PSYCH 1XX3 Lecture 7: 23
19 May 2018
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1.23 – MALIGNANCY ASSOCIATED THROMBOGENESIS
1. Cancer is a big risk factor for development (and recurrence) of VTE
• annual incidence is roughly 1:200
o although it could be higher than this because asymptomatic VTE is common and
unaccounted for, and clinical manifestations are non-specific due to background disease
• There is a 4-7x increased risk of VTE in cancer patients
• VTE is the second biggest killer in cancer patients; 1 in 7 cancer px die of a PE
o the longer the time between cancer and VTE diagnosis (presumably because of undetected,
asymptomatic disease) –t he greater the risk of dying
• Other VTE risk factors are age, stasis/surgery, family history of VTE, varicose veins, CHF/MI/Stroke,
lower leg fractures, OCP/HRT/pregnancy
• Idiopathic VTE may be a predictor of occult malignancy
• Tumour type/site influences risk of VTE:
RR
site
baseline risk
lung, colon, breast, ovary,
prostate
intermediate risk
>17x
leukaemia, liver,
cervical/uterus
highest risk
>25x
pancreas, lymphoma, brain
• Anti-tumour therapy may play a role in increasing
VTE risk too
o chemo (eg Thalidomide and Lenolidomide in
Multiple Myeloma)
o hormones
o surgery/immobility
2. The pathogenesis of VTE in cancer is complex and
probably poorly understood
• It is possible that malignant cells induce
monocytes/macrophages to produce TF
• Worth noting that cancer patients can often have
other co-exisiting thrombophilias eg F5 leiden
• some tumours eg adenocarcinoma produce pro-thrombotic mucin
3. The management/secondary prophylaxis of VTE in cancer may switch to long term use of LMWH
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Idiopathic vte may be a predictor of occult malignancy: tumour type/site influences risk of vte: baseline risk intermediate risk highest risk. >25x: anti-tumour therapy may play a role in increasing. Vte risk too: chemo (eg thalidomide and lenolidomide in. Multiple myeloma: hormones, surgery/immobility, the pathogenesis of vte in cancer is complex and probably poorly understood. Defects (dic/cpb/hus: dic is an excessive and inappropriate activation of coagulation which is always secondary to an underlying disorder. Increased degradation (by neutrophils) of antithrombin +/ impaired synthesis of antithrombin. [snake venoms activate factor 10/2: high levels of pai-1 which depresses fibrinolysis. There are four main causes of dic: cancer (acute leukaemia, obstetric (septic abortion, placental abruption, Infections (g-ve sepsis, malaria) eclampsia) tissue necrosis (burns, trauma, liver disease) <50 (cid:858)(cid:373)oderate i(cid:374)crease(cid:859) prolonged by >6s (cid:858)stro(cid:374)g i(cid:374)crease(cid:859) The surface is lined with polyurethane, polypropylene and pvc: preventing excessive blood loss in cardiac surgery reduced mortality and decreases need for transfusions.
