Bleeding, Clotting and Hematologic Malignancies - Cheat Sheet
Your last-minute revision companion for high-stakes hematologic nursing topics. Master platelet disorders, clotting defects, malignancies, and transfusion safety in 30 minutes.
Normal Hemostasis & Bleeding Risk Thresholds
Common values
Value
150,000–400,000/µL
Symbol
PLT
Quantity
Normal platelet count range
Value
<10,000/µL
Symbol
PLT
Quantity
Critical bleeding threshold
Important facts
- Normal platelet count: 150,000–400,000/µL
- Below 50,000/µL → bleeding risk with trauma or surgery
- Below 20,000/µL → risk of spontaneous bleeding (CRITICAL threshold)
- Below 10,000/µL → severe, spontaneous, life-threatening hemorrhage risk (including intracranial)
- Hemostasis requires: intact vessels + adequate platelets + functional clotting factors
Key definitions
Hemostasis
Example
When you cut your finger, hemostasis seals the wound within minutes.
The physiologic process that stops bleeding through vessel integrity, adequate platelets, and functional clotting factors.
Thrombocytopenia
Example
A patient with 18,000/µL platelets is at risk for spontaneous, life-threatening hemorrhage.
Platelet count below 150,000/µL; bleeding risk escalates as count falls.
Diagrams to know
- Three-component model of normal hemostasis (vessels, platelets, factors)
Thrombocytopenia and Immune Thrombocytopenic Purpura (ITP)
Important facts
- ITP causes: antibodies attack platelet surface → phagocytosis by spleen
- Clinical signs: petechiae, purpura, ecchymoses, mucosal bleeding (gums, epistaxis), menorrhagia
- Diagnosis: low platelets + normal WBC/Hgb + increased megakaryocytes in marrow
- HIT is a medical emergency; stop ALL heparin immediately (even flushes)
- ITP first-line treatment: corticosteroids (prednisone), IVIG (IV immunoglobulin)
- Anti-D immunoglobulin used in Rh-positive ITP patients
- Splenectomy reserved for corticosteroid-refractory cases
- Thrombopoietin receptor agonists (romiplostim, eltrombopag) for chronic ITP
Key definitions
Immune Thrombocytopenic Purpura (ITP)
Example
A woman with ITP presents with petechiae, epistaxis, and a platelet count of 15,000/µL.
Autoimmune disorder in which antibodies coat platelets; spleen destroys them → severe thrombocytopenia.
Heparin-Induced Thrombocytopenia (HIT)
Example
Patient on heparin develops falling platelet count AND thrombosis; all heparin must be stopped immediately.
Paradoxical immune reaction to heparin causing platelet consumption AND clotting simultaneously.
Diagrams to know
- ITP pathophysiology: antibody coating → splenic destruction
- HIT paradox: thrombocytopenia + thrombosis together
Nursing Management of Thrombocytopenia
Important facts
- BLEEDING PRECAUTIONS: soft toothbrush, electric razor, no aspirin/NSAIDs, no IM injections, avoid invasive procedures
- Monitor for signs of internal bleeding: abdominal pain, headache, vision changes, hematuria
- Monitor for intracranial hemorrhage (ICH): confusion, altered LOC, severe headache
- Educate: avoid contact sports, use stool softeners to prevent straining
- Platelet transfusions only when platelet count <10,000/µL or with active bleeding <20,000/µL
- Do NOT transfuse unless bleeding or count critically low (may alloimmunize)
Disseminated Intravascular Coagulation (DIC)
Important facts
- DIC is ALWAYS secondary to an underlying trigger (never primary)
- Top triggers: sepsis (MOST COMMON), obstetric emergencies, massive trauma/burns, malignancy, transfusion reactions
- Paradoxical process: clotting → microthrombi → organ ischemia, acral cyanosis, THEN bleeding
- Classic lab triad: LOW platelets + LOW fibrinogen + PROLONGED PT & aPTT
- Elevated D-dimer and fibrin degradation products (FDP) from clot breakdown
- Manifestations: oozing from IV sites, petechiae, hematuria, GI bleeding, oliguria, respiratory distress
- Treatment: TREAT THE UNDERLYING CAUSE FIRST (only definitive therapy)
- Supportive: platelets, fresh frozen plasma (FFP), cryoprecipitate (fibrinogen)
- Heparin use selective and controversial (mainly when thrombosis predominates)
- Monitor strictly for bleeding and thrombosis simultaneously
Key definitions
Disseminated Intravascular Coagulation (DIC)
Example
Septic patient develops fever, acral cyanosis, oozing from all sites, low platelets, low fibrinogen.
Secondary disorder of widespread clotting activation producing microthrombi, consuming factors, then paradoxical uncontrolled bleeding.
Diagrams to know
- DIC cascade: trigger → widespread coagulation → microthrombi & consumption → bleeding
Hemophilia A & B
Common values
Value
Hemophilia A
Symbol
F VIII
Quantity
Factor VIII deficiency
Value
Hemophilia B
Symbol
F IX
Quantity
Factor IX deficiency
Important facts
- Inheritance: X-linked recessive → affects MALES, females are CARRIERS
- Hemophilia A = Factor VIII deficiency (MOST COMMON, ~80%)
- Hemophilia B = Factor IX deficiency (~20%)
- Lab hallmark: PROLONGED aPTT with NORMAL PT, normal platelet count, normal bleeding time
- Manifestations: prolonged bleeding after minor injury/surgery, HEMARTHROSIS (bleeding into joints), deep muscle bleeds, hematomas
- Hemarthrosis hallmark: pain, swelling, limited mobility; repeated episodes → joint destruction
- Treatment: FACTOR REPLACEMENT (concentrate) at first sign of bleeding and prophylactically before procedures
- Desmopressin (DDAVP) raises factor VIII levels; used for MILD hemophilia A only
- Joint bleed management: RICE (rest, ice, compression, elevation) + analgesia + factor replacement
- Avoid: aspirin, NSAIDs, IM injections, contact sports
Key definitions
Hemophilia A
Example
8-year-old boy presents with hemarthrosis (bleeding into knee joint) after minor fall.
Inherited X-linked recessive deficiency of clotting factor VIII; most common (80% of hemophilia cases).
Hemophilia B (Christmas Disease)
Example
Adult male with hemophilia B has prolonged bleeding after dental extraction.
Inherited X-linked recessive deficiency of clotting factor IX.
Diagrams to know
- X-linked inheritance pattern: affected males, carrier females
- Intrinsic pathway defect (prolonged aPTT)
Acute Leukemia
Important facts
- Types: ALL (acute lymphocytic) vs. AML (acute myelogenous) vs. CLL (chronic lymphocytic) vs. CML (chronic myelogenous)
- ALL: MOST COMMON in CHILDREN; good treatment response
- AML: MOST COMMON acute leukemia in ADULTS
- CML: associated with PHILADELPHIA CHROMOSOME; treated with tyrosine kinase inhibitors (imatinib)
- Marrow failure triad: ANEMIA + INFECTION (neutropenia) + BLEEDING (thrombocytopenia)
- Infection is the LEADING CAUSE OF DEATH in leukemia
- Diagnosis: CBC (abnormal WBC with blasts) + bone marrow biopsy (confirmatory)
- Treatment: chemotherapy (induction, consolidation, maintenance), targeted therapy, hematopoietic stem cell transplant
- Tumor lysis syndrome (TLS) risk: rapid cell death → K+, uric acid, phosphate ↑; K+ → cardiac arrhythmias, death
Key definitions
Acute Leukemia
Example
A 6-year-old with ALL presents with fatigue, fever, petechiae, and a WBC of 120,000/µL with 85% blasts.
Malignant proliferation of immature WBCs (blasts) in bone marrow; crowds out normal hematopoiesis.
Marrow Failure Triad
Example
Leukemia patient has low Hgb, ANC <500, platelets 15,000/µL.
Anemia (fatigue, pallor, dyspnea) + Neutropenia (infections) + Thrombocytopenia (bleeding).
Diagrams to know
- Leukemia types by cell line and course
- Tumor lysis syndrome cascade
Nursing Care in Acute Leukemia
Common values
Value
<500/µL
Symbol
ANC
Quantity
Critical ANC threshold for infection risk
Important facts
- INFECTION PREVENTION (absolute priority): protective isolation for ANC <500, strict hand hygiene, avoid crowds
- Monitor ANC (absolute neutrophil count) closely; fever in neutropenic patient = medical emergency (treat empirically)
- Maintain bleeding precautions (soft toothbrush, electric razor, no aspirin/NSAIDs)
- Manage chemotherapy side effects: nausea/vomiting, mucositis, alopecia, cardiotoxicity
- Tumor lysis syndrome (TLS) prevention: aggressive hydration (IV fluids), allopurinol/febuxostat (↓ uric acid), monitor labs (K+, uric acid, phosphate)
- Emotional support for parents/child; prepare for long-term treatment and possible relapse
Hodgkin vs. Non-Hodgkin Lymphoma
Important facts
- Hodgkin: Reed-Sternberg cells present (diagnostic)
- Hodgkin: starts in SINGLE cervical lymph node region → spreads ORDERLY, CONTIGUOUSLY
- Hodgkin: bimodal age distribution (young adults + older adults); GOOD prognosis, especially localized disease
- NHL: NO Reed-Sternberg cells
- NHL: usually WIDESPREAD, MULTIPLE-NODE involvement at diagnosis
- NHL: unpredictable spread pattern; MORE COMMON in OLDER ADULTS
- NHL: prognosis varies by subtype (some indolent, some aggressive)
- B symptoms present → advanced disease, worse prognosis
- Most common presentation: painless lymphadenopathy
- Treatment Hodgkin: chemotherapy ± radiation (highly curable)
- Treatment NHL: chemotherapy ± immunotherapy (rituximab) ± stem cell transplant
- Late effects of radiation: second malignancies, cardiac/pulmonary toxicity, infertility
Key definitions
Hodgkin Lymphoma
Example
Young adult with painless cervical lymphadenopathy; biopsy shows Reed-Sternberg cells.
Lymphoma defined by presence of Reed-Sternberg cells; orderly, contiguous spread from single node region.
Non-Hodgkin Lymphoma (NHL)
Example
Elderly patient with widespread lymphadenopathy, no Reed-Sternberg cells, multiple organ involvement.
Diverse group WITHOUT Reed-Sternberg cells; widespread multiple-node involvement, unpredictable spread pattern.
B Symptoms
Example
Lymphoma patient reports 12 kg weight loss, night sweats soaking sheets, fever >38.5°C.
Fever, drenching night sweats, unexplained weight loss (>10%); indicate advanced disease and worse prognosis.
Diagrams to know
- Hodgkin vs. NHL: Reed-Sternberg cells, spread pattern, prognosis
Multiple Myeloma
Common values
Value
Serum/urine electrophoresis
Symbol
M-spike
Quantity
M protein detection
Important facts
- Disease centered on BONE DESTRUCTION and RENAL INJURY
- CRAB criteria (diagnostic): hyperCalcemia + Renal failure + Anemia + Bone lesions
- Manifestations: bone pain (especially back), pathologic fractures, lytic 'punched-out' lesions on imaging
- Hypercalcemia from bone breakdown → nausea, constipation, polyuria, altered mental status, cardiac arrhythmias
- Renal failure from Bence Jones protein in tubules + hypercalcemia
- Recurrent infections from suppressed normal immunoglobulin production
- Diagnosis: M protein on serum/urine electrophoresis, Bence Jones proteinuria, marrow plasmacytosis >10%, lytic lesions
- Treatment: chemotherapy (bortezomib, lenalidomide, melphalan) + corticosteroids + stem cell transplant
- Bisphosphonates (zoledronic acid, pamidronate): protect bone, reduce hypercalcemia
- CRITICAL nursing: encourage HYDRATION 3–4 L/day + MOBILITY to prevent renal failure and manage hypercalcemia
Key definitions
Multiple Myeloma
Example
Elderly man with bone pain, pathologic fracture, Hgb 8 g/dL, Ca 12 mg/dL, Cr 3 mg/dL; serum protein electrophoresis shows M spike.
Malignant proliferation of plasma cells in bone marrow producing abnormal immunoglobulin (M protein).
Bence Jones Protein
Example
Myeloma patient has positive urine Bence Jones protein and elevated creatinine.
Light chains of immunoglobulin excreted in urine; causes renal tubular damage and 'myeloma kidney.'
Diagrams to know
- CRAB criteria for myeloma diagnosis
- Pathophysiology: plasma cells → M protein → bone breakdown + renal damage
Blood Transfusion: Administration & Safety
Common values
Value
2 mL/min
Symbol
Rate
Quantity
Initial transfusion rate
Value
4 hours
Symbol
Time limit
Quantity
Maximum transfusion time per unit
Important facts
- Two-nurse verification at bedside: patient identity (TWO identifiers), blood type/Rh, crossmatch/unit number, expiration, bag integrity
- Obtain informed consent and baseline vital signs before starting
- NEVER transfuse if patient has pre-existing fever (masks early reaction signs)
- Use LARGE-BORE IV (18–20 gauge) and blood tubing with IN-LINE FILTER
- ONLY 0.9% NORMAL SALINE may infuse with blood
- NEVER use dextrose (causes RBC hemolysis) or lactated Ringer's (calcium triggers clotting)
- START SLOWLY: ~2 mL/min initially; STAY WITH PATIENT first 15 minutes (most severe reactions occur early)
- Recheck vitals at 15 minutes, then per policy
- Transfuse each unit WITHIN 4 HOURS (risk of bacterial growth beyond that)
- Prime tubing and change per facility policy
- Document: unit number, patient verification, start time, completion time, patient response
Key definitions
Blood Administration Set (Y-Set)
Example
Y-set connected: one line to blood unit, one to normal saline for dilution/flush.
Tubing with in-line filter for transfusion; allows two fluid sources (blood + saline).
Diagrams to know
- Y-set configuration and blood transfusion circuit
- Transfusion timeline: baseline → 15 min → 1 hour → completion
Transfusion Reactions: Types & Management
Important facts
- IF ANY REACTION SUSPECTED: STOP transfusion immediately, keep vein open with normal saline via NEW tubing
- Notify provider and blood bank; recheck vitals; send blood bag, tubing, and blood/urine samples to lab
- Acute hemolytic: MOST DANGEROUS; usually from clerical/ID error (wrong blood type); rapid fever, chills, flank/back pain, hypotension, hemoglobinuria, shock, DIC, AKI
- Acute hemolytic management: STOP immediately, maintain airway, treat shock (fluid, vasopressors), monitor urine output closely (maintain >200 mL/hr with fluids/diuretics to prevent AKI)
- FNHR: fever/chills only; prevent with leukocyte-reduced blood; treat with antipyretics; transfusion may resume if mild
- Mild allergic: hives/itching; treat with antihistamines; resume slowly if mild and symptoms resolve
- Anaphylactic: wheezing, bronchospasm, hypotension, shock; STOP, maintain airway, give IM epinephrine immediately; use washed/IgA-deficient blood products in future
- TACO: dyspnea, crackles, hypertension, distended neck veins; SLOW/STOP transfusion, sit upright, give diuretics, oxygen; prevent in at-risk (cardiac, elderly) with slower infusion
- TRALI: acute dyspnea within 6 hours, bilateral infiltrates, hypoxia; supportive respiratory care
- Delayed reactions: hemolysis (days later), graft-vs-host disease, infection transmission
Key definitions
Acute Hemolytic Transfusion Reaction
Example
Patient transfused with wrong blood type: fever 39.5°C, chills, severe flank pain, hypotension, dark urine (hemoglobinuria), progresses to shock.
Most dangerous reaction; caused by ABO incompatibility (antigen-antibody mismatch); rapid onset within minutes.
Febrile Non-Hemolytic Reaction (FNHR)
Example
Patient develops fever and chills 30 minutes after transfusion starts; blood smear shows no hemolysis.
Most COMMON reaction; caused by recipient antibodies to donor leukocytes; fever/chills without hemolysis.
Allergic Reaction
Example
Hives and itching appear 10 minutes into transfusion; resolves with antihistamine, transfusion resumes.
Mild-to-severe immune response to donor plasma proteins; ranges from urticaria to anaphylaxis.
Anaphylactic Reaction
Example
IgA-deficient patient receives transfusion: sudden wheezing, bronchospasm, hypotension, shock within minutes.
Severe, rapid reaction in IgA-deficient recipients exposed to IgA in donor plasma; life-threatening airway/shock emergency.
Transfusion-Associated Circulatory Overload (TACO)
Example
Rapid transfusion in elderly patient: dyspnea, crackles bilaterally, hypertension, distended neck veins, pink-tinged sputum.
Acute pulmonary edema from too much volume too fast, especially in cardiac or elderly patients.
Transfusion-Related Acute Lung Injury (TRALI)
Example
Patient develops acute hypoxia, bilateral infiltrates on CXR 2 hours after transfusion; improves with supportive care.
Acute respiratory distress within 6 hours from donor antibodies; mimics ARDS.
Diagrams to know
- Transfusion reaction classification and decision tree
- Acute hemolytic vs. febrile non-hemolytic vs. allergic presentations
DIC Laboratory Findings & Diagnosis
Common values
Value
200–400 mg/dL
Symbol
Fibrinogen
Quantity
Normal fibrinogen
Value
<500 ng/mL
Symbol
D-dimer
Quantity
Normal D-dimer
Important facts
- DIC labs = CONSUMPTIVE COAGULOPATHY: low platelets, low fibrinogen, prolonged PT, prolonged aPTT
- Elevated D-dimer and fibrin degradation products (FDP) from massive clot breakdown
- Classic DIC picture: low platelets + low fibrinogen + prolonged PT & aPTT + high D-dimer = DIAGNOSTIC
- Antithrombin III (AT III) low (consumed in clotting cascade)
- Hematocrit may drop from consumption coagulopathy or active bleeding
- Sequential lab monitoring critical: worsening platelets + fibrinogen = DIC progression
Must remember
- BLEEDING RISK TIERS: <20,000/µL spontaneous bleeding; <10,000/µL life-threatening hemorrhage (NLE HIGH-YIELD)
- ITP = autoimmune platelet destruction by spleen; treat with corticosteroids, IVIG, splenectomy; avoid aspirin/NSAIDs (NLE FREQUENT)
- DIC = clotting then bleeding paradox; ALWAYS secondary; labs show low platelets + low fibrinogen + prolonged PT/aPTT + high D-dimer; TREAT UNDERLYING CAUSE FIRST (NLE CRITICAL)
- Hemophilia = X-linked (males affected); A = Factor VIII, B = Factor IX; hemarthrosis is hallmark; prolonged aPTT + normal PT/platelets (NLE CLASSIC)
- Leukemia triad = anemia (↓Hgb) + infection (↓ANC, fever) + bleeding (↓platelets); infection is LEADING CAUSE OF DEATH; ANC <500 = infection risk (NLE PRIORITY)
- Hodgkin = Reed-Sternberg cells, single region start, orderly spread, good prognosis; NHL = no Reed-Sternberg, widespread, unpredictable, variable prognosis (NLE DISTINCTION)
- Multiple myeloma = CRAB (hyperCalcemia, Renal failure, Anemia, Bone lesions); push hydration 3–4 L/day + mobility; Bence Jones protein → kidney damage (NLE APPLICATION)
- TRANSFUSION: ONLY normal saline (never dextrose/LR), large-bore IV, start 2 mL/min, stay 15 min, finish within 4 hours (NLE PROCEDURE)
- Transfusion reaction: STOP immediately, new tubing + NS, notify provider/blood bank; acute hemolytic = most dangerous (ABO error), febrile = most common (NLE PROTOCOL)
- HIT = heparin paradox (falling platelets + clotting); STOP ALL HEPARIN immediately including flushes (NLE EMERGENCY)
Last minute tips
- When you see 'platelet count + bleeding manifestations,' think FIRST of the specific threshold: <20,000 = spontaneous risk; <10,000 = life-threatening. Don't just say 'low' — quantify.
- DIC is always a SECONDARY disorder with an UNDERLYING TRIGGER (sepsis, trauma, obstetric crisis). If the question doesn't mention a trigger, re-read. Also remember the paradox: clots form FIRST (microthrombi, acral cyanosis), then bleeding begins as factors are consumed.
- Hemophilia X-linked means ONE factor deficiency (VIII or IX) on the intrinsic pathway → prolonged aPTT ONLY (PT/platelets stay normal). Hemarthrosis is SO characteristic that if you see it, think hemophilia immediately.
- Leukemia infections are a PRIORITY — neutropenic fever = medical emergency requiring EMPIRIC antibiotics without waiting for culture. ANC <500 is the danger zone; this is what kills leukemia patients, not the cancer directly.
- Transfusion reactions: if the question mentions ANY symptom during transfusion (fever, rash, dyspnea, pain), your FIRST action is ALWAYS 'STOP the transfusion and keep line open with NS via new tubing.' Everything else (diagnosis, treatment) comes after this stop-and-flush.
Comparison tables
Hemophilia A vs. Hemophilia B
| Feature | Hemophilia A | Hemophilia B (Christmas Disease) |
|---|---|---|
| Deficiency | Factor VIII | Factor IX |
| Frequency | ~80% of hemophilia | ~20% of hemophilia |
| Inheritance | X-linked recessive | X-linked recessive |
| aPTT | Prolonged | Prolonged |
| PT | Normal | Normal |
| Platelet count | Normal | Normal |
| DDAVP effective? | YES (mild hemophilia A only) | NO |
| Treatment | Factor VIII concentrate, DDAVP for mild | Factor IX concentrate (prothrombin complex) |
Hodgkin Lymphoma vs. Non-Hodgkin Lymphoma
| Feature | Hodgkin Lymphoma | Non-Hodgkin Lymphoma |
|---|---|---|
| Pathognomonic finding | Reed-Sternberg cells | NO Reed-Sternberg cells |
| Spread pattern | Orderly, contiguous from single region | Widespread, random multiple nodes |
| Common starting site | Cervical lymph nodes | Variable, often multiple sites |
| Age group | Bimodal (young + older adults) | More common in older adults |
| Prognosis | Generally good, especially localized | Varies by subtype (indolent to aggressive) |
| Treatment response | Highly curable with chemotherapy ± radiation | Variable; may add immunotherapy (rituximab) |
| B symptoms | Indicate advanced disease | Indicate advanced disease |
Acute vs. Chronic Leukemia
| Feature | Acute Leukemia (ALL, AML) | Chronic Leukemia (CLL, CML) |
|---|---|---|
| Onset | Rapid (days to weeks) | Insidious (months to years) |
| Blast percentage | >20% blasts | <5% blasts initially |
| Most common type | ALL in children, AML in adults | CLL in older adults, CML in any age |
| Marrow failure severity | Severe, rapid-onset anemia/infection/bleeding | Mild to moderate, gradual |
| Treatment urgency | URGENT (days), intensive chemotherapy | May be monitored initially ('watch & wait') |
| Prognosis | Variable; ALL better in children | CML: excellent with imatinib; CLL: variable |
Common Transfusion Reactions at a Glance
| Reaction Type | Onset | Cause | Key Signs | Management |
|---|---|---|---|---|
| Acute Hemolytic | Minutes to hours | ABO incompatibility (ID error) | Fever, chills, flank/back pain, hemoglobinuria, hypotension, shock | STOP, maintain airway, treat shock, keep urine output >200 mL/hr |
| Febrile Non-Hemolytic (Most Common) | 30–60 min into transfusion | Donor leukocyte antibodies | Fever, chills (NO hemolysis) | Antipyretics; leukocyte-reduced blood for future; may resume if mild |
| Mild Allergic | 10–30 min | Donor plasma proteins | Urticaria, itching | Antihistamines; resume slowly if mild |
| Anaphylactic | Seconds to minutes | IgA deficiency + IgA in donor blood | Wheezing, bronchospasm, hypotension, shock | STOP, maintain airway, IM epinephrine, use IgA-deficient products future |
| TACO (Volume Overload) | During/after transfusion | Too much volume too fast | Dyspnea, crackles, hypertension, distended neck veins | Sit upright, slow/stop, diuretics, oxygen |
| TRALI | Within 6 hours | Donor antibodies → pulmonary inflammation | Acute dyspnea, bilateral infiltrates, hypoxia | Supportive respiratory care |
Platelets vs. Clotting Factors (Function & Defects)
| Component | Normal Count/Level | Function | Defect Causes | Bleeding Pattern |
|---|---|---|---|---|
| Platelets | 150,000–400,000/µL | Primary hemostasis; plug formation | Thrombocytopenia, ITP, DIC, chemotherapy | Petechiae, purpura, mucosal bleeding (gums, nose) |
| Clotting Factors (intrinsic: VIII, IX, XI, XII) | 50–150% of normal | Secondary hemostasis; stable clot formation | Hemophilia A/B, vitamin K deficiency, liver disease, DIC | Deep muscle bleeds, hemarthrosis, prolonged bleeding after trauma/surgery |
Diagrams
Bleeding Disorders: Classification & Key Features
Mind map showing the three major categories of bleeding disorders: platelet disorders (ITP, HIT, thrombocytopenia), clotting factor defects (hemophilia A & B), and consumption disorders (DIC). Each branch shows key diagnostic and management features.
Transfusion Reaction Decision Tree
Decision tree for managing transfusion reactions. Starts with immediate STOP action, then branches by clinical presentation to specific diagnoses and management for acute hemolytic, febrile non-hemolytic, allergic, anaphylactic, and TACO reactions.
DIC Cascade & Laboratory Profile
Flowchart showing the DIC cascade from trigger through microthrombi formation, consumption of platelets and clotting factors (resulting in prolonged coagulation times), clot breakdown (elevated D-dimer/FDP), and finally the bleeding phase. Emphasizes that treating the underlying cause is the primary intervention.
Leukemia Marrow Failure Progression
State diagram showing the progression from normal bone marrow through blast infiltration and marrow failure, leading to the classic triad of anemia, neutropenia (infection risk), and thrombocytopenia (bleeding risk). Highlights that infection from neutropenia is the leading cause of death in leukemia.
Hemophilia Diagnosis: Lab Pattern
Diagnostic flowchart for hemophilia showing the characteristic lab pattern (prolonged aPTT, normal PT/platelets/bleeding time) and differentiation between Hemophilia A (Factor VIII) and B (Factor IX) based on specific factor assays. Shows inheritance pattern and treatment options for each.
Leukemia Types by Frequency
Pie chart showing the approximate frequency of leukemia types. CLL is most common overall, but ALL is most common acute leukemia in CHILDREN, and AML is most common acute in ADULTS. Useful for remembering epidemiology for NLE.
Blood Transfusion Timeline & Monitoring
Timeline showing critical time points in blood transfusion administration. Emphasizes early-reaction window (0-15 min) when nurse must remain at bedside, vital sign rechecks, and maximum 4-hour infusion window to prevent bacterial growth.