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

W9: Thrombotic Disorders :((( Flashcards

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

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

A

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

22
Q

treatment of dvt

A

Anti-coagulation, thrombolytic therapy

23
Q

prevention of dvt

A

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

24
Q

prognosis of dvt

A

3% risk of fatal pulmonary embolism (PE)

25
Q

what increases ur long term tisk of venous thromboembolism (VTE)?

A

thrombophilia - can be acq or gen

26
Q

what are the 7 inherited causes of thrombophilia?

A

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
Q

name some inhibitors of coag

A

anti-thrombin III
protein C & protein S (activated by thrombomodulin)
plasminogen

28
Q

anti-thrombin III

A

Inactivates serine proteases (e.g. thrombin)
Prod by liver
Slowly degraded by thrombin
Heparin increases ATIII activity (works 2000-4000x faster)

29
Q

protein C & protein S inhibit…

A

FV & FVIII

30
Q

plasminogen inhibits…

A

fibrin

31
Q

actions of protein C & S

A

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
Q

anti-thrombin III def

A

Autosomal dominant disorder (chr 1).
1:5000
~50% develop clot in lifetime.
25-50x risk of VT.
(affects XIa, IXa, Xa & thrombin)

33
Q

protein C def

A

Autosomal dominant/recessive disorder (chr 2) .
1:500.
10-15x risk of VT.
(affects VIIIa & Va)

34
Q

protein S def

A

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
Q

factor V leiden

A

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
Q

Prothrombin G20210A allele

A

Autosomal dominant disorder (chr 11).
Elevated prothrombin levels.
2-3x risk of VT.

37
Q

Dysfibrinogenaemia

A

Autosomal dominant disorder (chr 4).
Dysfunctional fibrinogen may cause
thrombosis (10%)
haemorrhage (50%)
asymp (40%).
V. Rare (~200 families)
Variable risk of VT.

38
Q

may-thurner syndrome

A

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
Q

11 reasons for acquired thrombophilia

A

Previous thrombosis
Age
Immobilisation
Surgery
Malignancy
Oral contraceptives
Hormone replacement therapy
Antiphospholipid syndrome
Essential thrombocytosis
Polycythaemia vera
Paroxysmal nocturnal haemaglobinuria

40
Q

acquired thrombophilia: prev thrombosis

A

prev DVT is the strongest risk factor, ↑ risk by 5x.

41
Q

Acquired Thrombophilia: age

A

less active (stasis of blood in venous system), ↓ prod of inhibitors??

42
Q

Acquired Thrombophilia: immobilisation

A

less active (stasis of blood in venous system)

43
Q

Acquired Thrombophilia: surgery

A

less active (stasis of blood in venous system)
Most likely in the elderly / obese.
Major abdominal operations
Major orthopaedic operations

44
Q

Acquired Thrombophilia - malignancy

A

4x risk. Tumour cells may express TF. Occult cancer should be considered.

45
Q

Acquired Thrombophilia: oral contraceptives & HRT

A

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
Q

Acquired Thrombophilia: Antiphospholipid antibody syndrome

A

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
Q

Acquired Thrombophilia: Essential thrombocytosis or thrombocytheamia

A

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
Q

Acquired Thrombophilia: Polycythaemia Rubra Vera

A

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
Q

Acquired Thrombophilia: Paroxysmal Nocturnal Haemaglobinuria

A

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)

Clinical Biomedicine (23 decks)

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