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thrombophilia Flashcards

1
Q

give a general explanation of thrombophilia

A
  • procoagulation is enhanced

- pathological formation of a thrombis (clot)

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2
Q

where can thrombis formation occur?

A

arteries and veins

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3
Q

what are the early stage effects of a thrombis? (2)

A
  • ishcemia (restriction of blood flow)

- hypoxia (deprivation of cells/tissues from oxygen)

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4
Q

what are the late stage effects of a thrombis? (1)

A

infarction (nercrosis/tissue death due to long term deprivaton of oxygen)

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5
Q

define embolisation

A

severe complication where thrombis breaks from site of formation (now called embolus) and travels through circulation and becomes lodged in the lungs

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6
Q

where do venous thrombosis’ genrally occur?

what are the two classifications of a venous thrombosis?

A
  • in veins thrombi form at the valves bs high levels of turbulance
  • can occur superficially or deep
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7
Q

define superficial thrombophlebitis

what is the risk of embolism for these patients?

A
  • characterized by localized pain along the vein with red streak-like patterns
  • can usually palpate the thrombis
  • risk of embolism = low
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8
Q

where is deep venous thrombosis (DVT) most common?
what is the risk of embolism for these patients?
what is a life threatening posibility from this pathology?

A

-most common in leg
-proximal DVTs (above knee) are more likely to embolize
than distal DVTs
-pulmonary embolism (PE) can occur when DVT embolizes and travels through heart and lodges in pulmonary circulation

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9
Q

is venous thromboembolism (VTE) more common in men or women?

A

men

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10
Q

does the risk of VTE increase or decrease with age?

A

increases

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11
Q

50% of the time the cause of VTE is:

other 50%?

A
  • uknown (idiopathic)

- associated with other risk factors

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12
Q

5-8% of the population have ______ that increase their risk of thrombophilias

A

genetic risk factors

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13
Q

in addition to genetic risk factors, ______ factors can accumulate over a lifetime

A

acquired risk factors (environmental/pathological)

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14
Q

in combination to genetic and/or aquired risk factos there can be ______ that lead to the development of a venous thrombosis

A

acute triggering events

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15
Q

what are inherited risk factors that increase the risk of developing a venous thrombosis?

A
  • increase coagulation factor activity
  • decrease in anticoagulatn proteins
  • abnormalities in the fibrinolytic system
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16
Q

what are acquired factors that increase the risk of developing a venous thrombosis?

A
  • acute/triggering risk factors (immobilization, surgery, estrogen)
  • chronic or more permanent risk factors (cancer, obesity, history of blood clots)
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17
Q

explain relative risk

why do we have this term?

A
  • every risk factor does not contribute equally to the development of the disorder
  • instead have an associated relative risk (ratio of the probability of an outcome in an exposed grp to the prob of an outcome in an unesposed grp)
  • e.g. for thrombophilia - likelihood an individual w a risk factor develops a thrombis vs someone wout that risk factor
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18
Q

explain 2 techniques for diagnosing DVT

A

(1) venography (GOLD STANDARD) - IV is inserted into patients foot and die is injected for x-ray imaging
(2) compression ultrasonography (MOST COMMON) - probes placed on the skin to compress veins where DVTs suspected, veins are compressible but DVT is not

19
Q

what are possible signs and symptoms of DVT?

A
  • shortness of breath
  • pleuritic chest pain
  • cough
  • leg pain
  • tachycardia
  • pleural rub
  • syncope
20
Q

explain 2 techniques for diagnosis a PE

A

(1) pulmonary angiography (GOLD STANDARD) - contrast die injected via catheter inserted into groin and threaded up to pulmonary circulation followed by imaging (thrombus appears as filling defect or cutt off of blood flow)
(2) CT pulmonary angiography (MOST COMMON) - die delivered through IV then CT imaging

21
Q

limitations to pulmonary angiography

A
  • invasive
  • need well trained physician
  • only offered at tertiary centrs
  • cost
  • risk of neurotoxicity due to die
22
Q

benefits/risk of CT pulmonary angiography

A
  • increased availability bc IV not catheter to heart
  • lower cost
  • dont need as trained person
  • risks worth it bc PE is life threatening
23
Q

explain the 3 goals of management of VTE

A

(1) to prevent thrombus extension/embolisation/recurrance
(2) prevent post-thrombic syndrome
(3) thrombolysis only in most severe cases

24
Q

are PE and DVT treated the same?

A

yes

25
Q

why do we only use thrombolysis in most severe cases?

A

serious risk of adverse bleeding bc breaks down clot formation

26
Q

when is treatment via thrombolysis appropriate?

A

(1) presence of hypotension (low bp related to PE)
(2) severe hypoxemia (low o2 related to PE)
(3) severe right sided heart failure (related to PE)
(4) cases of extensive/severe DVT

27
Q

what is the most common thrombolytic?
how is it administered?
what is its mechanism of action?

A
  • tissue plasminogen activator (tPA)
  • given intravenously when thromolysis is required
  • converts plasminogen to plasmin - promotes breakdown of thrombus into degredation products
28
Q

if a patient has a clearly identifiable reversible risk factor (e.g. birth control), how long would treatment with an anticoagulant last?

A
  • remove the risk factor

- treatment lasts 3 months

29
Q

if a clear risk factor can not be identified, how long would treatments with anticoagulants last?

A

long-term

30
Q

what are the three classifications of anticoagulant?

do they all act on the same parts of the coagulation cascade?

A
  • direct oral anticoagulants (DOACs)
  • heparins
  • other oral anticoagulants
  • all act on diff parts of the coagulation cascade
31
Q

explain the mechanism for direct oral anticoagulants (DOACs)

what are the benefits? limitations?

A
  • either directly inhibit thrombin or FXa
  • benefits: oral pill, no monitoring required, rapid onset of action
  • limitations: antidote not available (issues for emergency surgery)
32
Q

explain the mechanism of action for unfractioned heparins (UFH)
what are the benefits? limitations?

A
  • acts via antithrombin to inhibit FIIa, FXa, FIXa, FXIa and FXIIa
  • benefits: rapid onset of action, short half life, reverse agent available
  • limitations: requies injection (usually IV), requires constant monitoring every 6 hours
33
Q

explain the mechanism of action for low molecular weight heparins (LMWH)
what are the benefits? limitations?

A
  • extracted MW fraction of UFH
  • acts primarily on inhibiting FXa
  • benefits: more predictable pharmokinetics, injection can be given by patients at home, longer 1/2 life than UFH
  • limitations: no direct reverisble agent available
34
Q

explain the mechanism of action for warfarin (other oral)

what are the benefits? limitations?

A
  • vitamin K antagonist - interferes w carboxylation of vit. K dependent factors (VII, IX, X, II, protein C/S)
  • benefits: longer 1/2 life, direct reversible agent available
  • limitations: peek effect seen in 4-5 days - needs to be combined w faster acting drug if used acutely
35
Q

what are the adverse effects of all anticoagulants?

A

-bleeding safety

36
Q

what are the adverse effects specific to DOACs?

A

no data about pregnancy

37
Q

what are the adverse effects specific to heparins?

A
  • thrombocytopenia - low platelet counts - result of adverse immune reaction
  • osteoporosis after long term use
38
Q

what are the adverse effects specific to warfarin?

A
  • embryopathy (developmental defect in fetus’)

- can cause allergic reactions (rash)

39
Q

when is genetic testing of inherited thrombophilias done?

A

in patients with a strong family history who present at a young age

40
Q

pros of genetic testing?

A
  • easy - simple blood test
  • offers explanation for sudden occurance of a VTE without known risk factor
  • can find multiple defects - improves long-term treatment
41
Q

cons of genetic testing?

A
  • knowing if an inherited thrombophilia is present doesn’t affect initial treatment
  • can lead to unessecary/aggressive family testing
  • asymptomatic individuals - potential risk to future insurability
42
Q

is timing of thrombophilia testing critical?

A
  • FVL and PGM are reliable anytime bc look for a mutation

- PC, PS and AT must be done when patient is well for an accurate result (treatment affects levels in blood)

43
Q

what are the most common thrombophilic conditions that are tested for?

A
  • FVL (factor V leiden - specific gene mutation)
  • PGM (prothrombin gene mutation)
  • protein C deficiency (pheotypic assay by blood test)
  • protein S deficiency (pheotypic assay “)
  • antithrombin deficiency (pheotypic assay “)

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