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Hem 240 > Week 10 > Flashcards

Week 10 Flashcards

1
Q

What is coagulation

A

formation of a blood clot AFTER injury to blood vessel

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2
Q

What is thrombosis

A

formation of a blood clot inside a intact blood vessel which obstructs the flow of blood through the circulatory system

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3
Q

What is embolus

A

when a portion of a large clot breaks free and travels around the body

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4
Q

What are the 4 manifestations of thrombosis

A

DVT
pulmonary PE
Stroke
MI

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5
Q

What are some types of VTE

A

Venous Thromboembolic Events

DVT- in calf or leg, in deep veins, caused by loss of mobility like illness or long flights
-pain, swelling, redness and heat
-Erythema and edema

Pe Pulmonary emboli
-Blood clot in pulmonary artery blocking blood flow to lung caused by a portion of a DVT clot that has travelled up to the lung - FATAL due to ischemia of lung tissue
-symptoms are similar to pneumonia

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6
Q

How is DVT examined

A

Ultrasonography

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7
Q

What is Arterial Thrombosis

A

-Formation of atherosclerotic plaque on walls of small arteries
-if plaques are unstable they rupture causing wall damage and platelet activation
-pts take aspirin to prevent AT
-Ebolisms to organs originates in heart or large arteries and then occludes arterioles, coronary arteries and carotid arteries

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8
Q

What can Arterial Thrombosis cause

A

Stroke:
-clot blocks brain vessel resulting in ischemia and loss of brain function
-most strokes are caused by blockage of carotid arteries

Coronary Artery Disease
-blot blocks coronary artery
-thrombi that block the coronary arteries result in MI

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9
Q

What are some risk factors to thrombosis

A

Acquired - lifestyle
Secondary - systemic disease
Congenital - inherited

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10
Q

What is thrombophilia

A

hypercoaguble state
-increases the risk of thrombosis
- caused by acquired and congential factors
- needs a combination of risk factors before thrombosis (clot formation) occurs

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11
Q

What are the three main factors that predispose to thrombosis and make up the virchows triad

A

Endothelial injury (BV wall damage)
- causing PLT activation
-TF exposure
-athersclerosis , catheter

Abnormal blood flow
-venostasis
-when plts are brought in contact with endothelium due to flow of blood
-bed rest, paralysis, A fib

Hypercoagulability/reduced inhibition
-increase of coag factor activation so there are more procoag factors in the plasma or a reduction of inhibitory factors of coag pathway

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12
Q

Acquired Thrombosis Risk Factors

A

Age/Immobility - after 50 your risk doubles due to abnormal blood flow

Diet/Lipid metabolism - eating fatty foods, not enough folate , high chol, high LDL leads to plaque formation
-BV wall damage

Elevated estrogen - pregnancy / birth control increases risk 4x
-stimulation of coag factors

post op trauma - DIC , endothial injury

Smoking - depends on degree - endothlial injury and abnormal blood flow

Inflammation - endo injury increases coag factors

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13
Q

Acquired Thrombosis Risk Factors
Secondary associated with systemic risk factors

A

Chronic inflammation /autoimmune disorder- lupus

Hepatic and Renal disorders - decreased production of inhibitory factors (hypercoagulability) or excretion of factors through urine

Myeloproliferative disorders
Essential thrombocytopemia ET
Polycythemia vera PCV

Leukemia - increases risk for DIC. Some tumors release TF which activate coagulation

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14
Q

Lupus SLE

A

-inflammatory and autoimmune disease
-produces Anti DNA, ACAPN, Lupus anticoagulant LAC - which targets phospholipids

-varied manifestations
-tissue damage from AB and complement fixing

-more common in women
-recurrent miscarriages and butterfly rash

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15
Q

how to detect Lupus in LAB

A

ANA- ana nuclear AB test - GOLD
-only some lupus pts have LAC , it can also be detected in RA
-LA causes prolonged APTT and normal PT
-LA is an AB to protein - phospholipid complexes

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16
Q

What is Lupus Anticoagulant or Antiphospholipid Syndrome APS

A

not all pts with SLE develop SLE some get APS
-complication from anti phospolipid AB
-IgM or IgG AB to phospholipid
-promote coagulation in vivo but anticoagulant in VITRO
-prolonged phospholipid dependent tests- PTT
-associated with SLE

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17
Q

Antiphospholipid Syndrome (APS) – Clinical Criteria:

A

Thrombosis = - venous and arterial at the same time

-pregnancy loss- 3 or more unexplained (through impaired nitric oxide release, atherosclerotic plaque development, promotes clotting, TF expression, increased Thromboxane -increase PLT)

-slight hemolytic anemia

-thrombocytopenia

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18
Q

Laboratory Criteria for LA / Antiphospholipid Syndrome (APS)

A

initial PTT is prolonged with LAC presence

but PTT can be prolonged due to Factor deficiency , inhibitors (non specific LAC), Anticoagulants

differentiate between these by doing mixing studies

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19
Q

How to do a mixing study

A

Normal plasma with sample plasma 1:1 ratio

Corrects- factor deficiency or factor inhibitor
Not Correct - non specific inhibitor like LAC - DRVVT -assay for lupus anticoagulant

if corrects then make new 1:1 and incubate

corrects- factor deficiency - do factor assays
Not correct - specific factor inhibitor - do factor inhibitor assays

20
Q

What is drvvt

A

dilute russel viper venom test

-initiates coag cascade at FX (intrinsic) not affected by inhibitors or factor deficiencies of FXI, XII, IX or VII (intrinsic)

If a prolonged time is seen with drvvt then its likely due to anti phospholipid antibodies like LAC

21
Q

Laboratory Criteria for LA / APS

A

if you suspect an antiphospholipid AB then you need to confirm with
dRVV or PTT with high phospholipid conc

the high phospholipid concentration neutralizes the AB so the dRVVT is corrected to normal through the AB:AG reaction

confirm with immunoassay
ACAPN
ANTI B1 glycoprotein AB

22
Q

What are the criteria for the diagnosis of LA

A

1-prolonged phospholipid dependent clot formation when using an assay like low phospholipid PTT or DRVVT

2-failed to correct the prolonged clot time when mixed with normal platelet poor control plasma

3-correction of prolonged screen with the addition of excess phospholipids

4-exclusion of coagulopathies

23
Q

DIC

A

-starts with excessive clotting (small clots form throughout bloodstream and block blood vessels) caused by a substance that enters the blood
part of disease process
complication of child birth
surgery or trauma
toxins - venom, TSS

Coag pathway will be activated and excess circulating thrombin will activate PLTs, catalyze fibrinogen to fibrin
The fibrinolytic pathway is activated due to excess clot formation but in DIC the fibrin will FAIL to polymerize and circulate freely instead therefore the plasmin response will be delayed

24
Q

DIC pathophysiology

A

normal anticoagulant and fibrinolytic systems are overwhelmed and coagulation activation cant be contained

fibrin microthrombi occlude small vessels causing PLT, coag factor and protein consumption
Red cells are fragmented as they travel through blood vessels
-Fibrin degradation products or D dimers are generated
-leads to excessive bleeding which depletes PLTs and clotting factors needed to control bleeding

25
Q

Diagnosis of DIC

A

Type of MAHA
-thrombocytopenia
-shistocytes on PBS

prolonged PT and PTT
increased D dimer
fibrinogen is decreased because fibrinolysis via plasmin is occuring

26
Q

D dimer

A

Negative D dimer means its NOT DIC, PE or DVT
-Normal is <0.5 mg/L
- in DIC levels are 10000 - 20000 ng/L or 10mg/L
in PE or DVT they are a bit lower

27
Q

What tests could you do for testing of D dimer

A

-latex fixation slide test (Qualitative)
-ELISA -turbidimetric with decease of transmitted light at 405; change is plotted on a standard curve to establish the concentration if D dimer

1)If D-dimers are present, they will agglutinate the latex particles > Clumps
2)If D-dimer absent, solution remains clear

28
Q

What Conditions Resulting in Increased Risk of Thrombosis (inheritied )

A

Deficiencies in:
Antithrombin
Protein C
Free PS
TPA

Mutations of:
Factor V
F V Leiden (APCR)
Prothrombin
G20210A
Fibrinogen
dysfibrinogenemia
Plasminogen
PAI-1 (elevation)

order a thrombosis panel to narrow down what is causing the issue
most common are VENOUS thrombosis AT, PC, PS, APC-R

29
Q

Antithrombin (AT) Deficiency:
lab assessment

A

congenital deficiency
-serine protease inhibitor that neutralizes thrombin
acquired in prolong heparin therapy, DIC, Liver disease etc

most cases are due to reduced production or due to mutations that cause abnormalities in protease binding site or heparin binding site

Lab assessment :assays, Clot based and chromogenic AT assay , immunoassay for AT concentration

30
Q

AT Chromogenic Functional Assay:

A

pt AT binds heparin and is activated
AT + HEP bind to reagent FXa
chromogenic substrate is added but it will be hydrolyzed by the excess FXa not bound to AP+HEP

the color produced is inversely proportional to amount of AT

31
Q

Immunoassay for AT Concentration

A

consists of a reagent made up of latex microbeads coated with monoclonal AB directed at AT

the AT in pt plasma binds the beads causing latex agglutination and increases turbidity

AT concertation is directly proportional to rate of light ABs change

32
Q

Chromogenic vs Immunoassay for AT

A

Fuctional (chromogenic)
detects both quantitative (amount present) and qualitative (ability to bind protease) AT deficiencies

Immunoassay
Detects only quantitative AT (amount present)
DOESNT TEST FOR FUNCTIONALILITY

33
Q

Inherited Protein C or S Deficiency

A

Thrombin binds Thrombomodulin which activates Protein C (APC). APC binds free Protein S to stabilize APC-S complex. This complex will go inactivate FVa and FVIIIa

Therefore, without Protein C or Protein S, NO inhibition of FVa and FVIIIa, so clotting continues

Protein C def and Protein S deficiency - are Vit K dependent (DIC, Liver Disease)
No complexes formed
no inhibition of FVa or FVIIIa

do chromogenic or clot based assays
enzyme immunoassay

34
Q

Chromogenic Protein C Assay

A

1)Patient Plasma is mixed with Reagent containing Snake Venom (which is activator of Protein C)
2)Second reagent containing colour substance is added
3)APC in patient plasma will hydrolyze the substrate and create colour

Intensity of color is proportional to the activity of Protein C

35
Q

Clot-Based Protein C Assay

A

1)Patent plasma is mixed with Protein C-depleted Normal Plasma
—This ensures normal levels of all factors EXCEPT Protein C
2) Reagent containing snake venom and APTT reagent is added
3) Time to clot is measured

Prolongation is proportional to plasma protein C activity (because APC will prolong PTT)

APC prolongs APTT

36
Q

Chromogenic
Clot based

A

both can affect molecule’s serine protease site (site which binds to FVIIIa and FVa)

**listen

37
Q

Enzyme Immunoassay for Pro C

A

Uses ELISA method – Quantitative and Qualitative

-Plate coated with monoclonal Ab directed to Pro C. These monoclonal Ab are used to capture patient’s plasma Pro C
-Add an enzyme linked monoclonal antibody (also directed to Pro C)
-Add a substrate that changes colour when in contact with that enzyme
-Concentration of Pro C is measured by colour development
-Assay determines if low functional activity is due to non-functional Pro C (Qualitative) or if there is a quantitative deficiency (Quantitative – normal levels, dysfunctional protein)

38
Q

Protein S Assays
Clot-Based Assay

Immunoassay

A

Pt plasma + protein S depleted normal plasma +reagent (APC, venom, and PTT)
time to clot is measured
prolonged = high protein S- proportional

Immunoassay - similar to Prc assay for qualitative and quantitative

39
Q

Factor V Leiden (FVL) Mutation

A

Activated Protein C Resistance (APC-R)

FVa is usually inactivated by APC-Protein S complex , in FVL is there is a mutation on FV molecule
Maintains normal co factor ability so coagulation is normal

arginine is the site of APC/PS cleavage
Va not inactivated!!! > Remains active
No reduction in prothrombinase production
Continued clotting

40
Q

F V Leiden / APC-R Lab Analysis

A

-suspected based on history
PT and PTT is normal

screen with APC-R assay
pt plasma+ FV deficient plasma (all factors but V )
that way you are assessing only the presence of Fv in pt plasma

Two aliquots
both contain APTT reagent + FV-depleted normal plasma + Patient plasma

First aliquot:
1) Add CaCl
2)Measure time to clot

Second aliquot
1)Add CaCl and APC.
2)Measure time to clot

APC should inactivate patient’s FVa and prolong APTT
–Second aliquot should be prolonged by AT LEAST 1.8x of the first aliquot

If person is APC-Resistant (aka has FVL) > there would be normal clotting bc FV is not inactivated (Fv L mutation confirmed by molecular genetics)

determine zygosity as homozygous state is high risk
LAC interferes with APC-R so go directly to genetics

41
Q

Prothrombin G20210A

A

prothrombin mutation FII

G to A mutation
increased risk of DVT
increased Prothrombin level = more thrombin
-molecular genetics to diagnose

42
Q

Dysfibrinogenemia

A

-functional or structural abnormality of the fibrinogen molecule

-Abnormalities in structure results in resistance to plasmin
-Plasmin cant recognize cleaving site so the clot won’t be able to be digested
-This means clotting will continue

Test - Fibrinogen concentration or Thrombin Time (TT) Assay
Decreased Fibrinogen levels
Abnormal TT (prolonged) bc abnormal structure makes it so there’s issues with cleaving fibrinogen to fibrin

43
Q

Plasminogen:

how does the assay work

A

Without plasminogen, patient is unable to breakdown clots

Use of thrombolytic therapy (e.g Recombinant TPA) useless without plasminogen

Chromogenic Substrate Assay can be used to measure Plasminogen levels
1)Patient’s plasma is mixed with Reagent containing streptokinase (plasminogen activator)
2)Patient’s plasminogen will be converted to plasmin
3)Plasmin will react with chromogenic substrate to release colour

Colour intensity will be proportional to the concentration of plasminogen in patient

44
Q

Tissue Plasminogen Activator

how does the assay work

A

deficiency associated with Myocardial Infarction (MI), stroke & DVT
-Without TPA, plasminogen cannot be converted - no clot breakdown

Chromogenic Substrate Assay to measure TPA activity:
1)Known constant conc of Plasminogen is added to patient plasma
2)Patient’s TPA will convert plasminogen to plasmin
3)Plasmin will react with chromogenic substrate

Intensity of colour substrate is proportional to TPA activity

45
Q

Plasminogen Activator Inhibitor 1

A

Deficiency associated with mild bleeding
INCREASED PAI-1 = thrombosis, primary inhibitor of fibrinolysis – increased levels stops TPA from activating plasminogen – clots don’t get broken down

PAI-1 overproduction is measured using indirect approach:
1)Patient plasma is mixed with a fixed amount of reagent and TPA in excess
2)Patient’s PAI-1 will inactivate reagent TPA.
3)The residual TPA that hasn’t been inactivated will activate reagent plasminogen to plasmin. This will react with chromogenic substrate

Colour intensity is INVERSELY proportional to patient’s PAI-1 activity

46
Q

Factor XII, PK, HMWK deficiency

A

involved in activating plasminogen , if there is a deficiency then fibrinolytic activity is reduced

FXII deficiency doesn’t always result in bleeding disorders it can be bypassed as a contact factor by direct activation of FXI thrombin

47
Q

Tissue Factor Pathway Inhibitor (TFPI) Deficiency

A

inhibits the Extrinsic Tenase complex

TFPI binds directly and inhibits the Xa & TF–FVIIa complex therefore inhibiting continued activation of FXa

Low levels of TFPI are a risk factor for clotting disorders
Allows for continued FXa activity

Hem 240 (6 decks)

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