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Clinical Biomedicine > W9: Thrombotic Disorders :((( > Flashcards

W9: Thrombotic Disorders :((( Flashcards

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1
Q

normal haemostasis: what happens in 3 steps

A
  1. injury to BV, collagen exposed, platelet adhesion
  2. platelet activation, secretion & aggreg
  3. fibrin strands trap cells forming a stable thrombus
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2
Q

thrombotic pathology assoc w/ platelet plug formation

A

arterial thrombosis
MI, ischaemic stroke, (PAD - peripheral arterial disease)
bc atherosclerosis occurs in arteries

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3
Q

thrombotic pathology of coag step

A

venous thrombosis
DVT
bc of stasis

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4
Q

arterial thrombosis caused by inapprop activation of platelets - why?

A

atherosclerosis only in arteries (high pressure - corners, branches_
rupture of plaque exposes lipids which are thrombogenic

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5
Q

arterial thrombosis: S&S depend on location…

A

ischaemic stroke: disruption of blood supply to brain
MI: disruption of blood supply to heart muscle (coronary arteries)
(PAD - leg arteries)

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6
Q

signs vs symptoms

A

physician measures vs pt reports

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7
Q

symptoms of MI

A

Central chest pain, that may radiate to the jaw & arms, SoB, sweating, nausea/vomiting.

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8
Q

signs of MI

A

Tachycardia, low grade fever, pale clammy skin, hypo or hypertension, altered heart sounds.

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9
Q

diagnosis of MI

A

ECG, elevated troponin levels (protein released by damaged heart muscle), elevated creatine kinase levels (released by damaged heart muscle).

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10
Q

treatment of MI

A

Thrombolytic therapy, anti-platelet therapy, b-blockers, PCTA, CABG

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11
Q

prognosis of MI

A

23% ppl die before reaching hospital
5% die each year thereafter

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12
Q

ischaemic stroke = blockage of which arteries?

A

carotid/cerebral

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13
Q

ischaemic stroke symptoms

A

FAST

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14
Q

ischaemic stroke signs

A

Muscle weakness, paralysis, loss of sensation

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15
Q

ischaemic stroke diagnosis

A

Clinical (from S&S) but neuroimaging necessary to distinguish haemorrhagic vs ischaemic (CT or MRI).

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16
Q

ischaemic stroke treatment

A

Thrombolytic therapy, anti-platelet therapies, carotid endarectomy.

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17
Q

ischaemic stroke prognosis

A

Complete neurologic recovery occurs in ~10%.
Use of affected limb usually limited, & most deficits that remain after 12 months are permanent. Subsequent strokes often occur, & each tends to worsen neurologic function.
~20% pts die in the hospital; mortality rate ↑ w/ aging.

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18
Q

why does inapprop activation of coag in the veins (Venous thrombosis) occur?

A

virchow’s triad:
stasis
endothelial damage
hypercoagulability (Genetic variation- makes blood more “clotty”)

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19
Q

causes of venous thrombosis

A

Commonly occurs in the deep veins of the legs (DVT)
Often caused by immobility eg. bed rest / post-surgery, long flights / car journeys

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20
Q

venous thrombosis S&S

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A

sympt: pain in leg
signs:
Tenderness, swelling, redness, heat (unilateral). Fever, general malaise, ↑ WBC & erythrocyte sedimentation rate (measure of inflammation)

Embolism of venous thrombi travel to heart but gets stuck in lungs bc vessels smaller (capillaries)

21
Q

diagnosis of dvt

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A

Ultrasound, venogram (x-ray w/ contrast dye), elevated D- dimers (by-product of fibrinolysis)

22
Q

treatment of dvt

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A

Anti-coagulation, thrombolytic therapy

23
Q

prevention of dvt

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A

Exercising the legs, wearing support stockings, prophylactic anti-coagulation (heparin)

24
Q

prognosis of dvt

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A

3% risk of fatal pulmonary embolism (PE)

25
what increases ur long term tisk of venous thromboembolism (VTE)?
thrombophilia - can be acq or gen
26
what are the 7 inherited causes of thrombophilia?
Antithrombin deficiency Protein C deficiency Protein S deficiency Factor V Leiden Prothrombin 20210A Dysfibrinogenemia May-Thurner Syndrome Most inherited causes of venous thrombosis result from hypercoagulability. Often deficiencies in the inhibitors of coag
27
name some inhibitors of coag
anti-thrombin III protein C & protein S (activated by thrombomodulin) plasminogen
28
anti-thrombin III
Inactivates serine proteases (e.g. thrombin) Prod by liver Slowly degraded by thrombin Heparin increases ATIII activity (works 2000-4000x faster)
29
protein C & protein S inhibit...
FV & FVIII
30
plasminogen inhibits...
fibrin
31
actions of protein C & S
Thrombin binds thrombomodulin (TM) Protein C (enzyme) binds thrombomodulin & is activated by proteolytic cleavage by thrombin Protein S (cofactor) and endothelial phospholipid (PL) bind complex APC (activated protein C) cleaves FV or FVIII (inactivating them)
32
anti-thrombin III def
Autosomal dominant disorder (chr 1). 1:5000 ~50% develop clot in lifetime. 25-50x risk of VT. (affects XIa, IXa, Xa & thrombin)
33
protein C def
Autosomal dominant/recessive disorder (chr 2) . 1:500. 10-15x risk of VT. (affects VIIIa & Va)
34
protein S def
Autosomal dominant / recessive disorder (chr 3). 10x risk of VT. Prot S levels higher in♂. Levels drop in pregnancy, contraceptive pill and HRT. (affects VIIIa & Va)
35
factor V leiden
a mutation in FV so can’t be inhibited by protein C (activated protein C resistance APCR). Autosomal dominant disorder (chr 1). Most common cause of thrombophilia. 80x risk of VT (homozygotes) 3-5x risk of VT (heteros). APCR more common in pregnancy, contraceptive pill and HRT. (affects Va)
36
Prothrombin G20210A allele
Autosomal dominant disorder (chr 11). Elevated prothrombin levels. 2-3x risk of VT.
37
Dysfibrinogenaemia
Autosomal dominant disorder (chr 4). Dysfunctional fibrinogen may cause thrombosis (10%) haemorrhage (50%) asymp (40%). V. Rare (~200 families) Variable risk of VT.
38
may-thurner syndrome
congenital anatomic variation that predisposes to DVT in left leg. Compression of left common iliac vein by right common iliac artery. Causes stasis (Virchow’s triad)
39
11 reasons for acquired thrombophilia
Previous thrombosis Age Immobilisation Surgery Malignancy Oral contraceptives Hormone replacement therapy Antiphospholipid syndrome Essential thrombocytosis Polycythaemia vera Paroxysmal nocturnal haemaglobinuria
40
acquired thrombophilia: prev thrombosis
prev DVT is the strongest risk factor, ↑ risk by 5x.
41
Acquired Thrombophilia: age
less active (stasis of blood in venous system), ↓ prod of inhibitors??
42
Acquired Thrombophilia: immobilisation
less active (stasis of blood in venous system)
43
Acquired Thrombophilia: surgery
less active (stasis of blood in venous system) Most likely in the elderly / obese. Major abdominal operations Major orthopaedic operations
44
Acquired Thrombophilia - malignancy
4x risk. Tumour cells may express TF. Occult cancer should be considered.
45
Acquired Thrombophilia: oral contraceptives & HRT
Oestrogen therapy: incr plasma levels of factors II, VII, VIII, IX AND X decr levels of anti-thrombin III decr levels of protein S Prot S levels higher in ♂. Prot S levels decr in pregnancy, contraceptive pill & HRT decr levels of tPA Therefore, careful screening for other thrombophilic risk factors necessary before prescribing.
46
Acquired Thrombophilia: Antiphospholipid antibody syndrome
Autoantibodies (IgG/IgM) to phospholipid (aPL) Found in 5% healthy popn. 18% of young stroke patients, 21% of young MI patients In vivo associated with increased arterial AND venous thrombosis, and recurrent pregnancy loss. In vitro causes prolonged aPTT!
47
Acquired Thrombophilia: Essential thrombocytosis or thrombocytheamia
A raised platelet count above normal range of 150-400 x 109/L Can cause thrombosis (excess platelets) or bleeding (platelet function can be defective). One of the myeloproliferative neoplasms (MPDs) (excess production of myeloid blood cells): Essential thrombocytosis (excess platelets) Polycythaemia vera (excess RBCs) Chronic Myeloid Leukaemia (excess granulocytes) Primary myelofibrosis (bone marrow replaced with connective tissue)
48
Acquired Thrombophilia: Polycythaemia Rubra Vera
Another myeloproliferative neoplasm Excess production of RBCs A raised Hct (>48% in females, >52% in males) A raised HGB (>16.5g/dL in females, >18.5g/dL in males).
49
Acquired Thrombophilia: Paroxysmal Nocturnal Haemaglobinuria
Lysis of RBCs results in Hb in urine. Due to urine concentration overnight, it appears darker in morning. However, the lysis is occurring all the time. Defect in forming GPI-anchors, so loss of GPI-anchored proteins from the surface of blood cells Effects: Haemolytic anaemia Venous thrombosis at atypical sites (e.g. Hepatic portal vein) Bone marrow failure (pancytopenia)

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