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Heme/Lymph 1 > Pathologic Hemorrhage and Thrombosis > Flashcards

Pathologic Hemorrhage and Thrombosis Flashcards

1
Q

Hemorrhage vs thrombosis

A

Hemorrhage - porrly controlled escape of blood from circulation

Thrombosis - pathologic clot fomrmation in circulation not associated with bleeding

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2
Q

Result of alterations of blood composition, flow dynamis, and vessels

A

Composition - unbalanced procoag and anticoag factors
Dynamics - stasis, turbulence (bedridden, vascular constriction, AF), increased visocisity (sickle cell, polycythemias, waldenstrom macroglobulinemia, leukemic leukostasis)
Vessels - vascular malformations…injury exposed vWF, collagen, and TF

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3
Q

Pathologic hemorrhage

A

Composition - procoagulant def, presence of anticoagulants, excessive firbinolysis

Flow - hypertension, vascular congestion, reduced viscosity

Vessels - trauma, surgery, dz

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4
Q

Bleeding disorders due to

A

Primary/secondary hemostatic disorders and fibrinolytic disorders

NONE due to anticoagulation disorders

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5
Q

Primary hemostatic disorder clinical presentation

A

Mucosal bleeding
Easy bruising
Petechiae
Prolonged bleeding from cuts

Make sure to take a good history and ask lots of questions

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6
Q

Thrombocytopenia

A

Platelet disorder
Decreased marrow production, increased peripheral desturction, increased sequestration in an enlarged spleen
PLatelet counts low

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7
Q

ITP

A

Immune thrombocytopenia

Platelet life is very short so the platelets in circulation are younger and function better

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8
Q

Platelet production disorder

A

Normal distribution of platelet ages but might have greater risk of pbleeding

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9
Q

Congenital platelet dzs

A

Bernard Soulier Syndrome - GPIb receptor def
Glanzmann’s thrombasthemia - def of GP2b/3a
Storage pool diseases - something wrong with platelet granules, inhibits activation and recruitment of other platelets
Congenital aspirin like defect - defect in platelet intracellular signaling for activation

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10
Q

Acquired platelet dzs

A

Drug effect or uremia (granule def or vWF dysfunction)

More common than congenital

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11
Q

Uremic platelet dysfunction

A

Anemia plays rehologic role in bleeding
Increases NO synthesis of platelets
Degree of azotemia does not correlate with bleeding risk
Poorly characterized uremic toxins (not urea or creatinine) are the culprits
Txs include DDAVP and cryoprecipitate (increased vWF)…estrogens will reduce NO synthesis
Dialysis may help

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12
Q

Causes of acquired platelet dysfunction

A 
Liver dz, diabetes, trauma, extracorporeal circuits, CP bypass
Dysproteinemias 
Myeloprol disorders (essential thrombocytosis or CML)
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13
Q

vWD

A

Most common inherited
Most are type 1 (70-80)
Then type 2A (15)
Then type 2B (5)

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14
Q

Types 1 and 3 of vWD

A

1 - decreased level of normal vWF
3 - absent vWF
Acquired - anti-vWF blocking ABs, marked thrombocytosis clearing vWF from circulation, cleavage of molecule in high flow environemtns like tight aortic stenoiss or extracorporeal circuits)

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15
Q

Type 2s of vWD

A

2a - no ultra large monomers…bleeding results when needed
2b- exposes GPIb receptor permitting IV platelet binding and splenic clearance of complexes leading to thrombocytopenia
2M - platelet binding too week due to loss of function
2N - binding of F8 defective so undefended from protein C…mild hemophilia like d

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16
Q

Platelet type vWD

A

Similar to vWD type 2B…gain of function in GPIb receptor

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17
Q

vWF factoids

A

Increased by thyroxine and estrogens (but not progestins)
vWF is an acute phase reactant
Ultra large molecules (storage form) can be depleted by DDAVP or stress

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18
Q

How to characterize secondary bleeding disorder

A

Hematomas with deep tissue and joint bleeding

Delayed posttraumatic bleeding

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19
Q

Liver failure

A

Decreased factor production and dysfibrinogenemia
Cirrhotic patients at risk of bleeding AND thrombosis because both pro and anticoagulant proteins are decreased…multifactoral thrombocytopenia

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20
Q

Hemophilia A, B and C

A

A - X-linked def of F8
B - x linked def of F9
C - auto rec of def of F11

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21
Q

Parahemophilia and congenital F13 def

A

Parahemophilias - F5 def…auto rec

Congenital F13 def - delayed wound hemorrhage

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22
Q

F8 vs F9

A

F8 is a larger molecule and an actue phase reactant

F9 is smaller and not an acute phase reactant…need twice as much F9 in replacement therapy

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23
Q

Hemophilia A notes

A

Most have severe…if acquired with AI dz, will make anti-F8 ABs…severely depleted could also make anti-F8 antibodies

24
Q

Heparin induced thrombocytopenia

A

Heparin therapy activates platelets….they are then cleared by the spleen and then it declines

PF4 is released by alpha granules of platelets…forms complex with heparin in circulation…complex activates other platelets leading to positive feedback loop…PF4-hep complex also immunogenic and IgG will attach after about 5 days….AB-hep-PF4 complex also indcues platelet activation and continue positive feedback loop…declining platelet count and further release of PF4…if it stops here, it is HIT type 1 and benign, never causes bleeding problems

25
Q

HIT type 2 or HIT-T

A

Heparin induced thrombocytopenia with thrombosis
IgG ABs formed to heparin-PF4 may cross react with endothelial surface leading to endothelial activation and risk of thrombosis…release IL-6, vWF…venous and arterial platelet-rsi hwhite thrombis

26
Q

How to diagnose HIT-T

A

Patient on heparin suffers 50% decline in platelet count 5-10 days into therppy…withdraw heparin permanently

27
Q

TTP

A

Thrombotic thrombocytopenia purpura
Decreased ADAMTS activty leads to inadequate cleavage of vWF into small size
Excess multimer leads to excess vWF activity
Unwanted platelet plug formation in microvasculatiure of critical tissues and ischemia

Will see schistocytes

28
Q

DIC

A

Disseminated IV coagulation
Secondary to other diseases
Infection - bacterial endotoxin and some viruses activate endothelium exposing TF
Trauma - endothelial injury leading to TF exposure
Obstetric catastrophe - amniotic fluid embolization
Neoplasia - high in TF expression or release cytokines that upregulate TF expression

Circulation NOT normally exposed to TF…brain and placental villi are especially likely to be involved

29
Q

DIC pathology

A

Fibrin microthrombi formed and trapped in microvasculature…tissue ischemia
Vascular occlusion - endothelial release of tPA adding an important compoenet of fibrinolysis

Bleeding ensues when platelets and factors are consumed by intital hypercoagulability

Petechial hemorrhages, ecchymoses, oozing from surgical wounds and IV sites

30
Q

Waterhouse-Friderichsen syndrome

A

Adrenal infarction seen in the DIC accompanying meningococemia

31
Q

Lab testing for DIC

A 
PT and aPTT are prolonger
Fibrinogen decreased
Antithrombin decreased 
D-dimer increased
Microangiopathy on the periperal smear
32
Q

Tx of DIC

A

Treat underlying cause

Pro-coag - FFP, cryo, platelets

Anticoag- antithrombin and heparin

33
Q

Proteins C and S deficiencies and antithrombin def

A

Heterozygous prone to clotting disorders, homo die in utero

34
Q

APC resistance syndromes

A

Mutations in F5 gene that renders F5 resistant to APC….hypercoagulable…factor 5 leiden or cambridge

35
Q

Prothrombin gene mutation G20210

A

Excess prothrombin production

More F8 nd 9 so increased htrombosis risk

36
Q

APLs

A

Antiphospholipid antibodies
Directed toward phospholipid-protein complexes…some are associated with thrombosis risk
Some are virally induced…repeat positive test in 8-12 weeks

37
Q

Lupus anticoagulant/anticardiolipid antibodies

A

Lupus - Prolongation of clot based test
Lupus - Does NOT cause anticoagulatio in vivo, only by increased PTT

Both can cause catastrohpic antiphospholipid syndrome

APLs with coagulopathies are associated with loss of nromal pregnancies due to placental thrombosis

38
Q

Classification of thrombi

A

Arterial
Mural (cardiac chambers)
Valvular (cardiac valves)
Venous

39
Q

Risk for arterial thrombosis

A

Arterial atehroscleorosis
Areas of turbulent flow (bifurcations or aneurysms)
Endothelial damage
Abnormal stasis

40
Q

Venous thrombosis risk factors

A 
Older age, smoking history
bed rest 
Varicose veins 
Conditions cause endothelial cell damage
Thrombophlebitis 
Post op 
Severe burns, trauma, fracture
41
Q

Mural thrombi risk

A

Myocardial infarction - reduced wall motion and arrythmias cause stasis
Endocardial cell injury exposes tissue factor

42
Q

Valvular thrombi risk

A

Diseased heart valves
Rough surfaces
Abnormal blood flow
Formation of emboli

43
Q

Arterial thrombosis conseuqences

A

Sichemia
Infarction
Embolization (generally to systemic sites)

44
Q

Venous thrombosis consequences

A

COngestion and edema - blood flow blocked behind the clot…increased pressure…extravasation of lfuids into tissue
Infarction
Embolization - generally to the lung

45
Q

Potential outcomes of thrombosis

A 
Propogation of clot 
DIssolutioon ofclot
Embolization
Organization
Recenalization
46
Q

Embolization

A

Passage of material through circulation which lodges in a distant vessel and may produce partial or complete occlusion of the vessel

47
Q

Types of emboli

A 
Atherosclerotic 
Fat 
Air 
Amnitoic 
FB
Tumor
48
Q

Systemic thromboemboli

A

80% originate in heart
2/3 associated with LVMI
1/4 associtedwith dilated or fibrillating left atrium
Organs with most blood flow at greatest risk (brain and kidneys)

49
Q

Pulmonary embolism

A

95% from deep veins in the leg…travels through right heart and lodges in pulmonary vasculature
Most are siletn

50
Q

Types of PE

A

Peripheral lung field - small
Saddle - large and lodge in bifurcation
Paradoxial embolism - not pulmonary but venous in nature

51
Q

DIagnosiing thromboembolic dz

A

Spiral CT
VQ
Doppler
Imaging of heart

D-dimer levels
Genetics
Acquired predisposition

52
Q

Factors that influence infarction

A

Nature of supply
Rate of development
Vulnerability - neurons die quicker
Oxygen content of blood - anemia and hypoxia predispose

53
Q

White vs red infarctions

A

White - occur in tissues with end artery circulation….dense tissue minimizes hemorrhage

Red - Profuse bleeding into tissue…venous occlusion or tissue previously congested with blood (ovarian)…in organs with dual supply (lungs)…tissues re-perfused following infarction

54
Q

Morphology of infarcts

A

Gross - wedge shaped of white
Coagulative inheart
Liquefactive in brain
Abscess formation in sepsis

Otherwise termed bland

55
Q

MI

A

Death of myocardial tissue due to occluded coronary artery

Heme/Lymph 1 (14 decks)

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