Haemostasis & Coagulation — GCC Nursing Guide

Primary Haemostasis — Platelet Plug Formation

Vascular Injury

→

Vascular Spasm

→

vWF Exposed

→

Platelet Adhesion (GPIb)

→

Activation (ADP/TXA2)

→

Platelet Plug

Key Steps

Vascular Spasm: Immediate vasoconstriction reduces blood flow
Platelet Adhesion: vWF bridges collagen to platelet GPIb receptors
Platelet Activation: ADP, thromboxane A2 released — shape change
Platelet Aggregation: GPIIb/IIIa + fibrinogen cross-links platelets
Platelet Plug: Loose, unstable — requires secondary haemostasis

Clinical Notes

vWF deficiency → von Willebrand disease (mucocutaneous bleeding)
Aspirin irreversibly inhibits COX → blocks TXA2 → impairs activation
Clopidogrel/ticagrelor block P2Y12 ADP receptor
GPIIb/IIIa inhibitors (abciximab) block final aggregation
Thrombocytopenia <50×10⁹/L → impaired primary haemostasis
Bleeding time assesses primary haemostasis (platelet function)

Secondary Haemostasis — Coagulation Cascade

Key concept: In vivo, Tissue Factor (TF) + Factor VIIa is the dominant initiator. The intrinsic pathway amplifies coagulation. The "cascade" model is simplified — cell-based model is more accurate clinically.

Extrinsic Pathway (TF Pathway)

Tissue injury → TF released TF + VII → VIIa complex VIIa activates X and IX Measured by PT/INR

Intrinsic Pathway (Contact)

XII → XI → IX → VIII Amplifies TF-initiated coagulation Measured by aPTT

Common Pathway

X + V → prothrombinase complex Prothrombin (II) → Thrombin (IIa) Thrombin: fibrinogen → fibrin XIII cross-links fibrin (stable clot) Measured by both PT + aPTT

Coagulation Tests Interpretation

Test	Normal	Pathway	Clinical Use
PT/INR	11–13s / INR 0.9–1.1	Extrinsic + Common	Warfarin monitoring; liver function
aPTT	25–35s	Intrinsic + Common	UFH monitoring; haemophilia A/B
Fibrinogen	2–4 g/L	Common (end)	DIC, liver disease, PPH
D-dimer	<0.5 mg/L FEU	Fibrinolysis product	DVT/PE exclusion; DIC
Thrombin time	14–19s	Fibrinogen → Fibrin	Heparin effect; dysfibrinogenaemia

Pattern recognition:
Prolonged PT only → Factor VII deficiency or early warfarin
Prolonged aPTT only → Haemophilia A/B, VWD type 3, UFH
Both prolonged → Common pathway (X,V,II), DIC, liver disease, supratherapeutic warfarin

Fibrinolysis

tPA released

→

Plasminogen → Plasmin

→

Fibrin Degraded

tPA (tissue plasminogen activator) — endothelium releases on clot surface
Plasmin cleaves fibrin → FDPs and D-dimers
Alpha-2-antiplasmin inhibits plasmin (natural brake)
PAI-1 inhibits tPA (another natural brake)
Tranexamic acid / epsilon-aminocaproic acid — antifibrinolytics block plasminogen binding
Elevated D-dimer = fibrinolysis active (not specific for PE/DVT alone)

Natural Anticoagulants & Thrombophilia

Antithrombin (AT-III): Inhibits thrombin + Xa, IXa, XIa. Enhanced 1000× by heparin. Deficiency → thrombophilia
Protein C: Vitamin K-dependent; activated by thrombin-thrombomodulin. Inactivates Va + VIIIa. Deficiency → DVT/PE risk
Protein S: Cofactor for Protein C; free protein S assay. Deficiency similar to Protein C
TFPI (tissue factor pathway inhibitor): Inhibits TF/VIIa/Xa complex
Thrombophilia screen: Factor V Leiden, Prothrombin G20210A, AT, Protein C/S, APLS (anticardiolipin, lupus anticoagulant, anti-β2GP1)
Note: Do NOT test protein C/S or AT while on warfarin or acute thrombosis — false results

Anticoagulation Reversal Guide

Anticoagulant

Bleeding Severity

Last Dose (hours ago)

Reversal Agent & Dose

—

Additional Measures

—

Monitoring

—

Restart Anticoagulation

—

Haematology Consult

—

Clinical decision support only. Always follow local protocol and specialist guidance.

Warfarin (Vitamin K Antagonist)

MOA: Inhibits vitamin K epoxide reductase → reduces II, VII, IX, X, Protein C&S
Onset: 36–72 hours (Factor VII half-life 6h — PT changes first)
Monitoring: INR (target 2–3 for AF/DVT/PE; 2.5–3.5 for mechanical valves)
CYP2C9 interactions: Amiodarone, fluconazole, metronidazole ↑INR; rifampicin, carbamazepine ↓INR
Dietary: Consistent vitamin K intake (green leafy veg, khobz bread)

Reversal

Situation	Action
INR 4–6, no bleed	Omit 1–2 doses, recheck INR
INR >6, no bleed	Omit warfarin + Vit K 1–2.5 mg PO
Minor bleed, any INR	Omit warfarin + Vit K 1–5 mg PO
Major non-life-threatening	Vit K 5 mg IV slow + PCC 25–35 units/kg
Major life-threatening	Vit K 10 mg IV slow + 4-factor PCC 50 units/kg

UFH — Unfractionated Heparin

MOA: Binds antithrombin → inhibits thrombin (IIa) and Xa
Monitoring: aPTT 1.5–2.5× control (60–100 sec typically)
IV half-life: ~1 hour (SC 2–4h)
Reversal: Protamine sulfate 1 mg per 100 units heparin IV; max 50 mg; give over 10 min (risk of hypotension/bradycardia)
HIT monitoring: Platelet count every 2–3 days. Fall >50% within 5–10 days = STOP all heparin immediately
Anaphylaxis risk: Protamine in fish-allergic or prior vasectomy patients

HIT Alert: Stop ALL heparin including flushes/catheters. Use direct thrombin inhibitor (argatroban) or fondaparinux.

LMWH — Low Molecular Weight Heparin

Examples: Enoxaparin, dalteparin, tinzaparin
MOA: Preferentially inhibits Xa (less antithrombin effect than UFH)
Routine monitoring: Not required for most patients
Anti-Xa monitoring needed: Renal impairment (CrCl <30), extremes of weight (<50 kg or >100 kg), pregnancy
Anti-Xa target: BD dosing: 0.6–1.0 IU/mL; OD dosing: 1.0–2.0 IU/mL (4h post-dose)
Reversal: Protamine 1 mg per 100 anti-Xa units (only ~50–60% effective); repeat if needed
Renal dosing: Reduce or avoid if CrCl <30 mL/min — accumulation risk
Note: Can still cause HIT (less common than UFH)

DOACs — Direct Oral Anticoagulants

Drug	Target	Reversal Agent
Rivaroxaban	Xa	Andexanet alfa
Apixaban	Xa	Andexanet alfa
Edoxaban	Xa	Andexanet alfa (off-label)
Dabigatran	IIa (Thrombin)	Idarucizumab (Praxbind)

No routine monitoring required (predictable pharmacokinetics)
Andexanet alfa: 400 mg IV bolus + 4 mg/min infusion 120 min (standard) or 800 mg + 8 mg/min (high dose for rivaroxaban >10 mg, apixaban >5 mg)
Idarucizumab: 5 g IV (2×2.5 g) — fully reverses dabigatran within minutes
If no specific reversal: 4-factor PCC 50 units/kg as bridging measure
Renal consideration: Dabigatran 80% renal excretion — avoid in CrCl <30

DIC — Disseminated Intravascular Coagulation: Life-threatening. Simultaneous widespread clotting AND fibrinolysis → consumption of clotting factors + platelets → paradoxical bleeding + microvascular thrombosis (organ failure).

Pathophysiology

Trigger: Massive TF release or endothelial injury
Thrombin excess: Systemic activation of coagulation
Microvascular thrombosis: Fibrin deposits → organ ischaemia
Factor consumption: I, II, V, VIII, XIII, platelets depleted
Secondary fibrinolysis: Plasmin activated → FDPs, D-dimers ↑↑
Result: Bleeding from ALL sites + simultaneous thrombosis

Common Causes

Sepsis/Infection

Gram-negative septicaemia (most common)
Meningococcaemia
Viral haemorrhagic fever

Obstetric

Abruptio placentae
PPH (postpartum haemorrhage)
Amniotic fluid embolism
AFLP (acute fatty liver of pregnancy)
Eclampsia/HELLP syndrome

Trauma

Massive tissue injury
Crush injuries
Burns
Head trauma

Other

ABO-incompatible transfusion
Malignancy (APL — ATRA therapy)
Snakebite (GCC: viper envenomation)
Pancreatitis

ISTH DIC Score — Overt DIC Diagnosis +

Score ≥5 = Overt DIC (start treatment). Score 3–4 = Non-overt DIC (repeat in 1–2 days). Score <3 = DIC unlikely.

Parameter	Result	Score
Platelet count	>100×10⁹/L	0
	50–100×10⁹/L	1
	<50×10⁹/L	2
PT prolongation	<3 seconds	0
	3–6 seconds	1
	>6 seconds	2
Fibrinogen level	>1 g/L	0
	≤1 g/L	1

D-dimer / FDPs	No increase	0
	Moderate increase (<5× normal)	2
	Strong increase (≥5× normal)	3

DIC Management Algorithm +

Step 1 — TREAT THE UNDERLYING CAUSE FIRST. Antibiotics for sepsis. Deliver in obstetric DIC. Chemotherapy for APL.

Product	Indication	Target
FFP (Fresh Frozen Plasma)	Active bleeding + PT >1.5× normal OR aPTT >1.5× normal	10–15 mL/kg; correct to INR <1.5
Cryoprecipitate	Fibrinogen <1.5 g/L + bleeding	Fibrinogen >1.5 g/L (2 pools cryoprecipitate)
Platelets	<50×10⁹/L + active bleeding; <20×10⁹/L prophylaxis	>50×10⁹/L if bleeding
Tranexamic acid (TXA)	Hyperfibrinolytic DIC (trauma, PPH, APL with fibrinolysis)	1 g IV over 10 min, repeat at 30 min if needed
Heparin	NOT routine in overt DIC with bleeding; may be considered in thrombotic DIC (purpura fulminans)	Specialist-guided only
ATRA	Acute promyelocytic leukaemia (APL)-associated DIC	Haematology-directed

Nursing priorities: Monitor all IV sites for oozing. Avoid unnecessary venepuncture. Pressure 5–10 min on all sites. Avoid IM injections. Monitor UO for renal microthrombi. Continuous pulse oximetry. Document all bleeding sites and volumes.

Thrombocytopenia — Causes Framework

Decreased Production

Bone marrow failure (aplastic anaemia)
Chemotherapy / radiotherapy
Vitamin B12 / folate deficiency (megaloblastic)
Leukaemia / myeloma infiltration
Alcohol (bone marrow suppression)
Viral: HIV, EBV, CMV, hepatitis C

Increased Destruction

ITP — immune-mediated antiplatelet antibodies
HIT — heparin-induced thrombocytopenia
TTP — thrombotic thrombocytopenic purpura
DIC — consumptive
SLE / antiphospholipid syndrome
Drug-induced (quinine, vancomycin)
Hypersplenism (sequestration)

Dilutional

Massive transfusion (>10 units RBC)
IV fluid resuscitation (colloid/crystalloid)
Major surgery / CPB (cardiopulmonary bypass)

Threshold Guide

<150: Thrombocytopenia (define)
<100: Surgery risk ↑
<50: Spontaneous bleed risk
<20: Prophylactic platelet transfusion
<10: Critical — give platelets urgently

ITP — Immune Thrombocytopenic Purpura +

ITP = autoantibodies (anti-GPIIb/IIIa, anti-GPIb) → splenic platelet destruction + impaired megakaryocyte maturation

First-Line

Oral prednisolone 1 mg/kg/day (max 80 mg) × 3–4 weeks then taper
IVIG 1 g/kg/day × 2 days — for rapid rise (surgery, severe bleed). Onset 24–48h
Anti-D immunoglobulin (Rh+, non-splenectomised patients only)

Second-Line

Rituximab 375 mg/m² IV × 4 weekly doses (anti-CD20)
Splenectomy — removes main site of destruction; vaccinate first (PCV, MenACWY, Hib)

Refractory (TPO Receptor Agonists)

Eltrombopag (oral) — 50 mg OD; stimulates megakaryocytes
Romiplostim (SC weekly injection)
Avatrombopag (oral, pre-procedure)

HIT — Heparin-Induced Thrombocytopenia & 4Ts Score +

HIT = IgG antibodies to heparin-PF4 complex → platelet activation → paradoxical thrombosis (arterial + venous). Platelet count typically 20–80×10⁹/L.

4Ts Scoring System

Thrombocytopenia: >50% fall + nadir ≥20

2 pts

Thrombocytopenia: 30–50% fall OR nadir 10–19

1 pt

Timing: Day 5–10 OR within 1 day if prior heparin <30 days

2 pts

Thrombosis: New confirmed thrombosis / skin necrosis

2 pts

oTher causes: None apparent

2 pts

Score 6–8 = High probability. Score 4–5 = Intermediate. Score 0–3 = Low.

HIT Management — CRITICAL STEPS

STOP ALL HEPARIN immediately — including flushes, LMWH, heparin-coated catheters
Start alternative anticoagulant: Argatroban (IV) or Fondaparinux (SC) or Bivalirudin
Send HIT antibody test: PF4-heparin ELISA + serotonin release assay
Do NOT give platelets (unless life-threatening bleed) — may fuel thrombosis
Do NOT start warfarin until platelet count >150×10⁹/L (risk of limb gangrene from protein C depletion)
Bilateral lower limb Doppler — HIT causes DVT in 50% even without clinical signs

TTP — Thrombotic Thrombocytopenic Purpura & PLASMIC Score +

TTP: ADAMTS13 deficiency (congenital or acquired autoantibody) → ultra-large vWF multimers → platelet microthrombi in small vessels → MAHA + thrombocytopenia + neurological/renal/cardiac involvement.

Classic Pentad (not always all present)

Microangiopathic haemolytic anaemia (MAHA)
Thrombocytopenia (<30×10⁹/L typically)
Neurological symptoms (confusion, seizures)
Renal impairment (less severe than HUS)
Fever

Blood Film

Schistocytes (fragmented RBCs) >1% = key finding
Elevated LDH, low haptoglobin (haemolysis markers)
ADAMTS13 activity <10% = diagnostic

PLASMIC Score (pre-ADAMTS13 result)

Platelet count <30×10⁹/L

1 pt

Lysis (haemolysis — reticulocytes >2.5% or haptoglobin undetectable)

1 pt

Active cancer (no = 1 pt)

1 pt

Stem-cell or solid organ transplant (no = 1 pt)

1 pt

MCV <90 fL

1 pt

INR <1.5

1 pt

Creatinine <200 µmol/L

1 pt

Score 6–7 = High risk (96% sensitivity). Start plasma exchange immediately.

Treatment

Plasma exchange (PEX/TPE): Daily; removes antibodies + replaces ADAMTS13
Caplacizumab: Anti-vWF nanobody — given SC daily; reduces time to response
Steroids: Prednisolone 1 mg/kg or methylprednisolone IV
Rituximab: For refractory or relapsing TTP
Do NOT transfuse platelets — may worsen thrombosis

MTP — Massive Transfusion Protocol: Activation Criteria & Product Ratio +

MTP Activation Criteria (any 1 of)

Active haemorrhage + haemodynamic instability despite 2L crystalloid
>4 units RBC in 4 hours with ongoing bleeding
Anticipated requirement >10 units RBC in 24 hours
TASH score ≥16 (trauma associated severe haemorrhage)
ABC score ≥2 (assessment of blood consumption)
Clinical judgment: massive obstetric haemorrhage, ruptured aortic aneurysm

Call for help: Haematologist + Surgeon + Anaesthetist + Blood Bank simultaneously

Product Ratio — 1:1:1

RBC : FFP : Platelets = 1 : 1 : 1

Every 6 units RBC → 1 pool platelets

Cryoprecipitate if fibrinogen <1.5 g/L (2 pools)

TXA 1 g IV STAT + 1 g over 8h (within 3 hours of injury)

Calcium: CaCl₂ 1g IV every 4 units RBC (citrate chelation)

Target: Hb >80, Plt >50, Fib >1.5, pH >7.35, Temp >36°C

CRASH-2 Mnemonic — Major Haemorrhage Response

C — Control Bleeding

Direct pressure first
Tourniquet (limb haemorrhage)
Haemostatic dressings (Combat Gauze — kaolin-impregnated)
Wound packing for junctional bleeding
Surgical haemostasis (damage control)

R — Resuscitate with Blood Products

Avoid excessive crystalloid (dilutional coagulopathy)
MTP activation as above
Permissive hypotension (MAP 50–65 in trauma, until surgical control)
Warm all products (hypothermia worsens coagulopathy)

A — Antifibrinolytics

TXA 1 g IV within 3 hours of injury/PPH
CRASH-2 trial: reduces mortality in trauma
WOMAN trial: reduces PPH mortality
Repeat dose 1 g if continued bleeding

S — Surgery

Damage control laparotomy (pack + close)
Obstetric: B-Lynch suture, hysterectomy
Interventional radiology: embolisation
Endoscopy: GI haemorrhage

H — Haematology Consult

ROTEM/TEG guidance (viscoelastic testing)
Factor concentrates if specific deficiency
Fibrinogen concentrate vs cryoprecipitate
rFVIIa (NovoSeven) as last resort (off-label)

Epistaxis Management — BPPN

B — Bend Forward

Lean forward to prevent blood swallowing (nausea, airway risk)

P — Pinch Soft Part

Pinch the soft cartilaginous part of nose (Little's area — Kiesselbach's plexus)

P — Pressure 15 min

Continuous uninterrupted pressure for 15 minutes by clock

N — No Peeking

Do not release pressure to check — allows clot to reform

If fails: Silver nitrate cautery → nasal packing (anterior) → posterior balloon → ENT referral → consider Nasopore/BIPP packing. Check INR/platelets if recurrent.

GI Bleeding — Risk Scores & Management

Blatchford Score (pre-endoscopy — need for intervention)

Score 0 = low risk → outpatient management
Score ≥1 = requires endoscopy within 24h
Parameters: Urea, Hb, SBP, HR, melaena, syncope, liver disease, cardiac failure

Rockall Score (post-endoscopy — rebleed risk)

Score ≥8 = high rebleed + mortality risk
Parameters: Age, shock, comorbidities, endoscopy findings, stigmata of haemorrhage

Management

IV PPI: Omeprazole 80 mg bolus + 8 mg/h infusion (peptic ulcer)
Transfusion threshold: Hb <80 g/L (restrictive strategy, except ACS: <100)
Terlipressin: Variceal bleeding (portal hypertension)
Octreotide: Variceal + non-variceal haemorrhage adjunct
Sengstaken-Blakemore tube: Refractory variceal bleed (temporary bridge)

Subarachnoid Haemorrhage (SAH) — Haemostasis Considerations

Nimodipine 60 mg PO/NG q4h × 21 days — prevents delayed cerebral ischaemia from vasospasm (NOT to control bleeding)
Controlled BP: SBP <160 mmHg prior to aneurysm securing; avoid hypotension
Avoid anticoagulants in acute phase until aneurysm secured
TXA: Short-term (within 24h to aneurysm repair) reduces rebleed risk in some protocols

Coagulation check: Baseline PT, aPTT, platelets, fibrinogen pre-procedure
Reversal of anticoagulants required before coiling/clipping
Glasgow Coma Scale monitoring — coagulopathy worsens prognosis
Hunt-Hess grading guides surgical timing
Hydrocephalus monitoring — EVD insertion may require platelet ≥100×10⁹/L

GCC Haematology — Inherited Disorders

Sickle Cell Disease (SCD)

Autosomal recessive; HbS mutation (Glu→Val, position 6 β-globin); high prevalence in Gulf, Saudi Arabia, Oman
Vaso-occlusive crisis → microvascular thrombosis → ischaemia
Coagulopathy in SCD: Chronic hypercoagulable state; increased TF expression, platelet activation; elevated D-dimer; thrombocytosis may occur
Stroke risk: TCD screening in children; hydroxyurea reduces crises
Nursing: Hydration, analgesia, oxygen, transfusion threshold Hb <60 g/L or acute chest

Thalassaemia

Alpha/beta thalassaemia highly prevalent in GCC (consanguinity factor)
Thalassaemia major → chronic transfusion dependence → iron overload → organ damage
Coagulopathy: Chronic haemolysis → endothelial dysfunction → thrombosis risk especially in post-splenectomy; hypercoagulable
Deferasirox/desferrioxamine: Iron chelation therapy
Bone marrow transplant: Curative option; curative gene therapy emerging

G6PD Deficiency in GCC

G6PD deficiency is among the most common enzyme deficiencies globally — particularly prevalent in GCC, Middle East and Mediterranean populations.

Pathophysiology

X-linked recessive → males predominantly affected
G6PD protects RBCs from oxidative damage (generates NADPH)
Trigger → oxidative stress → Heinz bodies → acute haemolytic anaemia

Common Triggers

Fava Beans Primaquine Dapsone Nitrofurantoin Rasburicase Aspirin (high dose) Sulfamethoxazole Infection/Illness

Nursing: Patient education critical — avoid fava beans (ful medames — common in GCC diet). Medication reconciliation before prescribing. Blood film: Heinz bodies, bite cells.

Warfarin Clinic Management in GCC

INR monitoring frequency: Weekly until stable × 2 readings, then monthly
Dietary vitamin K: Consistency is key — not elimination. Common GCC high-K foods:

Spinach (Sabanekh) Parsley Coriander (Kuzbara) Khobz (Arabic bread) Green tea Fenugreek

Ramadan fasting: Dietary pattern change → INR fluctuation. Monitor INR more frequently during Ramadan
Herb interactions: Black seed (Nigella sativa) may ↑ anticoagulant effect; discuss herbal medicines routinely
Compliance: SMS reminders, pharmacy-led anticoagulant clinics in DHA/MOH hospitals
Sick day rules: Illness → altered diet + absorption → INR change; advise to contact clinic

DHA/DOH/SCFHS Competencies

DHA (Dubai Health Authority)

Haematology nursing exam covers: coagulation cascade, anticoagulant monitoring, transfusion reactions, DIC recognition
Competency: Correct blood sampling technique, EDTA vs citrated tubes, proper mixing/inversion
Blood transfusion: pre-transfusion checklist, vital signs monitoring, transfusion reaction management

SCFHS (Saudi Commission for Health Specialties)

Saudi Nursing Licence (SNL) exam: bleeding assessment, anticoagulation safety, patient education
Prometric: INR target ranges, reversal agents, HIT recognition are high-yield
Saudi MOH haematology nursing standards: anticoagulation stewardship programme

DOH (Department of Health — Abu Dhabi)

HAAD/DOH licence: clinical competency assessment includes haemostasis topics
Evidence-based practice: NICE/ASH guidelines adapted for UAE context

Islamic Bioethics & Blood Products in GCC

Islamic Jurisprudence (Fiqh)

Blood is considered najis (impure) under normal circumstances; however, the principle of darura (necessity) permits its use in life-threatening situations
Majority Islamic scholarly consensus: Blood transfusions and blood products (FFP, platelets, cryoprecipitate, albumin) are permissible when medically necessary
Fatwas from Al-Azhar, OIC Fiqh Academy, Saudi Permanent Committee: all permit blood transfusions when life is at risk
Autologous blood donation (own blood, pre-operative) is widely accepted

Clinical Implications in GCC

Jehovah's Witnesses are rare in GCC (predominantly non-Muslim community members); blood refusal is uncommon in GCC context
If blood refused: Explore the basis (cultural vs religious vs fear-based); involve hospital ethics committee; document informed refusal
Bloodless surgery: Cell salvage, erythropoietin, iron therapy — valid alternatives to discuss
Patient education: Reinforce Islamic permissibility; involve religious counsellor if requested
Documentation: Detailed informed consent; note the discussion in medical record

GCC Exam Prep — 5 MCQs: Haemostasis & Coagulation

Click an answer to check. Answers are based on SCFHS/DHA/DOH exam standards.

1. A patient on warfarin presents with an INR of 7.2 and no active bleeding. Which is the MOST appropriate immediate action?

A. Administer 4-factor PCC 50 units/kg IV immediately
B. Omit warfarin and administer vitamin K 1–2.5 mg orally
C. Continue warfarin at same dose and recheck INR in 2 weeks
D. Administer fresh frozen plasma 10 mL/kg IV

Correct: B. For INR >6 without bleeding: omit warfarin and give vitamin K 1–2.5 mg orally. PCC and FFP are reserved for major/life-threatening bleeding. Continuing the same dose is unsafe at INR 7.2.

2. A post-surgical patient on UFH develops a platelet count drop from 230×10⁹/L to 85×10⁹/L on day 7. The nurse suspects HIT. Which action is MOST critical?

A. Transfuse platelets to maintain count above 100×10⁹/L
B. Switch from UFH to LMWH immediately
C. Stop all heparin including flushes and start argatroban
D. Start warfarin immediately to prevent thrombosis

Correct: C. HIT management requires stopping ALL heparin products (including flushes and LMWH) and starting a non-heparin anticoagulant such as argatroban. Platelet transfusion may worsen thrombosis. LMWH can cross-react. Warfarin is contraindicated until platelets >150×10⁹/L.

3. In overt DIC (ISTH score ≥5) with active bleeding and fibrinogen of 1.1 g/L, which product should be prioritised AFTER treating the underlying cause?

A. Unfractionated heparin infusion to prevent further microthrombi
B. Cryoprecipitate to raise fibrinogen above 1.5 g/L
C. Aspirin to reduce platelet aggregation
D. Recombinant factor VIIa as first-line therapy

Correct: B. Cryoprecipitate is indicated when fibrinogen <1.5 g/L with active bleeding in DIC. Heparin is NOT routinely used in overt DIC with bleeding. Aspirin is contraindicated. rFVIIa is a last resort, not first-line.

4. A patient with G6PD deficiency is admitted with a urinary tract infection. Which antibiotic should be AVOIDED?

A. Amoxicillin-clavulanate
B. Ceftriaxone
C. Nitrofurantoin
D. Trimethoprim alone

Correct: C. Nitrofurantoin is a well-known trigger for haemolytic anaemia in G6PD deficiency (oxidative stress mechanism). Amoxicillin-clavulanate, ceftriaxone, and trimethoprim alone are generally considered safe alternatives for UTI in G6PD-deficient patients.

5. Tranexamic acid (TXA) is administered to a trauma patient. Its mechanism of action in haemostasis is:

A. Directly activating platelet GPIIb/IIIa receptors to enhance aggregation
B. Inhibiting vitamin K epoxide reductase to reduce clotting factor synthesis
C. Competitively blocking lysine binding sites on plasminogen, preventing fibrinolysis
D. Activating thrombomodulin to enhance protein C anticoagulant pathway

Correct: C. Tranexamic acid is an antifibrinolytic that competitively blocks the lysine binding sites on plasminogen and plasmin, preventing their attachment to fibrin and thus inhibiting fibrinolysis (clot breakdown). This preserves formed clots.