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NLE Hematologic Nursing — Bleeding, Clotting and Hematologic MalignanciesCheat Sheet

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Bleeding, Clotting and Hematologic Malignancies cheat sheet for NLE aspirants. If you could only take one sheet of paper into your review session, this is what it would look like. Professional Regulation Commission (PRC) — Board of Nursing's most-tested concepts, all in one place.

Exam context

For the Philippine Nurse Licensure Examination (PNLE), Professional Regulation Commission (PRC) — Board of Nursing tests Hematologic Nursing under a "Core" label, with Bleeding, Clotting and Hematologic Malignancies in the 2nd slot across 2 chapters. NLE candidates must clear the 75% weighted average with no sub-test below 60% cut on the 2026 paper, which draws about 50 Hematologic Nursing questions. Date to watch: Bi-annual.

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.

Sections

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

Section Title

Normal Hemostasis & Bleeding Risk Thresholds

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

Term

Hemostasis

Example

When you cut your finger, hemostasis seals the wound within minutes.

Definition

The physiologic process that stops bleeding through vessel integrity, adequate platelets, and functional clotting factors.

Term

Thrombocytopenia

Example

A patient with 18,000/µL platelets is at risk for spontaneous, life-threatening hemorrhage.

Definition

Platelet count below 150,000/µL; bleeding risk escalates as count falls.

Diagrams To Know

Three-component model of normal hemostasis (vessels, platelets, factors)

Section Title

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

Term

Immune Thrombocytopenic Purpura (ITP)

Example

A woman with ITP presents with petechiae, epistaxis, and a platelet count of 15,000/µL.

Definition

Autoimmune disorder in which antibodies coat platelets; spleen destroys them → severe thrombocytopenia.

Term

Heparin-Induced Thrombocytopenia (HIT)

Example

Patient on heparin develops falling platelet count AND thrombosis; all heparin must be stopped immediately.

Definition

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

Section Title

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)

Section Title

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

Term

Disseminated Intravascular Coagulation (DIC)

Example

Septic patient develops fever, acral cyanosis, oozing from all sites, low platelets, low fibrinogen.

Definition

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

Common Values

Value

Hemophilia A

Symbol

F VIII

Quantity

Factor VIII deficiency

Value

Hemophilia B

Symbol

F IX

Quantity

Factor IX deficiency

Section Title

Hemophilia A & B

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

Term

Hemophilia A

Example

8-year-old boy presents with hemarthrosis (bleeding into knee joint) after minor fall.

Definition

Inherited X-linked recessive deficiency of clotting factor VIII; most common (80% of hemophilia cases).

Term

Hemophilia B (Christmas Disease)

Example

Adult male with hemophilia B has prolonged bleeding after dental extraction.

Definition

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)

Section Title

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

Term

Acute Leukemia

Example

A 6-year-old with ALL presents with fatigue, fever, petechiae, and a WBC of 120,000/µL with 85% blasts.

Definition

Malignant proliferation of immature WBCs (blasts) in bone marrow; crowds out normal hematopoiesis.

Term

Marrow Failure Triad

Example

Leukemia patient has low Hgb, ANC <500, platelets 15,000/µL.

Definition

Anemia (fatigue, pallor, dyspnea) + Neutropenia (infections) + Thrombocytopenia (bleeding).

Diagrams To Know

Leukemia types by cell line and course
Tumor lysis syndrome cascade

Common Values

Value

<500/µL

Symbol

ANC

Quantity

Critical ANC threshold for infection risk

Section Title

Nursing Care in Acute Leukemia

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

Section Title

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

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

Common Values

Value

Serum/urine electrophoresis

Symbol

M-spike

Quantity

M protein detection

Section Title

Multiple Myeloma

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

Term

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.

Definition

Malignant proliferation of plasma cells in bone marrow producing abnormal immunoglobulin (M protein).

Term

Bence Jones Protein

Example

Myeloma patient has positive urine Bence Jones protein and elevated creatinine.

Definition

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

Common Values

Value

2 mL/min

Symbol

Rate

Quantity

Initial transfusion rate

Value

4 hours

Symbol

Time limit

Quantity

Maximum transfusion time per unit

Section Title

Blood Transfusion: Administration & Safety

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

Term

Blood Administration Set (Y-Set)

Example

Y-set connected: one line to blood unit, one to normal saline for dilution/flush.

Definition

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

Section Title

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

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

Common Values

Value

200–400 mg/dL

Symbol

Fibrinogen

Quantity

Normal fibrinogen

Value

<500 ng/mL

Symbol

D-dimer

Quantity

Normal D-dimer

Section Title

DIC Laboratory Findings & Diagnosis

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

Rows

Values

Factor VIII
Factor IX

Property

Deficiency

Values

~80% of hemophilia
~20% of hemophilia

Property

Frequency

Values

X-linked recessive
X-linked recessive

Property

Inheritance

Values

Prolonged
Prolonged

Property

aPTT

Values

Normal
Normal

Property

Values

Normal
Normal

Property

Platelet count

Values

YES (mild hemophilia A only)
NO

Property

DDAVP effective?

Values

Factor VIII concentrate, DDAVP for mild
Factor IX concentrate (prothrombin complex)

Property

Treatment

Columns

Feature
Hemophilia A
Hemophilia B (Christmas Disease)

Table Title

Hemophilia A vs. Hemophilia B

Rows

Values

Reed-Sternberg cells
NO Reed-Sternberg cells

Property

Pathognomonic finding

Values

Orderly, contiguous from single region
Widespread, random multiple nodes

Property

Spread pattern

Values

Cervical lymph nodes
Variable, often multiple sites

Property

Common starting site

Values

Bimodal (young + older adults)
More common in older adults

Property

Age group

Values

Generally good, especially localized
Varies by subtype (indolent to aggressive)

Property

Prognosis

Values

Highly curable with chemotherapy ± radiation
Variable; may add immunotherapy (rituximab)

Property

Treatment response

Values

Indicate advanced disease
Indicate advanced disease

Property

B symptoms

Columns

Feature
Hodgkin Lymphoma
Non-Hodgkin Lymphoma

Table Title

Hodgkin Lymphoma vs. Non-Hodgkin Lymphoma

Rows

Values

Rapid (days to weeks)
Insidious (months to years)

Property

Onset

Values

>20% blasts
<5% blasts initially

Property

Blast percentage

Values

ALL in children, AML in adults
CLL in older adults, CML in any age

Property

Most common type

Values

Severe, rapid-onset anemia/infection/bleeding
Mild to moderate, gradual

Property

Marrow failure severity

Values

URGENT (days), intensive chemotherapy
May be monitored initially ('watch & wait')

Property

Treatment urgency

Values

Variable; ALL better in children
CML: excellent with imatinib; CLL: variable

Property

Prognosis

Columns

Feature
Acute Leukemia (ALL, AML)
Chronic Leukemia (CLL, CML)

Table Title

Acute vs. Chronic Leukemia

Rows

Values

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

Property

Acute Hemolytic

Values

30–60 min into transfusion
Donor leukocyte antibodies
Fever, chills (NO hemolysis)
Antipyretics; leukocyte-reduced blood for future; may resume if mild

Property

Febrile Non-Hemolytic (Most Common)

Values

10–30 min
Donor plasma proteins
Urticaria, itching
Antihistamines; resume slowly if mild

Property

Mild Allergic

Values

Seconds to minutes
IgA deficiency + IgA in donor blood
Wheezing, bronchospasm, hypotension, shock
STOP, maintain airway, IM epinephrine, use IgA-deficient products future

Property

Anaphylactic

Values

During/after transfusion
Too much volume too fast
Dyspnea, crackles, hypertension, distended neck veins
Sit upright, slow/stop, diuretics, oxygen

Property

TACO (Volume Overload)

Values

Within 6 hours
Donor antibodies → pulmonary inflammation
Acute dyspnea, bilateral infiltrates, hypoxia
Supportive respiratory care

Property

TRALI

Columns

Reaction Type
Onset
Cause
Key Signs
Management

Table Title

Common Transfusion Reactions at a Glance

Rows

Values

150,000–400,000/µL
Primary hemostasis; plug formation
Thrombocytopenia, ITP, DIC, chemotherapy
Petechiae, purpura, mucosal bleeding (gums, nose)

Property

Platelets

Values

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

Property

Clotting Factors (intrinsic: VIII, IX, XI, XII)

Columns

Component
Normal Count/Level
Function
Defect Causes
Bleeding Pattern

Table Title

Platelets vs. Clotting Factors (Function & Defects)

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