deliver the baby if mom has HELLP?

A

As soon as possible

54
Q

What are some anesthesia consideration for HELLP?

A

Platelets may fall quickly

A drop in platelets by 30-40 thousand between two lab draws = epidural asap for immediate delivery

55
Q

Rupture of a subscapular hematoma of the liver may occur with?

A

HELLP syndrome

56
Q

Clinical management of HELLP:

A
  • Mag & antihypertensives
  • general or regional
  • Decadron and platelet count
  • platelet transfusion (<20K platelets)
  • LARGE IVs
57
Q

Preeclampsia with/without severe systemic organ involvement and seizures can first develop when?

A

In the postpartum period, probably compounded by early discharge, usually presents within 7 days of delivery

58
Q

“Late postpartum hypertension?”

A

Normotensive during gestation but develops hypertension from 2-6 weeks postpartum (she said 6 months & 140/90 and above)

Sometimes called pregnancy induced hypertension

59
Q

In what population is preeclampsia more common?

A

Primarily disorder of older, nulliparous women

young mom, old mom, more black & hispanic populations

60
Q

What is the incidences of pre-eclampsia?

A

Between 3-4%
25% are preeclamptic with severe features

61
Q

______ is one of the top three leading causes of maternal mortality (usually due to?)

A

Preeclampsia
Usually due to pulmonary edema and intracranial hemorrhage

62
Q

Neonatal mortality from PP HTN/PreE due to:

A

Impaired uteroplacental perfusion, placental abruption, and prematurity due to early onset disease

63
Q

What are risk Factors for developing Preeclampsia?

A
  • First pregnancy, family history of preeclampsia
  • > 40 years old, teens
  • Chronic HTN and Chronic renal disease, Diabetes, Vascular or connective tissue disease
  • Multiple gestation, in vitro fertilization
  • Obesity, Hispanic or Black race
64
Q

What are some protective factors of Preclampsia?

A

Smoking because nicotine inhibits thromboxane A-2 synthesis and/or simulates of nitric oxide release

65
Q

T/F: the fetus causes preeclampsia.

A

False, the placenta does & delivery of the placenta causes resolution of the disease

66
Q

Manifestations of Preeclampsia: Maternal Syndrome:

A

Hypertension, Proteinuria With/Without other systemic abnormalities

67
Q

Manifestations of Preeclampsia: Fetal Syndrome:

A

Fetal growth restriction, Oligohydramnios, Abnormal oxygen exchange

68
Q

Which etiology is consistent with vascular endothelial injury?

A

Preeclampsia

69
Q

Preeclampsia is a 2-stage disorder. What is the second stage?

A

Symptomatic second stage, caused by reduced perfusion of the intervillous space

Second stage: antiangiogenic factors from the intervillous space relased into circulation = endothelial dysfunction & systemic inflammatory response

70
Q

The 2nd stage of Preeclampsia is characterized by what?

A

Release of antiangiogenic (ability to grow new vessels) factors from the intervillous space into maternal circulation = widespread maternal endothelial dysfunction & accentuated systemic inflammatory response

71
Q

T/F: preeclampsia can occur without a fetus.

A

true

72
Q

In a normal pregnancy, what does the endothelium do?

A
  • Prevents platelet activation
  • Activates circulating anticoagulants
  • Buffers the response to vasopressors
  • Maintains fluid in the vascular compartment
73
Q

In Preeclampsia, normal endothelium functions are disrupted causing what?

A
  • Development of HTN and proteinuria
  • increased risk for HELLP, eclampsia and other end-organ damage
  • Usually manifest after 20 weeks gestation
74
Q

How does preeclampsia effect immune function?

A

Immune maladaptation

75
Q

During preeclampsia, macrophages, natural killer(NK) cells and dendrite cells are found in greater density where? Resulting in?

A

In the decidua, this causes impaired trophoblast invasion (excess inflammation)

76
Q

Aberrant hemostatic activation in preeclampsia causes what?

A

Abnormal placentation

77
Q

Increased tissue factor expression results in:

A

Activation of the clotting pathways in preE

78
Q

Abnormal protease-activated receptor 1
(PAR 1)
seen in?

A

Preeclampsia

79
Q

____ _____ to the angiotensin type 1 receptor (AT1) are involved in preE and result in?

A

Agonistic autoantibodies

increased production of soluble fms-like tryosine kinase-1 (sFLT-1) causing hypertension and proteinuria

80
Q

Prevailing hypothesis for preE:

A

Placenta becomes relatively hypoxic as pregnancy progresses
⬇️
overexpression & release of antiangiogenic factors
(sFlt-1 and soluble endoglin (sEng)
into maternal circulation

81
Q

Predominance of thromboxane w/ associated with?

A

Vasoconstriction, platelet aggregation, decreased uterine blood flow, and increased uterine activity

82
Q

______ has the opposite effect thromboxane

A

Prostacyclin

83
Q

______ may help prevent or decrease the severity of preeclampsia by?

A

Aspirin, inhibiting thromboxane production

start @ 12-14 weeks if high risk Pre-E

OB Final Exam (15 decks)

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