Respiratory CIS high yield handout 2 Flashcards
wells criteria 1.0 pts
malignancy
hemoptysis
what does GTPAL for obstetrical history taking stand for
G= gravidity (# of pregnancies)
Term births (term deliveries (full) births (38 wks or more)
Preterm births (preterm deliveries from viability up to 37 wks
Abortions/miscarriages
Living children
potential indications for thrombolytic therapy in venous thromboembolism
presence of hypotension related to PE presence of severe hypoxemia substantial perfusion defect RV dysfunction assocaited with PE extensive DVT
labs to consider checking for inherited thrombophilia
activated protein C/factor V leiden
homocysteine level
antithrombin III/protein C/protein S assay
antiphospholipid antibodies
what is tPA
clot buster
naturally occurring enzyme produced by endothelial cells
binds fibrin, increases its affinity for plasminogen and enhances its activation
are hormones pro thrombotic
yes
HRT and estrogen
S2 splitting during cardiac exam
physiologic splitting of S2 on inspiration can be normal
persistent splitting of S2 during inspiration and expiration can be sensitive and specific for
- heart disease in adults, most likely RBBB
- RV pressure overload situations such as acute massive PE
managment if no personal or family history of VTE but have antithrombin deficiency
propylatic anticoag postop, during pregnacny, and postpartum
types of shock
hypovolemic
cardiogenic
distributive
obstrucive (PE, tension pneumothorax) (pericardial tamponade)
managment of thrombofilia with family history of VTE only (no personal history of it themselves)
if no other risk factor then routine care and education
if other risk factors: prophylactic antigcoag postoperatively, during pregnancy and postpartum
what is virchow’s triad
alteration in blood flow
vascular endothelial injury
alteration in constituents of blood
VTE risk
wells criteria 3.0 pts
clinical symptoms of DVT
other diagnosis less likely than pulmonary embolism
what can be seen on ekg that is indicative of PE
S1 Q3 T3
S in lead 1
Q in III
inverted T in III
management of acute VTE
anticoag for at least 3-6 months
possible indefinite anticoag if:
- unprovoked VTE
- life threat PE
- male
- VTE at odd site
- strong family history of VTE
other risk factors of VTE
homozygous or compound heterozyougs for defect
or FVL or antithrombin defiecnicy
VTE in family member less than 50