Module 2.7 Hemostasis Flashcards

1
Q

Heparin reversal agent

A

Protamine Sulfate

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2
Q

Where does heparin act in the coagulation path

A

Inhibits Factor X to produce fibrin formation.

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3
Q

Which pathway does PTT measure?

A

Intrinsic (Play Table Tennis Inside)

Used to measure heparin effect

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4
Q

Which pathway does PT measure

A

Extrinsic (Play tennis outside)

Used to measure Warfarin effect.

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5
Q

How is platelet function measured

A

Bleeding time test.

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6
Q

3 phases of restoring hemostasis

A
  1. Vessel Spasm
  2. Formation of platelet plug.
  3. Blood Coagulation or development of an insoluble fibrin clot.

(Spazz, plug, clot)

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7
Q

Vessel spasm in hemostatic restoration

A

Spasm is transient (minutes-hours)

Mechanically slows blood flow to the area.

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8
Q

What initiates vessel spasm

A

cytokines

Prostaglandins (Thromboxane A2, Prostacyclin)

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9
Q

Thromboxane A2

A

causes constriction

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10
Q

Prostacyclin

A

Causes dilation, inhibits platelet aggregation in normal uninjured vessels

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11
Q

Half life of platelets

A

8-12 days

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12
Q

What produces platelets

A

megakaryocytes

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13
Q

Listen at 7:30

A

Listen at 7:30

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14
Q

Vitamin K is soluble in

A

fat only

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15
Q

Requirements for clotting

A

Platelets
Von Willebrand Factor
Clotting Factors

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16
Q

Where is Von Willebrand factor generated

A

by the vessel endothelium

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17
Q

Where are clotting factors synthesized

A

in the Liver using Vitamin K

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18
Q

Antithrombin III

A

Contains naturally occurring heparin

Protects against uncontrolled thrombus formation

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19
Q

Protein C

A

Plasma protein

Acts as anticoagulant by inactivating factors V and VIII

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20
Q

Intrinsic Pathway

A

Slow

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21
Q

Extrinsic Pathway

A

Fast

Trauma response

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22
Q

Where do the intrinsic and extrinsic pathways become the same

A

Activation of Factor X

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23
Q

Describe the activation of the coagulation pathway after factor X

A

Xa activates prothrombin to thrombin

Thrombin activates fibrinogen to fibrin

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24
Q

Listen to 13:50 Mark)

A

Listen to 13:50 Mark)

25
Listen to khan academy vid on clotting
Listen to Khan Academy vid on clotting
26
Protein S
Accelerates the action of protein C
27
Negative feedback systems in clotting cascade
Proteins S and C Plasminogen > Plasmin breaks down fibrin mesh into fibrin degradation products Thrombin stimulates anti-thrombin production
28
Anti-thrombin action
inhibits conversion of prothrombin to thrombin | By inhibiting activation of factor X (which is the common pathway!!)
29
Warfarin MoA
Affects vitamin K and therefore dependent factors NOT IMMEDIATELY REVERSABLE
30
Heparin MOA
Affects factor X without other clotting factors IMMEDIATELY REVERSIBLE
31
Heparin is measured with
PTT
32
Warfarin (Coumadin) is measured with
PT
33
What may also decrease vitamin K levels other than Coumadin
Antibiotics (kills bacteria needed for absorption) | Clofibrate
34
Conditions that cause increased platelet function
``` Atherosclerosis Diabetes Smoking HLD and high cholesterol Pregnancy (estrogen increases coagulation) Protein S and C deficiency ```
35
Leiden mutation
Factor V mutation Decreased Protein C effect Hypercoagulability
36
Virchow's Triad
Vessel Injury Stasis Hypercoagulable state
37
Antiphospholipid syndrome
IgG antibodies directed against phospholipids Recurrent venous and ARTERIAL thrombi DVT's, arterial thrombosis in coronary, renal and peripheral arteries Recurrent pregnancy loss TIA's
38
Risk factors for hypercoagulability states
``` Pregnancy and puerperium Oral contraceptives (estrogen) Post-surgical state Virchow's Triad/immobility Congestive Heart Failure Malignant diseases ```
39
Thrombocytosis
>1,000,000 platelets/uL | Due to increased thrombopoietin production
40
Primary thrombocytosis
bone marrow disorders - increased platelet production. Often dysfunctional platelets.
41
Secondary Thrombocytosis
Disease states causing more platelet production ``` Post-op Infection cancer CHRONIC INFLAMMATORY CONDITIONS Myeloproliferative disorders. ```
42
Arterial thrombi are associated with
turbulent blood flow.
43
Venous thrombi are associated with
stasis
44
Thrombocytopenia
<150,000 platelets/uL | clinical issues really start at <100k though.
45
Causes of thrombocytopenia
Decreased platelet production secondary to decreased thrombopoietin. Increased sequestration of platelets in spleen. Decreased Platelet survival Impaired platelets function
46
Types of thrombocytopenia
Drug induced Immune thrombocytopenia purpura (ITP) Thrombotic hrombocytopenia purpura
47
Immune thrombocytopenia purpura (ITP)
autoimmune increased platelet antibody formation usually follows viral infections in children DOESN'T INVOLVE CLOTTING FACTORS
48
Manifestations of thrombocytopenia
Bleeding (nose, mouth, GI Petechiae - pinpoint purple-red spots Purpura - PURPLE areas Splenic enlargement in ITP due to sequestration. Possible Splenectomy.
49
Vitamin K deficiencies
Antibiotics - kill bacteria needed for absorption | Impaired fat absorption (bile salts!)
50
Hemophilia A
Factor VIII deficiency (30% of new cases are new mutations!!!) X-linked recessive ayyyy 8
51
Hemophilia B
Factor IX deficiency | X-Linked Recessive
52
Von Willibrand Disease
Autosomal Dominant (type 1 and 2) Autosomal recessive for type 3 (rare) Normal platelet count Increased bleeding time
53
Hemorrhagic Telangiectasia
Autosomal Dominant | thin walled vessels, dilated capillaries and arterioles
54
Cushing Diseases
protein wasting and loss of vessel tissue support due to increased cortisol
55
Vit. C Deficiency
Scurvy | Poor collagen synthesis and failure of endothelial cells to cement together
56
Senile Purpura
old person bruising
57
Disseminated Intrvascular Coagulation (DIC)
Consumptive process. System wide clotting cascades via INTRINSIC system. All components of cascade wiped out. Severe Hemorrhage occurs. Caused by some other disease or injury.
58
Causes of DIC
``` Gram negative sepsis Obstetric complications Any trauma Hypoxia Shock Hypotension ```