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heme/onc > wk 6 > Flashcards

wk 6 Flashcards

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1
Q

What is the difference between bleeding and thrombosis?

A

Bleeding = hypocoagulable, Thrombosis = hypercoagulable.

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2
Q

What is the role of fibrin in clotting?

A

Fibrin stabilizes the platelet plug. Thrombin converts fibrinogen to fibrin.

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3
Q

What is the earliest response to vascular injury?

A

Vasospasm.

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4
Q

What does von Willebrand Factor (VWF) do?

A

VWF helps with platelet adhesion.

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5
Q

What test is associated with the intrinsic pathway? What factors are involved?

A

aPTT (table tennis indoors). Factors: 12, 11, 9, 8 (especially 8 and 9).

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6
Q

What causes a prolonged PTT?

A

Deficiency of factors 8, 9, 11, 12, VWF, heparin, or direct factor Xa inhibitors.

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7
Q

What test is associated with the extrinsic pathway? What factors are involved?

A

PT (tennis outdoors). Factors: 7 (primary), and 3.

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8
Q

What causes a prolonged PT?

A

Factor 7 deficiency, mild vitamin K deficiency, liver disease, DIC, or warfarin use.

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9
Q

What factors are involved in the common pathway?

A

Factors 10, 5, 2, 1, and 13.

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10
Q

What causes deficiencies in the common pathway?

A

Deficiencies of prothrombin, fibrinogen, factor 5, factor 10, liver disease, DIC, severe vitamin K deficiency, or supratherapeutic anticoagulation doses.

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11
Q

What factors are vitamin K-dependent, and where are they synthesized?

A

Factors 2, 7, 9, and 10. They are synthesized in the liver.

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12
Q

What does a mixing study differentiate between?

A

Factor deficiencies and factor inhibitors.
○ Take patients plasma and pooled normal plasma
○ If clotting test normalizes = Factor deficiency
○ If clotting test does not normalize = Factor inhibitor

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13
Q

How does a mixing study work?

A

Mix patient plasma with pooled normal plasma: - Normalizes = Factor deficiency. - Does not normalize = Factor inhibitor.

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14
Q

What causes hemophilia?

A

Inherited hemorrhagic disorder caused by deficiency of factors 8, 9, or 11.

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15
Q

What is the inheritance pattern for Hemophilia A and B?

A

X-linked recessive. Females with a single mutated gene are generally asymptomatic.

  • 1/3 happen spontaneously
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16
Q

What happens if a father has hemophilia and the mother does not carry the gene?

A

Each son has a 0% chance of having hemophilia. Each daughter has a 100% chance of being a carrier.

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17
Q

What happens if the mother carries the hemophilia gene?

A

50/50 chance for sons and daughters to inherit or not, depending on the X chromosome they receive.

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18
Q

What are the inheritance odds if both parents have hemophilia?

A

100%

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19
Q

What is Hemophilia A?

A

X-linked, Factor 8 deficiency, most common hemophilia.

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20
Q

What is Hemophilia B, and what is it also called?

A

Factor 9 deficiency, 10% of cases, milder than Hemophilia A. Also called Christmas disease.

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21
Q

What is Hemophilia C, and who is it common in?

A

Factor 11 deficiency (Rosenthal syndrome), autosomal recessive. Common among Ashkenazi Jews.

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22
Q

What are the shared signs and symptoms of hemophilia?

A

Bleeding into joints/muscles, bruises easily, prolonged bleeding after surgery/injury, frequent nosebleeds, blood in urine.

PTT: prolonged
PT: normal

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23
Q

What is compartment syndrome, and what causes it?

A

Complication of bleeding into muscles, causing pressure on arteries/nerves. Symptoms: weakness, pallor, swelling, numbness, severe pain, paralysis.

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24
Q

How are Hemophilia A and B treated?

Study These Flashcards
A

Hemophilia A:
- recombinant factor VIII, cryo
- mild = DDVAP (stimulate vWF release from storage sites in endothelial cells and stabilize factor VIII) -> only lasts 6-8 hrs

Hemophila B:
- recombinant factor IX, FFP
- NO DDVAP

25
How is Hemophilia C treated?
Fresh frozen plasma (FFP).
26
What does DDAVP do?
Stimulates release of VWF from endothelial cells. Lasts 6-8 hours.
27
What is von Willebrand Disease (VWD)?
Most common hereditary bleeding disorder (1 in 100). Blood doesn’t clot properly. - autosomal dominant - Abnormal/heavy menstrual bleeding, gum bleeding, easy bruising, frequent nosebleeds, skin rash. Test: VWF antigen testing. Type 3 VWD resembles severe Hemophilia A; risoterin cofactor activity - effectiveness of vWF, factor VIII assay low
28
How is mild VWD treated? vs severe
mild: DDAVP to raise VWF and reduce bleeding risk. severe: Replacement of VWF and factor 8 using concentrates.
29
What is Disseminated Intravascular Coagulation (DIC)?
Simultaneous presence of thrombin and plasmin. Presents as both bleeding and thrombosis. MC underlying disorder = sepsis ELEVATED D-DIMER (fibrin degredation product) tx: Treat the underlying condition, replace platelets, FFP, and cryoprecipitate.
30
What causes vitamin K deficiency?
Nutritional deficiency (alcoholics), antibiotics, warfarin use.
31
How does liver disease affect coagulation?
Liver synthesizes clotting factors. Reduced factor 5 distinguishes liver dysfunction from vitamin K deficiency.
32
What defines a massive transfusion, and how is it managed?
More than 1.5 times a patient’s blood volume in 24 hours. Administer 1 unit FFP and calcium chloride for every 4-6 units PRBCs.
33
What does FFP contain, and when is it used?
Contains all soluble clotting factors (including fibrinogen, factors 5 and 8). Used for multiple factor deficiencies with bleeding.
34
What does cryoprecipitate contain, and when is it used?
Contains fibrinogen, factor 8, VWF, and factor 13. Used to treat hypofibrinogenemia and VWD.
35
What medications can cause bleeding/bruising?
Aspirin, clopidogrel, heparin, NSAIDs, warfarin.
36
How long does aspirin’s antiplatelet effect last?
The life of a platelet (7-10 days).
37
Can hemophilia arise without a family history?
Yes, it can arise from a spontaneous gene mutation.
38
What is HIT, and how is it managed?
Heparin-induced thrombocytopenia. Management = stop the heparin.
39
What is thrombosis? main cause?
Formation of a blood clot inside a blood vessel. Platelet plug = temporary blockage. cause = Virchow’s Triad: Hemostasis, endothelial injury, hypercoagulability.
40
What are venous thromboses made of, and what are examples?
Largely fibrin and RBCs. Examples: DVT, PVT, RVT, JVT, Budd-Chiari syndrome, Paget-Schroetter disease.
41
What diagnostic test is the gold standard for calf DVT?
Contrast venography.
42
What complication can arise from a DVT?
Pulmonary embolism (PE).
43
How is PE diagnosed?
Spiral CT.
44
What are arterial thromboses made of?
Platelet aggregates (white thrombus). MC manifestations: Stroke, MI, limb ischemia (6 Ps: pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia), hepatic artery thrombosis. Test: CTA.
45
How is arterial thrombosis treated?
Aspirin (lasts 7-10 days), clopidogrel, ticagrelor, oral anticoagulants (warfarin), NOACs (rivaroxaban, dabigatran, apixaban).
46
What is the most common hereditary cause of thrombosis?
Factor V Leiden (base pair mutation inactivating factor 5).
47
What is the prothrombin G20210A mutation, and how is it diagnosed?
An inherited thrombosis risk - increased prothrombin levels in blood - autosomal domninant Diagnosed via DNA PCR.
48
What are the causes of acquired thrombosis?
Age, immobilization, major surgery, pregnancy.
49
What is antiphospholipid syndrome, and what is it associated with?
Venous/arterial thrombosis, thrombocytopenia, recurrent fetal loss. Associated with lupus, RA.
50
What is LMWH, and what are its uses?
Low molecular weight heparin (e.g., enoxaparin). Administered SC. Prevents venous thrombosis.
51
What are complications of LMWH and regular heparin?
Bleeding, hypersensitivity reactions, thrombosis, thrombocytopenia (HIT).
52
What are the types of HIT, and how do they differ?
- Type 1: Non-immune, Day 1-4, mild, no complications. - Type 2: Immune-mediated, Day 4-16, moderate-severe, life-threatening thromboembolism possible.
53
How is HIT treated?
Stop heparin, treat with Lepirudin.
54
What is the goal INR for warfarin therapy?
INR 2-3 (without heart valve). Bleeding risk >3; clotting risk <2. Target = ~2.5.
55
How is warfarin overdose treated?
Fresh frozen plasma (FFP) and vitamin K. (best is PCC but not this class)
56
How do NOACs compare to warfarin?
NOACs (e.g., Eliquis) are generally better than warfarin. - NOAC (non vitamin K): rivaroxaban, dabigatran, aprixaban (Eliquis)
57
What are fibrinolytics, and what do they do?
Clot busters: TPA, streptokinase, urokinase.
58
How is Factor 8 deficiency treated?
Factor 8 concentrate, cryoprecipitate, FFP. DDAVP can be used for mild cases.
59
How is VWF deficiency treated?
DDAVP can be used.

heme/onc (4 decks)

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