Chapter 14_1 flashcards

Question 1

Hemostasis: Definition

Answer 1

The physiological process that stops bleeding at the site of an injury.

Question 2

Two Main Processes of Hemostasis

Answer 2

1. Primary Hemostasis: Platelet aggregation to form a platelet plug.
2. Secondary Hemostasis: Deposition of fibrin (generated by coagulation cascade) to strengthen and stabilize the clot.

Question 3

Thrombus: Definition

Answer 3

A blood clot; a collection of aggregated platelets reinforced by fibrin.

Question 4

Platelets (Thrombocytes): Normal Range

Answer 4

150,000 to 400,000 cells per microliter (/uL).

Question 5

Thrombocytopenia: Definition & Value

Answer 5

A low number of platelets, fewer than 100,000/uL; can cause bleeding.

Question 6

Thrombocytosis: Definition & Value

Answer 6

An excessive number of platelets, more than 750,000/uL; can cause excessive clotting.

Question 7

Platelets: Origin & Precursor Cell

Answer 7

Originate from megakaryocytes in the bone marrow.

Question 8

Thrombopoietin: Source & Function

Answer 8

Hormone synthesized by the liver that stimulates platelet formation from megakaryocytes. Stimulated by reduced platelet numbers.

Question 9

Platelet Lifespan & Storage

Answer 9

Normal lifespan: 7 to 10 days. Almost one-third reside in the spleen; spleen can sequester up to 80% if enlarged/hyperactive.

Question 10

Platelet Activation & Aggregation Process

Answer 10

Endothelial injury exposes collagen & releases von Willebrand factor (vWF) -> Activates platelets -> Platelets release adhesive proteins, growth factors, thromboxane A2 -> More platelets drawn to site -> Activation of Glycoprotein (GP) IIb/IIIa receptor -> Binds fibrinogen -> Enhances platelet aggregation, forming a platelet plug.

Question 11

Glycoprotein (GP) IIb/IIIa Receptor: Role

Answer 11

Receptor on platelet surface that, when activated, binds to fibrinogen, acting as a bridge between adjacent platelets and enhancing platelet aggregation.

Question 12

Coagulation Cascade: General Purpose

Answer 12

A stepwise activation of proteins (coagulation factors) in the blood, leading to the formation of fibrin strands which strengthen the platelet plug.

Question 13

Intrinsic Pathway (Coagulation Cascade): Trigger & Measurement

Answer 13

Triggered by damage to endothelial lining of a blood vessel (e.g., inflammation, atherosclerosis) or stasis of blood (e.g., atrial fibrillation). Measured by activated partial thromboplastin time (aPTT).

Question 14

Extrinsic Pathway (Coagulation Cascade): Trigger & Measurement

Answer 14

Triggered by trauma to a blood vessel from external injury (e.g., laceration), exposing tissue factor (TF). Measured by prothrombin time (PT) or International Normalized Ratio (INR).

Question 15

Final Common Pathway (Coagulation Cascade)

Answer 15

Both intrinsic and extrinsic pathways converge to activate Factor X, which converts prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin.

Question 16

Essential Cofactors for Coagulation Cascade

Answer 16

Calcium and Vitamin K (obtained from diet; Vitamin K also synthesized by intestinal bacteria).

Question 17

Fibrinolysis (Clot Dissolution): Key Substances

Answer 17

1. Plasmin: Main enzyme responsible for breaking down clots.
2. Plasminogen: Precursor protein converted to plasmin.
3. Tissue Plasminogen Activator (tPA): Enzyme that changes plasminogen into plasmin.

Question 18

Therapeutic Use of Recombinant Tissue Plasminogen Activator (rtPA)

Answer 18

Drug (e.g., alteplase) used to break down existing clots (thrombolytic agent).

Question 19

Arterial (White) Thrombi vs. Venous (Red) Thrombi

Answer 19

Arterial Thrombi (‘White Thrombi’): Rich in platelets, scarce in RBCs.
Venous Thrombi (‘Red Thrombi’): Large number of RBCs, small number of platelets.

Question 20

Pathological Clotting Disorders: General Causes

Answer 20

Thrombocytosis (increased platelet number), enhanced platelet activity (due to blood flow disturbances, endothelial damage), or increased activation of coagulation factors (stasis of blood, increase in procoagulation factors, decrease in anticoagulation factors).

Question 21

Primary (Essential) Thrombocytosis vs. Secondary (Reactive) Thrombocytosis

Answer 21

Primary (ET): Occurs in bone marrow, cause unknown, increased number of platelets enhances clot risk.
Secondary: Elevated platelet count due to another condition (iron deficiency, cancer, inflammation, surgery); excessive platelets usually do not cause excessive clotting (may even cause bleeding if dysfunctional).

Question 22

Factors Increasing Platelet Activity (Risk for Clots)

Answer 22

Disturbances in blood flow (atherosclerosis), endothelial damage (smoking, high lipids/cholesterol, hypertension, diabetes, immune reactions).

Question 23

Factors Increasing Coagulation Activity (Risk for Clots)

Answer 23

Stasis of blood flow (immobility, heart failure, atrial fibrillation), high estrogen levels (oral contraceptives, pregnancy, postpartum), cancer (tumor cells secrete prothrombotic substances), deficiencies of natural anticoagulants (Antithrombin, Protein C, Protein S).

Question 24

Deep Vein Thrombosis (DVT) & Pulmonary Embolism (PE) Mechanism

Answer 24

DVT (often in lower extremities due to stasis) can break off, travel through inferior vena cava -> right heart -> pulmonary artery, lodging as a PE.

Question 25

Atrial Fibrillation & Stroke Mechanism

Answer 25

Non-contracting atrium -> stasis of blood -> arterial thrombus formation in left atrium -> travels to left ventricle -> aorta -> systemic arteries (commonly carotid -> brain, causing ischemic stroke).

Question 26

Bleeding Disorders: General Causes

Answer 26

Decreased platelet number (thrombocytopenia), platelet dysfunction, deficient/defective coagulation factors, or impaired vascular integrity.

Question 27

Causes of Thrombocytopenia (Decreased Platelet Number)

Answer 27

Decreased synthesis in bone marrow (aplastic anemia, leukemia, radiation, drugs), increased sequestration in spleen (hypersplenism), decreased platelet life span (antibody-mediated destruction like ITP, mechanical injury from prosthetic valves).

Question 28

Causes of Impaired Platelet Activity (Platelet Dysfunction)

Answer 28

Most common: Aspirin and other NSAIDs (aspirin irreversibly inhibits cyclooxygenase for platelet life). Renal failure (uremic toxins). Inherited disorders of adhesion. Other drugs.

Question 29

Causes of Defective Coagulation (Factor Deficiencies)

Answer 29

Defective synthesis (liver disease - e.g., cirrhosis), inherited defects (hemophilia, von Willebrand disease), increased consumption of clotting factors (DIC), Vitamin K deficiency (impairs synthesis of factors II, VII, IX, X).

Question 30

Assessment for Bleeding Disorders: Key History & Symptoms

Answer 30

History: Medications (aspirin, NSAIDs, anticoagulants), vitamin K status, liver disease, cancer, infections, autoimmune disorders, family history (hemophilia, vWD). Symptoms: Epistaxis (nosebleeds), spontaneous bruising (ecchymoses), petechiae, purpura, prolonged bleeding with trauma, GI/GU bleeding, menorrhagia.

Question 31

Assessment for Clotting Disorders: Key History & Symptoms

Answer 31

History: Immobility, surgery, atrial fibrillation, heart failure, cancer, oral contraceptive use, pregnancy, smoking, family history of thrombophilia. Symptoms: Depend on clot location - CVA (stroke), MI (heart attack), DVT (leg swelling/pain), PE (dyspnea, chest pain), PAD (limb ischemia).

Question 32

Prothrombin Time (PT): Measures & Normal Range

Answer 32

Measures integrity of extrinsic pathway (Factors I, II, V, VII, X) and time to clot. Normal range: ~10-14 seconds. Monitors warfarin therapy.

Question 33

Activated Partial Thromboplastin Time (aPTT): Measures & Normal Range

Answer 33

Measures integrity of intrinsic pathway (Factor XII through fibrin clot) and time to clot. Normal range: ~30-40 seconds. Monitors heparin therapy.

Question 34

International Normalized Ratio (INR): Purpose & Therapeutic Range

Answer 34

Standardizes PT measurement. Normal INR = 1. Therapeutic range for anticoagulation (e.g., warfarin): usually 2 to 3 (meaning blood takes 2-3x longer to clot than normal).

Question 35

Other Lab Tests for Bleeding/Clotting Disorders (Table 14-1)

Answer 35

D-dimer (measures fibrin degradation products; elevated indicates recent clotting). Fibrin degradation products. Fibrinogen levels. Platelet aggregation tests.

Question 36

Antiplatelet Drugs: General Use & Examples

Answer 36

Mainly prevent arterial clots (rich in platelets). Examples: Aspirin, Clopidogrel (P2Y12 inhibitor), Abciximab (GPIIb/IIIa receptor antagonist).

Question 37

Anticoagulant Drugs: General Use

Answer 37

Mainly prevent venous clots and clots from atrial fibrillation (rich in fibrin).

Question 38

Heparin (Unfractionated - UFH): Mechanism, Administration, Monitoring, Antidote

Answer 38

Mechanism: Activates antithrombin (natural anticoagulant), preventing clot formation/extension. Administration: IV or SQ. Monitoring: aPTT (therapeutic goal 2-3x control). Antidote: Protamine sulfate.

Question 39

Low Molecular Weight Heparin (LMWH): Mechanism, Advantages, Example, Antidote

Answer 39

Mechanism: Activates antithrombin (smaller fragments of heparin). Advantages: More predictable response than UFH, less monitoring, SC admin once/twice daily. Example: Enoxaparin (Lovenox). Antidote: Protamine sulfate (less effective than for UFH); often just stopping drug is sufficient.

Question 40

Fondaparinux (Arixtra): Mechanism & Use

Answer 40

Factor Xa inhibitor (inhibits prothrombin to thrombin). SC agent, once daily. Used for thromboprophylaxis (surgical/orthopedic patients). Predictable effect, no plasma protein binding.

Question 41

Warfarin (Coumadin): Mechanism, Monitoring, Antidote

Answer 41

Vitamin K antagonist; interferes with synthesis of factors II, VII, IX, X. Monitoring: PT/INR (INR target 2-3). Antidote: Vitamin K.

Question 42

Direct-Acting Oral Anticoagulants (DOACs): General Advantages

Answer 42

Target specific coagulation factors, predictable response, fixed dosing, no routine coagulation monitoring (usually), rapid onset/offset. Examples: Dabigatran, Rivaroxaban, Apixaban, Edoxaban.

Question 43

Dabigatran (Pradaxa): Mechanism & Reversal Agent

Answer 43

Direct thrombin (Factor IIa) inhibitor. Reversal agent: Idarucizumab (Praxbind).

Question 44

Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa): Mechanism & Reversal Agent

Answer 44

Oral Factor Xa inhibitors. Reversal agent for rivaroxaban & apixaban: Andexanet alfa (Andexxa).

Question 45

Thrombolytic Agents ('Clot-Busters'): Mechanism & Uses

Answer 45

Dissolve existing thrombi by converting plasminogen to plasmin, which degrades fibrin. Examples: Tissue Plasminogen Activator (tPA), alteplase. Uses: Acute MI, acute ischemic stroke, PE.