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AGPC 4!!!!!! > Lecture 7: Bleeding Disorders > Flashcards

Lecture 7: Bleeding Disorders Flashcards

1
Q

homeostasis: explain how a platelet plug is formed

A
  1. adhesion- Von willebrant factor- protein layer that is works like glue, very sticky- platelets stick to it, to become activated.
  2. aggregation- When platelets become activated they produce substances to call/ aggregate other platelets. Substance they produce- ADP, TXA2- contribute to aggregation of platelets.
  3. platelet plug- platelet plug/ clot will be formed at site of injury
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2
Q

How does ASA work?

A

Blocks TXA2 and therefore stops AGGREGATION

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3
Q

How does Plavix work?

A

Blocks ADP so therefore stops AGGREGATION

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4
Q

Why do we need clotting factors?

A

The platelet plug formed by platelets is not very stable- these are needed to form a more stable clot of fibrin

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5
Q

Where are clotting factors made and where do they live?

A

clotting factors are proteins produced in liver with the help of vitamin K, they are floating around in the blood waiting for opportunity to start clotting cascade

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6
Q

How do clotting factors work?

A

like a chain reaction. Tissue factor starts the clotting cascade- it is released from injured endothelial layer, which triggers factor 7 to be activated, which activates factor 10 which then causes Fibrinogen to turn into fibrin which converts the loose platelet plug to a stable fibrin clot- which is insoluble, so it has a stable base- problem is this is short lived. (this is the extrinsic pathway)

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7
Q

Why is the extrinsic pathway not very efficient?

A

it is short lived and the clot produced is more stable than a platelet plug but not as stable as it can be- only some fibrin is formed but you need the intrinsic pathway to help to form more fibrin. That is why the extrinsic pathway is also activated- amplifies formation of fibrin/ stable clot.

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8
Q

Extrinsic pathway is?

A

factor 12 –> factor 11–> factor 9 –> factor 8 –> factor 10

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9
Q

What happens if a pt has a vitamin K deficiency?

A

at risk for bleeding since liver won’t produce as many clotting factors

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10
Q

How does coumadin work?

A

It reduces vitamin K production, so pt will have reduced level of all factors = increased bleeding. (Coumadin is a INDIRECT anticoagulant since it works on production of factors in liver, not directly on factors)

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11
Q

How do eliquis (apixaban), and xarelto (rivaroxoban) work?

A

they work by directly inhibiting factor 10. (all have X in their name, X=10) they are all DIRECT anticoagulants.

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12
Q

How does Pradaxa (dabigatran) work?

A

directly affects thrombin- clot will not be produced (DIRECT anticoagulant)

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13
Q

How does Heparin work?

A

potentiates natural anticoagulant called anti-thrombin 3

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14
Q

What stops clot production to keep our system in balance of coagulation/ anticoagulation?

A

same injured endothelial cell that releases tissue factor to start clotting cascade also releases t- PA (tissue plasminogen activator)

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15
Q

What does t- PA do?

A

produced to break FRESH fibrin. t- PA only breaks fresh clots which is why you can only give it within 3.5 hours of a stroke.

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16
Q

What is the byproduct of broken down fibrin? What does it indicate?

A

D- dimer. So D- dimer indicates how fresh the clot/ fibrin is. Reflection of active coagulation.

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17
Q

Which meds work on platelets?

A

ASA and plavix- reduce aggregation

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18
Q

Which meds block the formation of fibrin?

A

coumadin and pradaxa through the direct blocking of thrombin; eliquis and xarelto through the direct blocking of factor 10 and heparin because it potentiates natural anticoagulation.

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19
Q

What tests are ordered for the evaluation of primary hemostasis?

A
  1. CBC- platelet count- to see how many platelets we have, should be (150,000- 450,000)- looks at how many NOT function
  2. bleeding time- barbaric test not done anymore- cut the skin and count how long it takes to stop bleeding (should be less than 10 min) only looks at function of platelets not clotting factors
  3. platelet function analysis- updated version of “bleeding time” analyze under microscope how platelets adhere to each other to form clot
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20
Q

What tests are ordered for the evaluation of secondary hemostasis?

A

PT (INR)- 11- 14 seconds for fibrin to be formed

PTT-25- 35 seconds for fibrin to form

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21
Q

What is the difference between PT/INR and PTT?

A

PT/ INR measures EXTRINSIC pathway aka function of clotting factor 7 and PTT measures INTRINSIC pathway aka all other clotting factors
(called extrinsic because you need that initial tissue factor from injury of endothelium to start reaction- added to tube of blood to initiate; with intrinsic all the factors are already in blood- don’t need to add anything to the blood)

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22
Q

If there is a deficiency of factor 8 which test will be abnormal?

A

PTT

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23
Q

What is the difference between INR and PT?

A

INR is standardized tissue factor (the stuff they add from outside) international normalized ratio, everyone uses same standardized tissue factor so you can compare results

24
Q

Why do we used PT/INR to adjust coumadin levels?

A

because factor 7 has very short half- life, so it will reflect changes first; it is the most sensitive indicator of ACUTE changes in the warfarin level

25
Q

Why do we use PTT to adjust Heparin levels?

A

because it affects factors 9 and 11 before 7 for some reason

26
Q

Which test is used for all meds that affect factor 10 (X meds)?

A

there is no good correlation, we don’t really use PT or PTT/ INR to monitor but they will be prolonged just like the others

27
Q

Which conditions do you give these X meds?

A

DVT, PE and non- valvular afib- all the ones that affect factor 10 can be given (xarelto, elaquis)

28
Q

Examples of primary hemostasis bleeding (platelets).

A

Superficial ( mucosal ) bleeding
epistaxis, gingival, vaginal
Skin bleeding (petechia, purpura)

29
Q

Causes of primary hemoastasis disorders?

A 
Inherited: Von Willebrant Disease
Acquired :
Idiopathic thrombocytopenic purpura (ITP)
Aspirin, NSAIDs, Clopidogrel 
Splenomegaly 
Viral infections ( HIV, HCV)
Uremia
30
Q

Examples of secondary hemostasis bleeding (clotting factors).

A

Deep bleeding to joints (hemarthrosis), muscles, retroperitoneal cavity

31
Q

Causes of secondary hemostasis disorders?

A

Hemophilia
Vitamin K deficiency (malnutrition)
Warfarin/ Heparin
Cirrhosis

32
Q

Idiopathic thrombocytopenic purpura

A

is an autoimmune disorder- antibodies attack own platelets “body psych disorder” body wakes up one day and doesn’t recognize its own platelets and attacks them

33
Q

What kind of bleeding causes fatal intracranial bleed?

A

Both

34
Q

Idiopathic thrombocytopenic purpura problem with number or function of platelets?

A

number of platelets- function is normal. It is ISOLATED thrombocytopenia (normal RBC,WBC, clotting factors)

35
Q

Symptoms of ITP?

A

Mostly ASYMPTOMATIC or “platelet-type bleeding” -

superficial bleeding- nose, gums and vagina

36
Q

How to treat ITP?

A

If asymptomatic- don’t need to treat, often comes and goes. But if severe (< 50,000) –> prednisone (reduces the ability of macrophages to bring platelets to spleen who eats them/ stores them) if it keeps happening have to get a splenectomy so there is nowhere for macrophages to bring them/ no one to eat them

37
Q

What is Von Willebrant Disease ( VWD)

A

disorder of platelets but problem is with function not amount of platelets. Von Willebrant factor is the glue, if no glue then the platelets don’t adhere. It’s the most common inherited bleeding disorder (1% of population); Von Willebrant factor also has minimal effect on factor 8- so PTT will be prolonged.

38
Q

What kind of bleeding will happen with ITP and VWD?

A

Superficial bleeding since they are platelet disorders.

39
Q

What kind of disorder it VWD?

A

Autosomal dominant (not on sex chromosome) gene on one chromosome so strong just need one defected gene to cause disease.

40
Q

If you have one parent affected, what are chances kid will get it?

A

50% chance kids will be affected with each pregnancy, regardless of being male or female.

41
Q

How to diagnose VWD with labs?

A 
CBC-  normal platelets 
Prolonged bleeding time (normal < 10 min) 
PTT -may be prolonged (factor VIII)  
PT- normal 
VWF level – decreased
42
Q

s/s of VWD?

A

VWD is usually mild and not diagnosed until surgery or trauma; women w/ menorrhagia – w/u for VWD

43
Q

treatment of VWD?

A

Desmopressin (DDAVP deamino-d-arginine vasopressin), a synthetic ADH - given IV or intra-nasally, induces endothelial cells to release VWF from stores

44
Q

What kind of disorder is hemophilia?

A

X-linked recessive disorder

Hemophilia A – deficiency of factor VIII
Hemophilia B- deficiency of factor IX – less common

45
Q

Who is affected by hemophilia?

A

Clinical features in MALE patients only

46
Q

What is the problem in hemophilia? What kind of bleeding does hemophilia cause?

A

It is a clotting problem (not a platelet problem) type A- deficiency of factor 8, type B- def of factor 9 (B less common). Both cause DEEP bleeding

47
Q

s/s of hemophilia?

A

deep bleeds: hemarthrosis (commonly knee) –> progressive joint destruction; dangerous bleeds are rare- retroperitoneal bleed, intracranial bleed

48
Q

Labs to diagnose hemophilia?

A 
Platelet count –normal 
Bleeding time – normal
PTT- increased (prolonged) 
PT- normal 
F. VIII or IX – decreased 
(these are the same lab results you would get with VWD but TYPE of bleeding is different)
49
Q

Treatment for hemophilia?

A

Clotting factors replacement (recombinant FVIII or FIX)- few times a week they need transfusions.
Patients treated with factor replacement (factor 8 or 9) these pts have near normal life expectancy unless they got infected with HIV back in the day.
To treat acute hemarthrosis – give analgesia and immobilization

50
Q

What is thrombophilia?

A

Pathologic formation of an intravascular blood clot- hypercoagulopathy because there is a lack or defect in anticoagulant proteins ( Increased risk of thrombosis)

51
Q

What are inherited causes of thombophilia?

A
  1. Protein C, protein S deficiency ( inhibits f. V, VIII)

2. Factor V Leiden* most common (mutation f. V > resistance to inactivation)

52
Q

What are acquired causes of thombophlia?

A
  1. Malignancy (production of substances w/ pro-coagulation activity, like tissue factor)
  2. Pregnancy up to 2 months postpartum
  3. Oral contraceptives (increase production of coagulation factors)
53
Q

Clinical features of inherited coagulopathy?

A
  • Age < 50 years
  • Recurrent venous thrombosis DVT and PE
  • Thrombosis is more often when other factors are present (pregnancy, oral contraceptives, immobility)
54
Q

Diagnosis of inherited thrombophilia?

A 
Protein C level 
Protein S level 
Molecular genetic testing for factor V Leiden (level is normal)
PT/INR (normal) 
Platelets (normal)
55
Q

Therapy of thrombophilia?

A

Treat DVT/PE with anticoagulation therapy (Warfarin, direct oral anticoagulants ) for a minimum of 3 months (optimal length of the treatment is unknown)

Indefinite anticoagulation should be considered for unprovoked thrombosis, recurrent thrombosis, life-threatening thrombosis

AGPC 4!!!!!! (10 decks)

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