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Final_Exam_Semester_4_Charts

Clotting Overview

  • Hemostasis: stopping bleeding; Clotting described as a mass of platelets (PLT) and clotting proteins.

  • Normal clotting sequence (hemostasis):

    • Injury and vasoconstriction: decreases blood flow to allow clotting factors to work.

    • Adhesion (stickiness): PLTs are sticky and adhere to exposed proteins.

    • Activation: PLTs change shape and bind to proteins.

    • Aggregation: PLTs recruit fibrinogen to stabilize the clot.

    • PLT plug formation.

    • Clot dissolution (fibrinolysis).

  • Clotting pathways:

    • Intrinsic pathway

    • Activated when a blood vessel is damaged; longer, more steps.

    • Reflects PTT: PTT ext{ (activated partial thromboplastin time)} \, \approx \, 25-35 \text{ s}.

    • Associated with vessel damage.

    • Extrinsic pathway

    • Extravascular injury causes tissue damage and release of clotting factors; shorter.

    • Reflects PT (Prothrombin Time): PT \, \approx \, 11-13 \text{ s}.

  • Bleeding precautions (RANDO/ RANDI-oriented):

    • Razor: electric (avoid if possible).

    • Aspirin: avoid.

    • Needles: use small-gauge needles.

    • Decrease needle sticks; protect injured areas.

  • Indications to implement bleeding precautions:

    • Anticoagulants, thrombolytics in use.

    • Platelets (PLT) below 150,000/µL.

    • Hemophilia or liver disease.

  • Subjective assessment (history):

    • Health history, medications, prior surgeries, use of blood thinners, contraception, genetic disorders, liver disease, activity level, prior stroke.

  • Objective assessment (physical):

    • Skin, lymph nodes, spleen (spleen only typically felt in kids or very thin adults).

    • RUQ exam: liver enlargement.

    • Bruising, redness, edema.

  • Diagnostic labs (DX):

    • CBC.

    • Coagulation studies: D-dimer, PT, PTT, INR (high when coagulopathy).

    • Peripheral smear.

    • Key reference ranges:

    • RBC: 4-6 \times 10^6/\text{µL}

    • Hgb: 12-18\ g/dL

    • Hct: 35-45\%

    • INR: \leq 1.1 (or 2-3 when on Warfarin)

    • aPTT: 30-40\text{ s} (with activator)

    • Fibrinogen: 200-300\ mg/dL

    • PLT: 150,000-400,000/\text{µL}

    • D-dimer: positive if > 1 (represents fibrin degradation fragments)

  • Warfarin (Coumadin)

    • Indication: chronic anticoagulation; PT/INR monitoring for baseline and ongoing.

    • Dosing and onset: typical initial dose around 5\text{ mg} (varies); takes time to become therapeutic.

    • Baseline testing: PT/INR prior to start; ongoing PT/INR monitoring.

    • Patient teaching: monitor potassium (K+), wear allergy/alert band, apply pressure to bleeding, inform dentist or clinicians about warfarin use.

  • Heparin (UFH)

    • Use: helps antithrombin inactivate clotting factors; not a clot buster but a clot preventer.

    • Pharmacokinetics: short half-life.

    • Administration: subcutaneous (SC) or continuous IV drip; often a bolus loading dose before drip; prophylactic SC dosing (3x daily) due to short half-life; preferred in renal impairment.

    • Considerations: baseline labs (aPTT, CBC, PLT); draw labs every 6 hours with sliding scale (aPTT or anti-Xa). Two RNs verify dose.

    • Peri-procedure management: hold 6-24 hours before procedures; stop a few hours before procedures; exception: epidural/neuro/spinal procedures – hold 18-24 hours.

    • Antidote: protamine sulfate.

  • Enoxaparin (Lovenox) – Low Molecular Weight Heparin (LMWH)

    • Use: prevention and treatment of DVT/PE; inhibits thrombin formation.

    • Administration: subcutaneous; preventive dosing is fixed; therapeutic dosing for DVT is weight-based: 1\ \text{mg/kg}; adjust for renal function.

    • Monitoring: monitor for HIT and platelet count; may monitor aPTT or INR in some settings.

  • Rivaroxaban (Xarelto)

    • Dose options: 10, 15, 20\ \text{mg/day}.

    • Mechanism: inhibits Factor Xa.

    • Contraindication: mechanical heart valve replacement.

    • Interactions: amiodarone, diltiazem, verapamil, macrolide antibiotics, ranolazine.

    • Pharmacokinetics: rapid onset; no routine blood test to monitor efficacy.

    • Administration: take at the same time every day; long-acting; once daily.

  • Apixaban (Eliquis)

    • Mechanism: inhibits Factor Xa; half-life ≈ 12\ \text{hours}; dosing typically 2 \times daily.

    • Indications: oral anticoagulant; 2.5-5 mg tabs.

    • Contraindication: severe renal impairment.

    • Antidote: none listed here.

  • Dabigatran (Pradaxa, direct thrombin inhibitor – ETA: Dabigatran)

    • Dose: 75-150\ mg; oral; must swallow whole; BID dosing.

    • Side effects: similar to Factor Xa inhibitors with GI disturbances; do not crush.

    • Antidote: listed as none here (note: clinically, idarucizumab exists as an antidote; not reflected in this source).

  • Clopidogrel (Plavix)

    • Class: antiplatelet; mechanism: prevents PLT aggregation.

    • Dosing: 75 mg/day; loading dose 300 mg.

    • Indications: often used after MI.

    • Renal impairment: generally okay.

    • Bleeding risk: lower than aspirin; often co-prescribed with PPI to reduce GI bleeding risk; caution with concurrent anticoagulants.

  • Fondaparinux (Arixtra) – LMWH

    • Does not cause HIT.

    • Dosing: subcutaneous; long-acting 2–4 days.

    • Indications: DVT prevention and treatment.

    • Cautions: renal disease and elderly patients.

Clotting Exemplar and Thrombocytopenia Overview (Page 4-5 content)

  • Thrombocytopenia: PLT < 150,000/\text{µL}

    • Severe bleeding not always present even with PLT as low as 100,000; not always necessary to transfuse PLT until critically low.

    • Usually an acquired disorder; main types: Immune thrombocytopenia purpura (ITP), Thrombotic thrombocytopenia purpura (TTP), Heparin-induced thrombocytopenia (HIT).

  • Common causes and manifestations:

    • Drug-induced (piperacillin, chemo, etc.).

    • Mucosal bleeding (nose/gums); petechiae; purpura; ecchymosis; heavy menstrual bleeding; splenomegaly; prolonged bleeding anywhere (e.g., needle sticks).

    • Signs of hypovolemia: tachycardia, hypotension; risk of brain hemorrhage when platelets very low.

  • Diagnostic approach:

    • Spleen assessment via ultrasound/CT is preferred over biopsy in bleeding patients.

    • Labs: CBC; coagulation studies; platelet count; peripheral smear.

  • Acute management principles:

    • Establish baseline status and monitor for changes.

    • Notify PCP of bleeding signs; avoid IM injections and other bleeding risks; careful oral care to prevent mucosal trauma.

    • Review medications that can worsen PLT function/number (list includes various drugs across categories).

  • Drugs that can contribute to PLT problems (selected examples from the list):

    • Diuretics (thiazide), alcohol; digoxin; chemo; estrogen.

    • NSAIDs (indomethacin, naproxen).

    • Aspirin (low-dose) can alter PLT aggregation.

    • Antibiotics (penicillin, cephalosporin, sulfonamides).

    • Antivirals/antifungals (rifampin, ganciclovir, amphotericin B).

    • Antipsychotics/antiseizure medications (haloperidol, valproate, lithium).

    • Platelet glycoprotein inhibitors (clopidogrel, abciximab).

    • H2 antagonists (cimetidine, ranitidine).

    • Herbs and vitamins (e.g., Vitamin E); Vitamin C not clearly stated here.

  • Immune thrombocytopenia purpura (ITP)

    • Pathophysiology: platelets coated with antibodies; spleen/macrophages destroy antibody-coated platelets; shortened PLT lifespan.

    • Population: more common in young women; often immunosuppressed states (Lupus, RA); may be asymptomatic.

    • Bleeding phenotype: variable; may present with bruising, mucosal bleeding, gum bleeding, GI/urinary bleeding; new or ongoing purpura.

    • Management: not always treated unless PLT < 30,000/\text{µL} or active bleeding; platelet transfusion may be ineffective if antibodies present.

    • Therapies (in decreasing order of common use in this source):

    • Corticosteroids – to suppress splenic macrophage response and antibody production; goal to increase PLT lifespan.

    • IVIG – to compete with antiplatelet antibodies for macrophage receptors; reduces platelet destruction; relatively few side effects.

    • Rituximab – monoclonal antibody; reduces immune response and platelet destruction; promotes longer PLT survival.

    • Thrombopoietin receptor agonists – stimulate bone marrow to produce more platelets.

    • Splenectomy – last resort; many patients achieve remission; risk of infection and RBC/PLT sequestration; may reduce antiplatelet antibodies.

  • Thrombotic Thrombocytopenic Purpura (TTP)

    • Characterized by lack of ADAMTS13 enzyme, leading to large von Willebrand factor multimers that promote widespread PLT aggregation and microemboli.

    • Pathophysiology: ADAMTS13 normally cleaves VWF; without it, platelets aggregate on VWF, forming microemboli.

    • Clinical progression: microemboli cause organ ischemia; platelets drop; high risk of death if untreated.

    • Causes: often idiopathic; drug-induced (OC pills, Plavix, chemo); pregnancy; autoimmune conditions.

    • Diagnostic clues: thrombocytopenia with normal coagulation studies; elevated LDH; evidence of tissue damage; schistocytes on smear.

    • Treatment: plasmapheresis (plasma exchange) to remove antibodies and excess VWF; rituximab if plasmapheresis not suitable; immunosuppressants; splenectomy as a last resort.

  • Heparin-Induced Thrombocytopenia (HIT)

    • Definition: thrombocytopenia associated with heparin or LMWH exposure; onset typically 5–10 days after therapy initiation.

    • Mortality: ~20% if untreated due to thrombosis.

    • Pathophysiology: heparin binds to platelet factor 4 (PF4) forming a complex and triggers IgG antibodies; platelet destruction and paradoxical thrombosis.

    • Risk factors: prior heparin exposure; prolonged heparin use; post-surgical prophylaxis.

    • Presentation: mucosal bleeding; thrombosis at IV sites; sometimes bleeding is not the first sign; Thromboembolism risk higher than bleeding.

    • Immediate actions: stop all heparin; document heparin allergy in med record; order PF4 antibody testing; avoid heparin and LMWH.

    • Management: start a direct thrombin inhibitor (Argatroban) to reduce thrombosis risk; maintain anticoagulation; warfarin initiated when PLT count reaches ~150,000/\text{µL}; Argatroban dosing example: 2\ \mu g/kg/min with titration by PTT to 1.5-3x baseline.

    • Alternatives/adjuncts: plasmapheresis for severe clotting; protamine sulfate to reverse heparin; consider thrombolytics or surgical removal of clots if indicated; be cautious with platelet transfusions (avoid unless life-threatening bleeding).

Blood Transfusion, Transfusion Reactions, and Transfusion Protocols (Pages 6-9 content)

  • Blood basics

    • Blood function: transport O2/CO2; maintain intravascular volume; coagulation; fight infection.

    • Hematopoiesis: occurs in bone marrow; erythropoiesis driven by erythropoietin from kidney for RBC production.

    • Blood components: Formed elements (45%) and buffy coat; Plasma (55%).

    • Formed elements:

    • RBC

    • WBCs (buffy coat—high bands indicate active infection)

    • PLT

    • Plasma: primarily water.

  • Blood products and indications:

    • Packed RBC (PRBCs)

    • Washed or Frozen RBCs

    • Platelets

    • Fresh Frozen Plasma (FFP)

    • Albumin

    • Cryoprecipitate

  • Jehovah’s Witnesses considerations: may reject whole blood, PRBCs, plasma; some components may be accepted (clotting factors, cryoprecipitate, albumin, IVIG, epidural patch cell saver). Respect advance directives and support patient in emergent situations.

  • Transfusion reactions (types):

    • Allergic reactions: itching, flushing, hives; treat with antihistamines/corticosteroids; epinephrine for severe reaction.

    • Febrile non-hemolytic reactions: fever, chills, anxiety; may premedicate with acetaminophen; use leukocyte-reduced products to minimize reactions.

    • Acute Hemolytic Reaction: incompatible blood; fever, back/abdominal/chest pain, hypotension, tachycardia, dark urine, jaundice; risk of renal injury; stop transfusion; treat shock; send samples for workup; cross-match new blood if continuing transfusion.

    • Transfusion-Related Acute Lung Injury (TRALI): pulmonary edema due to donor anti-leukocyte antibodies; presents with hypoxemia, frothy sputum, respiratory distress; management supportive; high mortality risk; donors with TRALI history are deferred.

    • Transfusion Associated Circulatory Overload (TACO): volume overload; signs include cough, crackles, dyspnea, JVD, HTN; manage with diuretics, oxygen, positioning; slow transfusion rate; consider reduced volume in high-risk patients.

  • Transfusion steps (Type & Screen and Transfusion workflow)

    • Step 1: Consent and Type & Screen (T&S)

    • Type & Screen is valid for ~72 hours; evaluates blood type and RH status; can take 1–2 hours.

    • Step 2: Supplies

    • Peripheral IV (PIV) or alternatives (PICC, midline, port);

    • 22G typically adequate in adults but bigger is better for rapid transfusion; pump; Y-type tubing with saline on one side and blood on the other; prime with saline; Y tubing typically good for 4 hours due to bacterial risk.

    • Hang blood within 30 minutes of blood from blood bank.

    • Step 3: Double verification

    • Verify with blood bank personnel and bedside with a second nurse; confirm consent, donor number, pt/donor blood tube, expiration date, and date of sample.

    • Step 4: Monitoring

    • Start at about 100-125\text{ mL/hr}, watch for tolerance; bags are often 250-350\text{ mL}; increase after 15 minutes if tolerated; monitor vitals every 15 minutes x2, then every 30 minutes until completion.

    • Step 5: Post-transfusion monitoring

    • Continue monitoring for stability; document start and stop times, toleration, and amount infused; check urine output; recheck Hb within 1 hour; watch for signs of volume overload.

    • Massive Transfusion Protocol (MTP)

    • Used in massive uncontrolled hemorrhage (ER/OR/Labor and Delivery, cardiac surgery, GI bleed).

    • Goal: expand intravascular volume and maintain perfusion and gas exchange.

    • Ratios: commonly 1:1:1 for PRBC:FFP:Platelets (or 4 units PRBC in 1 hour with simultaneous plasma/platelets as needed).

    • Amount goals: 10\ units\text{ of RBC in 24 h} or 4\ units\text in 1 \text{hour}; pediatric dosing often weight-based (e.g., 80 mL/kg).

    • Risks: hemostatic/metabolic complications, hypothermia, TRALI, TACO.

    • Nurse role: contact blood bank to initiate MTP; keep a timer; use a cooler with a timer; use 4-hour rule for blood in the cooler; transfuse 1–2 units rapidly if required; continuous labs and monitoring.

  • Transfusion reaction protocol (summary):

    • Stop transfusion immediately.

    • Keep the line open with normal saline if you need to resuscitate while evaluating.

    • Notify physician and blood bank; document reaction; send samples for workup; cross-match new units.

    • Follow institutional policy for further management.

  • Blood type compatibility (summary table reference):

    • PRBCs: compatible across ABO groups depending on donor compatibility; best to give matched units.

    • Plasma: ABO compatibility important (group AB universal recipient for plasma, but specifics vary by product and country).

    • Platelets: generally compatible with any ABO type; prefer to use the patient’s own blood type if possible.

    • Cryoprecipitate/FFP: used to supply clotting factors; cross-matching practicality depends on clinical scenario.

Blood Product Details (Page 7)

  • Packed Red Blood Cells (PRBC)

    • Indications: low RBC or low Hgb; active bleeding or ongoing loss (trauma, surgery); aplastic anemia.

    • Transfusion threshold: typically Hgb < 7\text{ g/dL} or active bleeding; for acute bleeding or specific conditions, higher thresholds may apply.

    • Administration: 1 unit PRBC increases Hgb by ~1 g/dL; one unit ~500 mL.

  • Washed or Frozen RBCs

    • Washed: reduce WBCs and plasma proteins to decrease allergic reactions.

    • Frozen: can be stored up to 10 years; used for rare needs (autologous transfusion); usable within 24 hours of thawing.

  • Platelets

    • Indications: PLT count <20,000/\text{µL} or significant bleeding due to thrombocytopenia; active bleeding with low PLT counts.

    • Dosing/units: single donor units or pooled packs from multiple donors.

    • Administration: ABO compatibility not strictly required; prefer patient’s own type but not always necessary; administer within 30 minutes or less; platelets are stable at room temperature and should be agitated during transfusion to prevent platelet clumping.

    • Monitoring: monitor for reaction for at least 15 minutes; prolonged monitoring may be needed.

  • Fresh Frozen Plasma (FFP)

    • Indications: DIC, liver disease; massive transfusion where clotting factors are needed; RBC transfusion alone will not replenish clotting factors.

    • Administration: within 30 minutes or less; can be infused rapidly; should be used within 24 hours of thawing; given for clotting factors rather than volume.

  • Albumin

    • Type: volume expander from plasma; moves intravascularly; significant impact on blood pressure with relatively small volumes.

    • Indications: dialysis-related volume management; hypovolemic shock; storage: up to 5 years; concentration options from 5-25%.

    • Cautions: used in dialysis patients with caution for volume overload.

  • Cryoprecipitate

    • Contents: concentrated sources of fibrinogen, Factor VIII, and Factor XIII.

    • Indications: low fibrinogen (<100\ mg/dL); DIC; liver disease; massive transfusion.

    • Administration: delivered by pump or IV push; caution with volume and dosing.

Transfusion Reactions: Key Features and Management (Page 8)

  • Acute Hemolytic Reaction (incompatible blood)

    • Signs: fever, back/abdominal pain, chest pain; tachycardia; hypotension; dark urine, jaundice; kidney injury; shock/DIC/death if severe.

    • Action: stop transfusion; treat shock/DIC; support BP with fluids/albumin; monitor output with Foley; send samples for testing; cross-match and select new blood if continuing.

  • Febrile Non-Hemolytic Reaction

    • Signs: sudden chills, rigor, fever (rise >2°C).

    • Action: stop transfusion if severe; treat with acetaminophen; consider leukocyte-reduced products for future transfusions; premedication may be used.

  • Allergic Reaction

    • Signs: flushing, itching, hives; mild to severe reactions.

    • Action: antihistamines; corticosteroids; epinephrine if severe; may resume transfusion with orders in mild cases.

  • Transfusion-Related Acute Lung Injury (TRALI)

    • Mechanism: reaction between donor antibodies and recipient leukocytes causing inflammation and capillary leak in lungs.

    • Severity: high mortality; treat with oxygen; avoid diuretics (may worsen leukocyte-related edema); chest imaging and ABG support; avoid re-exposure from the same donor.

  • Transfusion Associated Circulatory Overload (TACO)

    • Mechanism: volume overload from rapid transfusion in susceptible patients (renal disease, heart disease, hypertension).

    • Symptoms: cough, crackles, dyspnea, JVD, HTN.

    • Treatment: diuretics, oxygen, upright positioning; slow transfusion rate; use smaller volumes over longer periods; monitor carefully for signs of overload.

Disseminated Intravascular Coagulation (DIC) and HELLP (Page 9)

  • Disseminated Intravascular Coagulation (DIC)

    • Definition: abnormal systemic clotting and bleeding due to an exaggerated clotting cascade; widespread intravascular thrombin generation with widespread fibrin deposition and platelet consumption; then consumption of clotting factors leading to bleeding.

    • Primary trigger: shock or systemic inflammatory response; DIC occurs in ~10% of acutely ill patients with trauma or severe illness.

    • Sequence of events:
      1) Excess intravascular thrombin production.
      2) Fibrinogen converted to fibrin.
      3) Widespread fibrin and PLT deposition in capillaries/arterioles (clots).
      4) Activation of fibrinolysis.
      5) Release of fibrin degradation products (fibrin split products) that break down clots.
      6) Inhibition of normal clotting.
      7) Uncontrolled bleeding.

    • Labs/diagnosis: high D-dimer; low PLT; low fibrinogen; prolonged PT and PTT; schistocytes on peripheral smear; high fibrin split products.

    • Differentiation: DIC vs ITP/TTP/HIT based on coag studies and clotting markers.

    • Management principles: treat underlying cause; stabilize patient; supportive care with blood products; monitor baseline and repeatedly (q4h); continuous hemodynamic monitoring; consider blood products as needed (PLT transfusion for bleeding; cryoprecipitate for low fibrinogen; FFP for clotting factors); hesitance to use heparin/LMWH unless thrombosis risk outweighs bleeding.

  • HELLP Syndrome (Hemolysis, Elevated Liver Enzymes, Low Platelets)

    • Definition: a severe form of preeclampsia; can occur with or without overt preeclampsia; 70% of HELLP cases occur in the third trimester.

    • Features: hemolysis (elevated LDH), elevated liver enzymes (AST/ALT), low PLT count; may present with vague symptoms (HA, nausea/vomiting, RUQ pain, indigestion).

    • Timeline and risk factors: generally develops in the third trimester; risk factors include hypertension, prior HELLP, advanced maternal age (>25), caucasian, multiparity.

    • Classification (severity based on PLT):

    • Class I: severe thrombocytopenia PLT < 50,000/µL.

    • Class II: PLT 50,000–100,000/µL.

    • Class III: PLT 100,000–150,000/µL with AST > 40 U/L.

    • Management principles:

    • Early detection and delivery planning is critical; delivery is indicated at ≥34 weeks gestation; if pregnancy is earlier (24–34 weeks), corticosteroids are used to mature fetal lungs.

    • Bedrest and avoidance of ambulation to prevent placental rupture.

    • MgSO4 for seizure prophylaxis; BP control with appropriate antihypertensives.

    • Transfuse platelets if PLT < 25,000/µL or if significant bleeding or invasive procedures planned.

    • Monitor fetal well-being with biophysical profile, ultrasound, non-stress tests, and fetal movement monitoring.

Summary of Practical Points for Exams

  • Know the differences between intrinsic (PTT) and extrinsic (PT) pathways and how each is reflected in common lab tests (PTT, PT/INR).

  • Be able to interpret key lab values and what they imply for bleeding risk or anticoagulation therapy:

    • PT/INR: Warfarin monitoring; baseline and therapeutic ranges.

    • aPTT: Heparin monitoring; baseline and targets.

    • Fibrinogen: low levels (<200 mg/dL) in bleeding or DIC; indicate replacement needs.

    • D-dimer: elevated in active clot breakdown; not specific, used for ruling out other conditions.

  • Distinguish major anticoagulants and antiplatelets by mechanism, typical use, monitoring needs, and antidotes (as per this material): Warfarin (INR-based), Heparin/LMWH, DOACs (Xa inhibitors: rivaroxaban/apixaban; direct thrombin inhibitor: dabigatran), Clopidogrel, Fondaparinux.

  • Understand the approach to thrombocytopenia (ITP, TTP, HIT) and the typical management strategies and escalation steps.

  • Be able to outline the classic management plan for HIT, including stopping heparin, initiating a direct thrombin inhibitor like argatroban, and the timing for switching to warfarin once platelets recover.

  • Recognize the hallmark features and urgent management steps for DIC and HELLP syndrome, including the emphasis on treating the underlying cause and delivering the baby when HELLP is pregnancy-related.

  • Master the transfusion workflow (Consent/Type & Screen; supplies; double-check; monitoring; documentation) and the Massive Transfusion Protocol (MTP) ratios and logistics.

  • Know the common transfusion reactions, their presenting signs, and initial management steps.

  • Familiarize yourself with the indications for various blood products and the typical thresholds for administration (e.g., when to transfuse platelets, when to use FFP, when to use cryoprecipitate).

If you want, I can reorganize this into concise flashcards or expand any section with more examples or practice questions for exam prep.