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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
HIT type 2 or HIT-T
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
How to diagnose HIT-T
Patient on heparin suffers 50% decline in platelet count 5-10 days into therppy...withdraw heparin permanently
27
TTP
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
DIC
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
DIC pathology
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
Waterhouse-Friderichsen syndrome
Adrenal infarction seen in the DIC accompanying meningococemia
31
Lab testing for DIC
``` PT and aPTT are prolonger Fibrinogen decreased Antithrombin decreased D-dimer increased Microangiopathy on the periperal smear ```
32
Tx of DIC
Treat underlying cause Pro-coag - FFP, cryo, platelets Anticoag- antithrombin and heparin
33
Proteins C and S deficiencies and antithrombin def
Heterozygous prone to clotting disorders, homo die in utero
34
APC resistance syndromes
Mutations in F5 gene that renders F5 resistant to APC....hypercoagulable...factor 5 leiden or cambridge
35
Prothrombin gene mutation G20210
Excess prothrombin production | More F8 nd 9 so increased htrombosis risk
36
APLs
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
Lupus anticoagulant/anticardiolipid antibodies
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
Classification of thrombi
Arterial Mural (cardiac chambers) Valvular (cardiac valves) Venous
39
Risk for arterial thrombosis
Arterial atehroscleorosis Areas of turbulent flow (bifurcations or aneurysms) Endothelial damage Abnormal stasis
40
Venous thrombosis risk factors
``` Older age, smoking history bed rest Varicose veins Conditions cause endothelial cell damage Thrombophlebitis Post op Severe burns, trauma, fracture ```
41
Mural thrombi risk
Myocardial infarction - reduced wall motion and arrythmias cause stasis Endocardial cell injury exposes tissue factor
42
Valvular thrombi risk
Diseased heart valves Rough surfaces Abnormal blood flow Formation of emboli
43
Arterial thrombosis conseuqences
Sichemia Infarction Embolization (generally to systemic sites)
44
Venous thrombosis consequences
COngestion and edema - blood flow blocked behind the clot...increased pressure...extravasation of lfuids into tissue Infarction Embolization - generally to the lung
45
Potential outcomes of thrombosis
``` Propogation of clot DIssolutioon ofclot Embolization Organization Recenalization ```
46
Embolization
Passage of material through circulation which lodges in a distant vessel and may produce partial or complete occlusion of the vessel
47
Types of emboli
``` Atherosclerotic Fat Air Amnitoic FB Tumor ```
48
Systemic thromboemboli
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
Pulmonary embolism
95% from deep veins in the leg...travels through right heart and lodges in pulmonary vasculature Most are siletn
50
Types of PE
Peripheral lung field - small Saddle - large and lodge in bifurcation Paradoxial embolism - not pulmonary but venous in nature
51
DIagnosiing thromboembolic dz
Spiral CT VQ Doppler Imaging of heart D-dimer levels Genetics Acquired predisposition
52
Factors that influence infarction
Nature of supply Rate of development Vulnerability - neurons die quicker Oxygen content of blood - anemia and hypoxia predispose
53
White vs red infarctions
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
Morphology of infarcts
Gross - wedge shaped of white Coagulative inheart Liquefactive in brain Abscess formation in sepsis Otherwise termed bland
55
MI
Death of myocardial tissue due to occluded coronary artery

Heme/Lymph 1 (14 decks)

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