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OB Final Exam > Crash Course Module 9 > Flashcards

Crash Course Module 9 Flashcards

1
Q

which coag factors are increased in pregnancy

A

I, VII, VIII, IX, X, XI

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2
Q

1mg of protamine can neutralize ____________ of IV heparin

A

100 U

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3
Q

maternal side effects of protamine

A
  • hypotension (histamine release)
  • hypersensitivity/anaphylaxis
  • pulmonary hypertension
  • noncardio pulmonary edema
  • coagulation issues r/t thrombocytopenia
  • altered platelet aggregation
  • fibrinogen precipitation
  • reduced thrombin effect
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4
Q

AFE patho

A

Fetal material in maternal circulation can trigger massive cascade of inflammatory & hemostatic reactions
⬇️
CV collapse and DIC

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5
Q

AFE is traditionally diagnosed clinically by:

A

Acute respiratory distress
CV collapse
Coagulopathy

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6
Q

tissue factor binds to factor

A

VII

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7
Q

what activates the extrinsic pathway

A

factor VII

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8
Q

what triggers clotting

A

factor X

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9
Q

classic triad of AFE

A

respiratory distress, CV collapse and
coagulopathy near the time of delivery

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10
Q

AFE is a problem with which cardiac parameters

A

preload and cardiac output

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11
Q

____________ and ____________ can block serotonin and vagal stimulation, improving cardiovascular function with AFE

A

atropine and ondansetron

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12
Q

you can block the cause of coagulopathy by inhibiting thromboxane with

A

ketorolac

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13
Q

most cases of VTE in pregnancy are caused by

A

DVT

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14
Q

greatest risk increase for VTE is associated with which factor

A

V Leiden mutation

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15
Q

Virchow’s triad

A
  1. venous stasis
  2. vascular damage
  3. hypercoagulability
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16
Q

RV failure s/s

A

Split second heart sound, Jugular venous distention

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17
Q

where do most DVTs occur in pregnancy

A

left leg (88%)

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18
Q

D-dimer levels are ____________ in pregnancy

A

elevated

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19
Q

LMWH does not affect

A

aPTT

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20
Q

unfractionated heparin binds to

A

antithrombin III

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20
Q

unfractionated heparin potentiates

A

inactivation of other coagulation factors
ie: thrombin (factor IIa)

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21
Q

what lab should be checked with unfractionated heparin

A

aPTT q6 hrs

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22
Q

when should patient be transitioned from LMWH to UFH

A

36 weeks

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23
Q

when should UFH be discontinued

A

4-6 hrs before neuraxial/delivery

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24
Q

when should ASA be stopped in patients receiving thromboembolism prophylaxis

A

35-36 wks

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25
Q

Highest risk of thrombotic events are in

A

the first week postpartum

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26
Q

VAE occurs when the surgical field

A

is above the level of the heart

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27
Q

Millwheel murmur is associated with

A

VAE

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28
Q

s/s VAE

A

Sudden and dramatic hypotension, hypoxemia, dyspnea

Chest pain during uterine repair

Millwheel murmur

Right-sided heart failure, rhythm changes

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29
Q

during normal pregnancy, plasma volume ↑ by

A

approx 50%

but RBC ↑ by only 30% (dilutional anemia)

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30
Q

the most common cause of anemia in pregnancy

A

iron deficiency

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31
Q

thalassemias patho

A

A group of microcytic, hemolytic anemias that results from the reduced synthesis of one or more of the polypeptide globin chains

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32
Q

reduced synthesis in thalassemia leads to

A
  1. An imbalance in globin chain ratios
  2. Defective hemoglobin
  3. Erythrocyte damage resulting from excess globin subunits
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33
Q

silent carriers for α- thalassemia have ____________ functioning genes

A

3

34
Q

α- thalassemia trait has ____________ functioning genes

A

2

35
Q

hemoglobin H diseases has ____________ functioning gene

A

1

36
Q

αº- thalassemia or Bart’s hydrops

A

no functioning genes

incompatible with life

fetus usually dies of hydrops fetalis

37
Q

Rh incompatibility can cause

A

hydrops fetalis

Rh - mom & Rh + baby

38
Q

β- thalassemias have

A

one gene on each chromosome 11

39
Q

β- thalassemia patho

A

The production of β-chains is reduced
Usually have an excess of alpha chains that accumulate in RBC precursors

40
Q

it is unusual for patients with ____________ to get pregnant

A

β- thalassemia major

41
Q

if pregnant with β- thalassemia major…

A

Metabolic demands of pregnancy increase transfusion requirements

Goal: keep hgb >10 g/dL

Chelation agents are stopped in the first trimester

Increased incidence of spontaneous abortion, intrauterine fetal death & growth restriction

42
Q

β- thalassemia minor patients should receive high-dose ____________ during first trimester

A

folate

43
Q

Incidence of ____________ are more common with β- thalassemia minor

A

fetal growth restriction and oligohydramnios

44
Q

sickle cell disorder

A

refers to a state in which erythrocytes undergo sickling when
they are deoxygenated

45
Q

sickle cell disorder is characterized by….

A

a homozygous mutation (hemoglobin S)
where valine is substituted for glutamic acid in the B-chain

46
Q

main hgb in sickle cell anemia

A

Hgb S

47
Q

most important determinate in sickling

A

oxygen tension

48
Q

Factors that can increase the sickling risk:

A

Dehydration leading to increased blood viscosity
Hypotension causing vascular stasis
Hypothermia
Acidosis

49
Q

typical Hgb in sickle cell anemia

A

6-8 g/dL

50
Q

____________ are ↑ in sickle cell anemia

A

reticulocytes

51
Q

sickle cell pregnancy risks

A

Increased incidence of preterm labor, placental abruption, fetal growth restriction, preeclampsia, and eclampsia

52
Q

hgb goal in sickle cell

A

> 8 g/dL

53
Q

primary hemostasis

A

formation of a
friable platelet plugs

primary:(vWF) platelets adhere to exposed collagen; unstable platelet plug

secondary: deposition & stabilization of fibrin

54
Q

secondary hemostasis

A

coagulation; reinforcement of the friable platelet
plug by the formation of a firm fibrin
clot

55
Q

fibrinolysis

A

clot lysis and restoration of
blood flow through the recanalized
vessel

56
Q

Fibrinogen and fibrin degradation products are
____________ in normal pregnancy

A

↑

57
Q

is thrombocytopenia a specific indicator of DIC

A

no , sensitive indicator of DIC

58
Q

what happens to PT and aPTT during pregnancy

A

shortened

59
Q

gestational thrombocytopenia

A

most common cause of thrombocytopenia
in pregnancy

Usually considered a platelet count below 150

60
Q

autoimmune thrombocytopenia purpura (ATP)

A
  • increased platelet destruction byIgG antibodies
  • antibodies against platelet antigens are produced primarily in the spleen, where phagocytosis by macrophages occur.
  • Also can occur in liver & bone marrow
61
Q

____________ are administered if the platelet count is < 20-30k before
the onset of labor or <50k at the time of delivery

A

corticosteroids

62
Q

____________ is the hallmark of thrombocytopenia purpura (TTP)

A

DIC

63
Q

TTP is associated with deficiency of

A

enzyme ADAMTS13

64
Q

____________ is responsible for cleaving vWF multimers

A

ADAMTS13

65
Q

what differentiates TTP from DIC

A

The presence of vWF (but not fibrinogen) in platelet aggregates helps differentiate TTP from DIC. (In patients with DIC, fibrinogen but not vWF is found in platelet aggregates.)

66
Q

vWF 2 primary roles in coagulation

A

it forms a complex with factor VIII

it mediates platelet adhesion by binding to platelets
and collagen

67
Q

most common congenital bleeding disorder

A

Type 1 von Willebrand’s disease

68
Q

DDVAP can be used to treat…in pregnancy

A

type I or 2A von Willebrand’s disease

69
Q

for acute bleeding a/w von willebrand’s disease, ____________ can be administered

A

FFP or cryoprecipitate

70
Q

DIC leads to formation of large amounts of

A

thrombin

71
Q

DIC leads to activation of

A

the fibrinolytic system

72
Q

DIC depletes

A

coagulation factors

73
Q

most frequent causes of DIC

A
  • Preeclampsia
  • placental abruption
  • sepsis
  • retained dead fetus syndrome
  • PPH
  • acute fatty liver of pregnancy
  • AFE
74
Q

most common thrombophilia in pregnancy

A

Factor V Leiden mutation, prothrombin mutation, protein C deficiency, protein S deficiency, and antithrombin III

75
Q

most common hereditary thrombophilia

A

factor V leiden

76
Q

factor V leiden patho

A
  • factor V gene point mutation
  • a single amino acid switch (arginine to glutamine)
  • resistant to inactivation by activated protein C
77
Q

antithrombin III deficiency inactivates…

A

thrombin and factors IXa, Xa, XIa, and
XIIa

78
Q

antithrombin III is synthesized in

A

liver and endothelial cells

79
Q

heparin potentiates

A

activity of antithrombin III

UFH:
potentiates inactivation of other coagulation factors (thrombin/IIa)
binds to antithrombin III

80
Q

protein C deficiency patho

A

Occurs when the gene for protein C on both chromosomes #2 is affected

81
Q

protein C is….

A
  • vitamin K-dependent protein
  • synthesized in the liver
  • inhibits coagulation by proteolytic activation of factors V and VIII
82
Q

risk for thrombosis with protein C deficiency

A

is increased x5

83
Q

protein S acts as a cofactor for

A

protein C

OB Final Exam (15 decks)

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