CIS Resp Case 2 Flashcards

1
Q

What is GTPAL in regards to obstetrical history taking?

A
G = Gravidity = number of total pregnancies
T = term birth = term deliveries, (full) births (38 weeks or more)
P = preterm birth = preterm deliveries (from viability up to 37 weeks)
A = abortions/miscarriages = both surgical abortions and miscarriages
L = living children
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2
Q

What is a total hysterectomy?

A

Take uterus and ovaries, usually but not always cervix, too

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3
Q

CAD risk factors

A

Emotional stress

No exercise

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4
Q

Cause of S2 splitting during cardiac exam

A

Physiologic splitting of S2 on inspiration can be normal
Persistent splitting of S2 during inspiration and expiration can be sensitive and specific screening for
-heart disease in adults, most likely cause being RBBB
-RV pressure overload situations such as acute massive PE

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5
Q

What can be heard on pulmonary exam of pt with PE, 53% of the time?

A

Rales

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6
Q

What is an invasive by highly accurate way of measuring blood pressure constantly?

A

Arterial line (excellent in pts with any type of shock)

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7
Q

What labs are used to check for inherited thrombophilia?

A

Activated protein C/Factor V Leiden
Homocysteine level
Functional assays of antithrombin III/protein C/protein S
Antiphospholipid Abs

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8
Q

What is the most common finding on EKG in pt with PE?

A

Nonspecific ST-T wave abnormalities and sinus tachycardia

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9
Q

Gold standard imaging choice for PE?

A
CT angiogram (CTA) of chest (PE protocol) (spiral CT)
Need to consider stability of pt before taking him to radiology
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10
Q

what can be seen on EKG that is indicative of PE?

A

S1Q3T3 (S in lead I, Q in lead III, inverted T in lead III)

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11
Q

What is tPA?

A

Recombinant tissue type plasminogen activator (tPA, “alteplase”), “clot buster”
tPA is a naturally occurring enzyme produced by number of tissues including endothelial cells
It binds to fibrin, which increases its affinity for plasminogen and enhances plasminogen activation
Systemic thrombolysis preferred as more widespread availability and can give it rapidly as compared to taking to cath lab for angiogram and direct injection to clot itself

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12
Q

What are potential indications for thrombolytic therapy in venous thromboembolism?

A
Presence of hypotension related to PE
Presence of severe hypoxemia
Substantial perfusion defect
Right ventricular dysfunction associated with PE
Extensive deep vein thrombosis
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13
Q

What hormones are pro-thrombotic?

A

Hormone replacement therapy (HRT) of premarin (estrogen)

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14
Q

What is Factor V Leiden (FVL)? Discuss mutation

A

Mutant form of coagulation factor V
FVL mutation renders factor V (both activated and inactivated) insensitive to actions of activated protein C (aPC), a natural anticoagulant
As a result, pt who inherits mutation is at increased risk of venous thromboembolism (VTE)
FVL is extremely common in population, and many pts will never have VTE
VTE risk reduction (both primary prevention and recurrence prevention) involves challenging decisions

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15
Q

what is Virchow’s triad?

A

Pathogenesis of thromboembolism (VTE)

  • Alterations in blood flood (stasis)
  • Vascular endothelial injury
  • alterations in constituents of blood (inherited or acquired hypercoagulable state)
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16
Q

What are inherited thrombophilias that are risk factors for development of venous thrombosis?

A
Factor V Leiden mutation
Prothrombin gene mutation
Protein S deficiency
Protein C deficiency
Antithrombin (AT) deficiency
17
Q

What are acquired disorders that are risk factors for development of venous thrombosis?

A
Malignancy
Presence of central venous catheter
Surgery, especially orthopedic
Trauma
Pregnancy
Oral contraceptives
Hormone replacement therapy
Tamoxifen, thalidomide, lenalidomide
Immobilization
Congestive failure
Antiphospholipid antibody syndrome
Myeloproliferative disorders (polycythemia vera, essential thrombocythemia)
Paroxysmal nocturnal hemoglobinuria
Inflammatory bowel disease
Nephrotic syndrome
18
Q

What is Well’s Criteria?

A

Clinical symptoms of DVT (leg swelling, pain with palpation) = 3
Other diagnosis less likely than PE = 3
HR>100 = 1.5
Immobilization (>3 days) or surgery in previous 4 weeks = 1.5
Previous DVT/PE = 1.5
Hemoptysis = 1
Malignancy = 1

Traditional probability
High >6
Moderate 2-6
Low <2

Simplified (Modified Wells)
PE likely >4
PE unlikely <4

19
Q

What are absolute contraindications to fibrinolytic therapy for DVT or acute PE?

A

Prior intracranial hemorrhage
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months (excluding stroke within 3 hrs)
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-heart trauma or facial trauma within 3 months

20
Q

What are relative contraindications to fibrinolytic therapy for DVT or acute PE?

A

History of chronic, severe, poorly controlled HTN
Severe uncontrolled HTN on presentation (SBP>180 mmHG or DBP>110 mmHG)
History of ischemic stroke more than 3 months prior
Traumatic or prolonged (>10 min) CPR or major surgery <3 weeks
Recent (within 2-4 weeks) internal bleeding
Noncompressible vascular punctures
Recent invasive procedure
For streptokinase/antistreplase: prior exposure (more than 5 days ag) or prior allergic reaction to these agents
Pregnancy
Active peptic ulcer
Pericarditis or pericardial fluid
Current use of anticoagulant (warfarin sodium) that has produced elevated international normalized ratio (INR) >1.7 or prothrombin time (PT) > 15 sec
Age > 75 years
Diabetic retinopathy

21
Q

Hemodynamic profile of hypovolemic shock

A

Preload (pulmonary capillary wedge pressure)
-same (early) or decreased (late)

pump function (cardiac output)
-same (early) or decreased (late

afterload (systemic vascular resistance)
-increased

tissue perfusion (mixed venous oxyhemoglobin saturation)
>65% (early) or <65% (late)
22
Q

Hemodynamic profile of cardiogenic shock

A

Preload (pulmonary capillary wedge pressure)
-Increased

pump function (cardiac output)
-decreased

afterload (systemic vascular resistance)
-increased

tissue perfusion (mixed venous oxyhemoglobin saturation)
<65%
23
Q

Hemodynamic profile of distributive shock

A

Preload (pulmonary capillary wedge pressure)
-same (early) or decreased (late)

pump function (cardiac output)
-Increased or decreased (occasionally)

afterload (systemic vascular resistance)
-decreased

tissue perfusion (mixed venous oxyhemoglobin saturation)
>65%
24
Q

Hemodynamic profile of obstructive shock: PE, PH, tension pneumothorax

A

Preload (pulmonary capillary wedge pressure)
-same (early) or deceased (late)

pump function (cardiac output)
-same (early) or decreased (late)

afterload (systemic vascular resistance)
-increased

tissue perfusion (mixed venous oxyhemoglobin saturation)
->65%
25
Q

Hemodynamic profile of obstructive shock: pericardial tamponade

A

Preload (pulmonary capillary wedge pressure)
-Increased

pump function (cardiac output)
-decreased

afterload (systemic vascular resistance)
-increased

tissue perfusion (mixed venous oxyhemoglobin saturation)
<65%
26
Q

What is mean arterial pressure (MAP)?

A

Diastolic BP + ((systolic BP - diastolic BP)/3)
>65 = good perfusion to all organs
< 65 = hypotension/hypoperfusion