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26 Cards in this Set

  • Front
  • Back
Hyperemia
Local Inc in Vol of Bld
Active= local A. dilate
Passive= COngestion
Acute Passive Congestion
Shock, Sudden R-side Hrt Fail
Chronic Passive Congestion
L-Side Hrt Fail, Mitral Stenosis
Intra-Alveolar Hemosiderin Laden Macrophg= HrtFail Cells
Nutmeg Liver
dilated/congested Cent V and srrnding brwn/yellow fatty liver cells
Bc R-side Hrt Fail
(liver gets congested)
White Infarct
Heart, Spleen, Kidney
Red Infarct
Lung, GI
Bc redundant bld supply
Hemorrhage into infarct
Thrombosis
V. Stasis, CHF, Polycythemia, Sickle Cell, Visceral Malig, OC
Stabilize Platelet Plug
Fibrinogen Bridges
and Fibrin
Limit Platelet Plug Form
Prostacyclin (PGI2)
From Endothel Cells
Antag TXA2 so limit further Platelet Agg
Extrinsic Coag Path
Init by Tissue Factor
Eval by PT
Meas Factor 2, 5, 7, 10, and fibrinogen
Intrinsic Coag Path
Involve all Clot Factors (except 7,13)
Contact Activation: Factor12 (Hageman), PreK, HMWK, Factor11
Eval by PTT
Meas 2,5,8,9,10,11,12,Fibrinogen
Fibrinolysis
Pro-Enz Plasminogen to Plasmin (most imp fibrinolytic protease)
Splits Fibrin
Factor 5 Leiden
Most commn Hered Thrombophila
Abnrm Factor5 w/alt cleavage site for ActProtC
"Hereditary Resistnce to APC"
PT 20210A Transition
(Thrombophilia)
G to A Mut in 3'UTR of PT
Elev PT levels
Methylene THF Reductase Mut
(Thrombophilia)
Inc serum Homocysteine
A&V Thrombosis, Inc risk NT defect
supplemnt Folic Acid
Antiphospholipid Ab Synd
Prothrombotic D/O
V&A thromboemboli, Fetal loss, Thrombocytopenia
Incidental bc Elev PTT (paradoxical)
Some SLE (Lupus Anticoag)
Heparin Induced Thrombocytopenia
Ab to Hep-Platelet Cmplx
Arterial Thrombi
Lines of Zahn
(Drk platelet/Light fibrin)
Venous Thrombi
Drk Red
Bc grtr conc RBCs
Paradoxical Emboli
L-Side Emboli that arise in V. Circ
Access to A by RtoL Shunt
Fat Emboli
Chunks of Bone Marrow
Bc Severe/Mult Fractures
Fat Emboli Synd= Pulmo distress, Cut Petechia, Neuro manifest
Edema
Inc Hydrostatic Press (CHF)
Inc Cap Perm (inflam/burn)
Inc Na Retention (renal/CHF)
(Dec CO=Dec RBF=Act RAAS)
Anascara
Generalized Edema
Transudate
Non-Inflam
Bc Alt Intravasc Hydrostatic/Osmotic Press
Low Prot/SpecGrav<1.012
Exudate
Bc Inflam Inc Vasc Perm
High Prot/SpecGrav>1.02
But GLu low Bc leukos consume
Shock Stages
Nonprogressive (Early):
Compensatory Mech maint perfus
Progressive: Tiss Hypoperfus, Metab Acidosis
Compens no longer adeq
Irreversible: survival not possible