Patho Pharm module 4

Heparin

*Blood thinner

Drug Class: Anticoagulant; indirect thrombin inhibitor 

Route: IV or SC

Monitor: aPTT

Antidote: Protamine sulfate 

HIT (Heparin-Induced Thrombocytopenia)

*reaction to heparin

low platelets but increased clotting; stop all heparin products 

occurs when the body develops antibodies that attack platelets, leading to a decrease in platelet count (thrombocytopenia) and an increased risk of blood clots

Warfarin (Coumadin)

*blood thinner 

Class: oral anticoagulant

Antagonist: vitamin K (used if life-threatening bleeding occurs; IM or SC)

Use: prevents stroke, MI (myocardial infarction), DVT (deep vein thrombosis), and pulmonary embolism

Monitor: INR (test of how long blood takes to clot)

• Can take days to reach maximum effect

• Patient should not take any other OTC (over-the-counter) drugs

Heparin Bridge

Overlap Heparin+ warfarin during warfarin initiation 

a temporary period of anticoagulation with heparin, used to prevent blood clots (thrombosis) during or after a procedure or when oral anticoagulants (e.g., warfarin) need to be interrupted

Low Molecular Weight Heparin [LMWH] (Enoxaparin: lovenox)

*blood thinner

SC (subcutaneous); longer duration; predictable; less monitoring; no HIT risk

Role of Nurse: anticoagulants 

• The most serious side effect to assess is bleeding 

• To assess internal bleeding: 

  • monitor CBC, lumbar pain, abdominal bulging, & guaiac tests on stool (tests for blood in stool) 

• Assess coagulation studies (lab tests to evaluate blood clotting)

• bleeding risk increases when transitioning from heparin to warfarin

• Do not give warfarin to pregnant patients

• Heparin and LMWH can’t be given to pregnant patients

• Monitor intake of vitamin K-rich foods (limit garlic)

Antiplatelet Drugs

• Prolonged bleeding time by interfering with the clustering of platelets 

• Mechanism: alter the plasma membrane of platelets so they can’t cluster 

• Primary use: prevention of thrombi formation (the process of a blood clot forming in a blood vessel) after stroke or MI 

Aspirin

*Antiplatelet Drug

• OTC (over the counter) 

• indications:

  • pain & inflammation

  • prevention of stroke & MI

• dose varies depending on indication

Clopidogrel (Plavix)

*Antiplatelet; ADP receptor blocker

Mechanism: irreversible platelet inhibition

Duration: affects platelets for their lifespan

• used to reduce the rate of MI or stroke in patients with acute ST-elevation MI (heart attack characterized by a sudden blockage of a coronary artery) 

• Discontinue the drug at least 5 days before surgery 

Role of Nurse: Antiplatelet Agents

• monitor for bleeding

  • risk increases if given anticoagulants

• prolonged pressure needed to control bleeding at puncture sites

• monitor for gastrointestinal upset with warfarin

• may increase menstrual bleeding

Thrombolytics

*medications that dissolve blood clots

Mechanism: convert plasminogen to plasmin (digests fibrin & dissolves clots) 

Unwanted effects: Abnormal bleeding 

Contrainications: should not be used for patients with bleeding disorders, recent trauma, or surgery   

Primary Use: treat acute MI, deep vein thrombosis, and treat cerebrovascular accident, pulmonary embolism, arterial thrombosis, and to clear IV catheters 

Alteplase (Activase)

Class: Thrombolytic; TPA (Tissue Plasminogen Activator: medication used to dissolve blood clots)

Mechanism: Plasminogen → Plasmin → dissolves clots

Timing: immediately after symptoms start

• Unwanted effect: bleeding

  • Intracranial (rare) 

Contraindications: do not use if active internal bleeding, history of stroke or head injury, recent trauma or surgery, severe or uncontrolled hypertension, intracranial neoplasm, or arteriovenous malformation

Role of Nurse: Thrombolytics

• Assess for exclusions to therapy 

• Monitor baseline coagulation studies 

• Perform invasive procedures before administering if possible (ex. IV placement) 

• Monitor level of consciousness for symptoms of cerebral hemorrhage 

• Teach patient about increased risk of bleeding 

Anticoagulants Vs Antiplatelets

• Anticoagulants: Best for Venous thrombi (blood clots within the vascular system) [DVT- Deep Vein Thrombosis, PE- Pulmonary Embolism]

• Antiplatelets: Best for Arterial thrombi [MI- myocardial Infarction, stroke prevention]

DVT & VTE

Deep Vein Thrombosis

• lower extremity pain, redness, swelling, warmth (usually leg) 

• Risk factors: pregnancy, immobility, malignancy

Venous Thromboembolism 

• blockage of a vein caused by a thrombus (blood clot) 

• prophylaxis (prevention): heparin, compression socks, intermittent pneumatic stockings 

PE

Pulmonary Embolism

• dyspnea (shortness of breath), tachypnea (high respiratory rate), hypoxia (inadequate amount of oxygen), tachycardia (high heart rate), hemoptysis (coughing up blood), swelling, warmth 

Virchow’s Triad

Venous stasis (a condition where blood pools in veins)+ Hypercoagulability (a condition where blood has an increased tendency to form clots)+ Vascular injury = higher clot risk 

Hemostasis Steps

Hemostasis is achieved once a blood clot is formed, and the body is protected from excessive hemorrhage (loss of blood)

1. Vascular constriction 

2. Platelet plug (vWF for adhesion, ADP for aggregation) 

3. Coagulation cascade → fibrin 

Disorders: 

• Thrombosis: too much clotting 

• Bleeding: too little clotting 

PT vs aPTT

Both are blood-clotting tests used to see how long it takes to clot 

• PT: extrinsic pathway (activated when blood leaks out of vessel & enters tissue spaces); monitors warfarin; INR standardizes

• aPTT: intrinsic pathway (activated in response to injury); monitors heparin 

Von Willebrand Disease

• A condition where the body does not clot properly due to a problem with the protein called Von Willebrand factor (VWF). 

• Deficiency of vWF → impaired platelet adhesion + Factor VIII (a protein that plays a role in the clotting process) 

• Symptoms: spontaneous bleeding, excessive menstrual flow, & prolonged bleeding times

Hemophilia A

• Factor VIII deficiency 

• X-linked recessive disorder primarily affects males 

• Mild/moderate bleeding due to lesion or trauma 

• Symptoms: bleeding in the GI tract, joints, soft tissue 

• Treatment: Factor VIII replacement, avoid medications that cause bleeding

RBC Basics

• Lifespan: 120 days

• Function: oxygen transport via hemoglobin 

• Production: Bone marrow (stimulated by erythropoietin from kidneys) 

• Broken down by spleen 

Platelet Basics

• Lifespan: 8-12 days 

• Function: Hemostasis

• Normal Count: 150,000-450,00

Dissolution of Clots

• Fibrinolysis: clot removal 

  • starts within 24-48 hours of clot formation 

• Fibrinolysis is initiated by the release of tissue plasminogen activator (TPA: converts plasminogen to plasmin) 

  • Plasmin digests fibrin strands

Thrombocytosis 

Hypercoagulability associated with increased platelet function (your blood clots too easily because your platelets are more active than normal) 

Acquired Hypercoagulability

• Arterial Thrombi: associated with conditions that produce irregular blood flow and platelet adherence 

  • forms within arteries, away from the heart 

• Venous Thrombi: associated with conditions that cause inactivity of blood flow with increased concentration of coagulation factors 

  • forms within veins, towards the heart 

Accelerated activity in the clotting system: 

• pregnancy 

• use of oral contraception 

• post-surgical state 

• immobility 

• congestive heart failure 

• malignant disease 

Thromboembolic disease 

• Definition: a medical condition where a thrombus (blood clot) forms in a blood vessel and either blocks blood flow or a piece breaks off and travels to another part of the body to cause a blockage, an embolism

• thrombus: a stationary clot sticking to the vessel wall 

• embolus: floating clot in blood bloodstream 

• primary treatment: pharmacologic anticoagulation

Thrombocytopenia

• Happens when your body doesn’t make enough platelets, your spleen traps too many, or the platelets break down too quickly

• Drug-induced Thrombocytopenia

  • a condition where platelets are destroyed or their production is impaired due to the use of certain medications

• Visible symptoms: Petechiae (tiny red/purple dots on skin; when you have very few platelets), Purpura (large purple or bruised areas caused by bleeding under the skin)  

Inherited coagulation factor deficiencies

• Von Willebrand Disease

• Hemophilia A

Acquired coagulation factor deficiencies

• liver disease: responsible for the production of many clotting factors

• Vitamin K: needed to produce many clotting factors

  • Newborns are given a vitamin K injection at birth

  • Impaired fat absorption, gall bladder disease 

Labs Blood

• Complete Blood Count (CBC) 

  • Hb: hemoglobin

  • Hct: hematocrit 

  • WBC: white blood cell

  • Platelets

• Clotting Times 

  • PT 

  • PTT

  • INR

• Other Labs 

  • Liver function: AST, ALT

  • calcium

  • Fibrinogen: high (more clots), less (less clots)

Monitoring Blood

• Platelet Count

• Partial Thromboplastin Time (PTT/APTT)

  • measures activity of the intrinsic and final common pathways 

  • normal 30 secs 

• Prothrombin time (PT) 

  • measures activity of the extrinsic and final common pathways 

  • normal 15 secs 

• International Normalized Ratio (INR) 

  • standardizes evaluation of extrinsic pathways

Anemia

• Low RBC and/or hemoglobin (leads to impaired oxygen transport) 

Causes: 

• blood loss 

• destruction of RBCs (hemolysis) 

• Defection of RBC production 

• inadequate RBC production (bone marrow suppression)

Symptoms: 

• Mild hypoxia 

  • metabolic acidosis (too much acid in the blood) 

  • increase in heart rate 

  • peripheral vasoconstriction (blood vessels constrict) 

  • Diaphoresis (sweating)

  • Increase in BP 

  • Slight impairment of mental performance 

• Fatigue 

Blood loss anemia

• The rate of blood loss is important 

  • rapid blood loss: circulatory shock

  • slow blood loss: body has time to adjust/compensate 

• acute blood loss 

  • loss of volume 

Hemolytic anemia

• premature destruction of RBCs (shortened lifespan of RBCs) 

• When the body holds onto iron and other substances that come from the breakdown of red blood cells

• increase in erythropoiesis (process in which erythrocytes are produced) 

  • hyperactive bone marrow, increases immature RBCs 

Sickle Cell Disease

• recessive genetic disorder

• abnormal Hgb structure

• complications: 

  • anemia: reduced oxygen-carrying capacity 

  • blockage of vessels with sickled cells (vaso-occlusive crises) 

• symptoms: 

  • triggered by stress, dehydration, infection, hypoxia 

  • acute pain: ischemia (restriction of blood flow to body part) 

• No treatment focused on preventing sickling episodes 

Sickle Cell Anemia- Hydroxyurea (Droxia)

Drug name: hydroxyurea

Brand name: Droxia 

• increases production of fetal hemoglobin in the bone marrow 

• dilutes abdominal Hbg S 

• reduces frequency of sickling episodes 

• Unwanted effect: Bone marrow suppression → decreased WBCs, decreased platelets, & anemia 

• Contraindications: do not use if patient has severe anemia or leukopenia 

Iron deficiency Anemia

• iron is essential component of heme