Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MCC > Wk 2 Hemostasis & Coagulation > Flashcards

Wk 2 Hemostasis & Coagulation Flashcards

1
Q

What are the 4 main steps in hemostasis?

A

Vascular injury occurs ->
1. vasoconstriction
2. primary hemostasis = platelet plug formation
3. secondary hemostasis = fibrin formation/polymerization
4. thrombus and antithrombotic events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens with primary hemostasis?

A
  1. platelet adhesion to vascular injury. Collagen most IMP for this, vWF has role too
  2. platelet shape change
  3. granule release, promoted by platelet agonists like ADP, TxA2, which bind to the platelet surface receptors to promote the release
  4. recruitment of more platelets by granules
  5. aggregation (hemostatic plug): fibrinogen binds platelet GPIIb/IIIa receptors, connecting adjacent platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 primary tasks of primary hemostasis?

A
  1. platelet adhesion
  2. platelet activation
  3. aggregation

Main overall goal = form platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Main goal of secondary hemostasis

A

Make fibrin (and deposit it around the platelets in the plug)
-stabilizes the plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Analogy for primary and secondary homeostasis

A

platelets = bricks
fibrin = mortar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

4 steps in secondary hemostasis

A
  1. tissue factor
  2. phospholipid complex expression
  3. thrombin activation
  4. fibrin polymerization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the coagulation cascade?

A

Sequential enzymatic reactions -> formation of fibrin
-process is diff in lab (in vitro) and in body (in vivo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two pathways for activation of secondary homeostasis in vitro?

A
  1. intrinsic
  2. extrinsic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What components does each step of the coag cascade include?

A
  1. enzyme (activated coagulation factor)
  2. substrate (inactive coag factor - “pro-enzyme”)
  3. cofactor (helps rxn proceed)
  4. (-) charged phospholipid surface provided by platelets
  5. calcium (for steps w/ factors II, VII, IX, X)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the first step of the extrinsic pathway of secondary homeostasis?

A

Tissue injury ->
1. tissue factor (thromboplastin) activates F VII
2. FVII -> FVIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is the extrinsic pathway measured?

A

By the prothrombin time (PT) = time to fibrin clot formation

A long PT -> consider low FVII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the steps of the intrinsic pathway?

A

Starts w/ contact factors: prekallikrein, high molecular weight kininogen collagen (HMWK collagen) and FXII

Includes F XII, XI, IX, VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is the intrinsic pathway measured?

A

By partial thromboplastin time (aPTT)

Long aPTT -> consider low intrinsic pathway factors

Time to fibrin clot formation measured and reported as aPTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are components of the common pathway?

A

Starts w/ FX from either intrinsic or extrinsic pathway

Includes F X, V, II (prothrombin) and FI (fibrinogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is blood prepared for testing in the lab for coag factors?

A
  1. Pt whole blood sample collected in tube w/ anticoagulant (sodium citrate)
  2. Tube centrifuged to separate cells (RBC, WBC and platelets) from plasma

*Plasma = liquid portion of blood + coag factors, formed from centrifuged whole blood that did not clot in tube
*serum = liquid portion of blood -coag factors, formed from centrifuged whole blood that clotted in tube if not anticoag was added to tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

WHich sample is used for coag testing?

A

Plasma is used for PT and aPTT testing - need to have coag factors present to make fibrin from the sample

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a mixing study?

A

Can be done w/ aPTT or PT

If pt has long aPTT or PT, mix equal parts of the pt plasma and normal pooled plasma (has 100% of all coag factors) and then perform aPTT or PT on the mixture

2 possible outcomes:
1. corrects & shortens time to clot
2. fails to correct, clot formation still slow -> s/t other then coag factors is limiting clotting time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is a mixing study interpreted?

A
  1. Correction = factor deficiency
  2. No/partial correction or prolongation w/ incubation = factor inhibitor
    *usually, sometimes inhibitors are not directed at one clotting factor and are non-specific
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a factor inhibitor?

A

An antibody directed against a clotting factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In vitro vs in vivo clotting

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does thrombin do to the coag cascade?

A

Enhances it a several points

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens during in vivo clotting?

A
  1. Initiated most importantly by exposing TF at sites of endothelial damage
  2. TF activates FVII to FVIIa
  3. TF/FVIIa complex is the most IMP activator of FIX (FIX->FIXa) in vivo
  4. Thrombin enhances the cascade through feedback activation in vivo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 5 roles of thrombin?

A
  1. converts fibrinogen to fibrin
  2. stabilizes fibrin clot
  3. activates platelets
  4. pro-inflammatory
  5. anticoagulant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are 3 causes of bleeding disorders?

A
  1. vessel problems
  2. platelet problems (ie ITP)
  3. clotting factor problems (von Willebrand disease, hemophilia A and B, DIC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

INCOMPLETE

A
26
Q

Compare hemophilia A and B

A

-inherited factor deficiencies tend to affect only one factor
-acquired factors tend to affect multiple factors

27
Q

How are hemophilia A and B diagnosed?

A
  • Prolonged aPTT
  • Normal PT and platelet count
  • Diagnostic tests: Factor VIII activity or Factor IX activity
28
Q

What factors are vitamin K dependent?

A

II, VII, IX, and X

29
Q

What factors do hepatocytes make

A

All except VIII

30
Q

What factor would help distinguish b/w liver disease and vitamin K deficiency?

A

Factor V activity b/c it’s not vitamin K dependent

31
Q

What are 4 bleeding disorders w/ norm APTT and PT?

A
  1. von Willebrand Disease (usually) 2. Factor XIII deficiency
  2. Quantitative platelet disorder
    - Thrombocytopenia
  3. Qualitative platelet disorder
    –Acquired- Uremia, myeloproliferative neoplasms, antiplatelet drugs, post-cardiopulmonary bypass
    –Inherited- Glanzmann thrombasthenia, Bernard- Soulier syndrome, others
32
Q

How to interpret coag tests in a bleeding patient

A
33
Q

Reference range for PT and APTT

A

The reference range of the aPTT is 30-40 seconds. The reference range of the PTT is 60-70 seconds.

34
Q

VWF Fxn

A
  1. Mediates platelet binding to sites of vascular injury by binding to collagen and the platelet GPIb receptor (acts as a bridge)
  2. Carrier for coagulation factor VIII
35
Q

VWF Fxn

A
  1. Mediates platelet binding to sites of vascular injury by binding to collagen and the platelet GPIb receptor (acts as a bridge)
  2. Carrier for coagulation factor VIII
36
Q

What is the inheritance pattern of vWD?

A

autosomal dominant (most commonly)
1/100 - 1/10k

37
Q

vWD classifications

A

Type 1: Partial quantitative deficiency (most common)
Type 2: Qualitative deficiency
Type 3: Total quantitative deficiency

38
Q

How is vWD diagnosed?

A

aPTT often normal
* aPTT may be prolonged if FVIII is low enough (this is less common)
* Normal PT and platelet count
* Diagnostic tests- vWD panel
* vWF antigen (VWF:Ag in table in MCQ)
* vWF activity (ristocetin cofactor activity, VWF:Rco in table in MCQ) * Factor VIII activity- why? - often tightly bound to vWF

39
Q

What is fibrinolysis?

A

System regulated by activators and inhibitors to counterregulate hemostasis
The active enzyme plasmin breaks down fibrin clot
* Fibrin degradation products (FDPs), such as D-dimer*, are formed

40
Q

What is fibrinolysis?

A

System regulated by activators and inhibitors to counterregulate hemostasis
The active enzyme plasmin breaks down fibrin clot
* Fibrin degradation products (FDPs), such as D-dimer*, are formed

41
Q

What med induces fibrinolysis?

A

tPA = tissue plasminogen activator

42
Q

What are 3 forms of fibrolytic therapy?

A

Streptokinase, urokinase, tissue plasminogen activator (tPA)
-Convert plasminogen to plasmin to break down fibrin clot

43
Q

What do protein C and S do?

A

Protein C requires protein S as a cofactor
-together they inactivate factors Va and VIIIa to turn off coag cascade (along with antithrombin, which turns off thrombin, also IXa and Xa)

44
Q

What would happen w/ deficiency of protein C? S? Antithrombin?

A

Unregulated coagulation

45
Q

How does antithrombin work?

A

Inactivates thrombin, then F IXa and FXa

46
Q

What is a thrombus?

A

Results from inappropriate activation of hemostasis in an uninjured vessel or from thrombotic occlusion of a vessel after minor injury
-thrombi can obstruct vessels or form emboli

47
Q

What is Virchow’s Triad?

A

3 risk factors leading to thrombosis:
1. endothelial injury
2. abnorm blood flow
3. hypercoaguability

48
Q

What are 2 causes of hypercoaguability?

A
  1. inherited: factor V Leiden
  2. acquired: disseminated cancer
49
Q

What are 2 primary causes of endothelial injury?

A
  1. hypercholesterolemia
  2. inflammation
50
Q

What are 2 primary causes of abnormal blood flow?

A
  1. stasis (a-fib, bed rest)
  2. turbulence (atherosclerotic vessel narrowing)
51
Q

What are 3 pathological features of thrombi?

A
  1. firm
  2. focally attached to vessel wall
  3. have lines of Zahn - striped appearance w/ fibrin (differentiates from postmorten thrombi, which are more gelatinous)
52
Q

Where are 4 locations thrombi are found?

A
  1. venous - where there’s stasis
  2. arterial - where there’s turbulence or endothelial injury
  3. cardiac (mural thrombi) - turbulent or abnorm flow
  4. vegetations - thrombi on heart valves
53
Q

What are 4 fates of a thrombus?

A
  1. propagation - accum more platelets and fibrin
  2. embolization - parts break off, travel elsewhere
  3. dissolution - shrinkage due to fibrinolysis (recently formed thrombi)
  4. organization and recanalization - ingrowth of endothelial cells, smooth muscle cells and fibroblasts w/ capillary channels re-establishing the vascular lumen
54
Q

What are 2 other forms of emboli besides thromboemboli?

A
  1. fat embolism - occurs w/ fracture to long bones. Symptoms: pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, fatal in 5-15%
  2. air embolism = bubbles of gas in circ due to communcation b/w vasculature and outside air or decompression sickness. Can block perfusions or promote cytokine release -> intense inflammation
  3. amniotic fluid embolism = amniotic or fetal tissue introduced into maternal circ via placental membrane or uterine vein tear. Symptoms: sudden severe dyspnea, cyanosis, shock, severe neurologic impairment, DIC
    * 2 to 6 in 100,000 deliveries but up to 80% mortality rate
55
Q

What is hypercoagulability?

A
  • AKA thrombophilia
  • Blood disorder that predisposes to thrombosis
  • Can be either
  • Primary (inherited)
  • Secondary (acquired)
56
Q

What are 5 inherited thrombotic disorders?

A
  1. Factor V Leiden
  2. prothrombin mutation (increases FII)
  3. Protein S def
  4. Protein C def
  5. Antithrombin def

*FV and mutation are more common, but less risk

57
Q

What is Factor V Leiden?

A
  • Autosomal dominant
  • point mutation in coagulation factor V
  • Mutation makes factor V resistant to cleavage and inactivation by activated protein C
  • Activated protein C resistance
  • Greater risk for thrombosis in homozygotes (50-fold increase) than heterozygotes (5-fold increase)
58
Q

Is DIC primary? Why or why not?

A

NOT a primary disease. Associated w/ diseases that cause release of tissue factor or endothelial injury
* Infections, especially bacterial sepsis * Obstetric complications
* Preeclampsia/eclampsia
* Trauma, burns, tissue necrosis
* Venomous bites
* Malignancies
* Leukemia, others
* Severe immunological reactions
* Hemolytic transfusion reactions, transplant rejection
Must know underlying cause for tx

59
Q

How is DIC dx?

A
  1. elevated D-dimer (a fibrin degradation product)
  2. decreased fibrinogen
  3. prolonged PT and APTT
  4. decreased Hct
  5. Schistocytes
  6. decreased platelets
60
Q

What is a D-dimer?

A

2 D domains in crosslinked fibrin that plasmin has cleaved from the fibrin

61
Q

What does D-dimer detection imply?

A
  1. Fibrin has formed and polymerized * There is a thrombus
  2. Factor XIIIa has cross-linked fibrin * There is a stable thrombus
  3. Plasmin has degraded cross-linked fibrin * Fibrinolysis is occurring

MCC (44 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions