In ABO blood grouping, which is False?

ABO antibodies are natural and present since birth

IgM is most common antibody in ABO

Ab are present only if Ag is absent

Which of the following is not a part of basic essential obstetric care?

Administration of parenteral antibiotics

Administration of parenteral sedatives for eclampsia

Administration of parenteral oxytocic drugs

Blood Transfusion and Alternatives for INI-CET: High-Yield Pharmacology Lessons

Blood Products & Indications - What's in the Bag?

Product	Contents	Vol (mL)	Indications (Key Thresholds)	Storage	Notes
PRBCs	RBCs, residual plasma/WBCs/plts	~300	Anemia (Hb < 7 g/dL), Acute loss >20%	2-6°C; 35-42d	Leukoreduce, Irradiate
Platelets (PC)	Platelets, plasma	~50-70	Plt < 10,000/µL, Dysfunctional plts + bleeding	20-24°C (agitate); 5d	RDP/SDP
FFP	All clotting factors, plasma proteins	~250	Coagulopathy (INR > 1.5), TTP, DIC	≤ -18°C; 1yr	Thaw 30-37°C
Cryoprecipitate	Fibrinogen, FVIII, FXIII, vWF	~15	Fibrinogen < 100 mg/dL, FVIII/FXIII def, vWD	≤ -18°C; 1yr	Factor concentrate
Whole Blood	All components	~450	Massive hemorrhage, Exchange Txn	2-6°C; 21-35d	Rare; component therapy preferred

Compatibility & Crossmatching - Perfect Match Quest

ABO System (Landsteiner's Law): RBC Ag + plasma Ab.
Grp Ag Ab Donates RBC to Receives RBC from
A A Anti-B A, AB A, O
B B Anti-A B, AB B, O
AB A, B None AB A,B,AB,O (All)
O H Anti-A/B A,B,AB,O (All) O
Rh System: RhD Ag key. Rh(D)-neg: Anti-D (IgG) if sensitized (Rh+ exposure) → HDN risk.
Crossmatching: Pre-transfusion.
- Major: Donor RBCs + Recipient serum (Recipient Ab vs Donor Ag).
- Minor: Donor serum + Recipient RBCs.
📌 O RhD neg: Universal RBC Donor; AB RhD pos: Universal RBC Acceptor.

Grp	Ag	Ab	Donates RBC to	Receives RBC from
A	A	Anti-B	A, AB	A, O
B	B	Anti-A	B, AB	B, O
AB	A, B	None	AB	A,B,AB,O (All)
O	H	Anti-A/B	A,B,AB,O (All)	O

⭐ Bombay Blood Group (Oh): Lacks H antigen. Has anti-A, anti-B, anti-H. Can only receive Oh blood.

Transfusion Reactions - When Good Blood Goes Bad

Immediate Reactions (Minutes to hours)
- Acute Hemolytic Transfusion Reaction (AHTR)
  - Onset: Minutes
  - Symptoms/Signs: Fever, chills, hemoglobinuria (red urine), hypotension, DIC, flank pain.
  - Pathophysiology: ABO incompatibility; intravascular hemolysis (IgM mediated).
  - Prevention: Meticulous pre-transfusion testing.
  - Management: Stop transfusion, IV fluids, diuretics, manage DIC.
- Febrile Non-Hemolytic Transfusion Reaction (FNHTR)
  - Onset: 30 min - 6 hrs
  - Symptoms/Signs: Fever (↑ 1°C), chills, rigors.
  - Pathophysiology: Cytokines from donor WBCs. 📌 Mnemonic: Febrile = Cytokines from WBCs.
  - Prevention: Leukoreduction.
  - Management: Antipyretics; exclude hemolysis.
- Allergic/Anaphylactic Reaction
  - Onset: Minutes (anaphylaxis) to hours (mild allergic)
  - Symptoms/Signs: Urticaria, pruritus; (anaphylaxis: angioedema, bronchospasm, hypotension).
  - Pathophysiology: IgE mediated (recipient IgE vs donor plasma proteins); IgA deficiency (anaphylaxis).
  - Prevention: Antihistamines; washed RBCs for IgA deficient.
  - Management: Antihistamines, steroids; epinephrine for anaphylaxis.
- Transfusion-Associated Circulatory Overload (TACO)
  - Onset: Within 6 hrs
  - Symptoms/Signs: Dyspnea, orthopnea, hypertension, pulmonary edema.
  - Pathophysiology: Volume overload.
  - Prevention: Slow infusion, diuretics.
  - Management: Oxygen, diuretics, sit upright.
- Transfusion-Related Acute Lung Injury (TRALI)
  - Onset: Within 6 hrs
  - Symptoms/Signs: Acute dyspnea, hypoxia, bilateral pulmonary infiltrates, fever, hypotension.
  - Pathophysiology: Donor antibodies vs. recipient leukocytes.
  - Prevention: Screen donors (multiparous women).
  - Management: Supportive, oxygen, ventilation if needed.

⭐ Exam Favourite: TRALI: Donor antibodies vs. recipient leukocytes (immune); TACO: Simple volume overload, often in elderly or cardiac patients. Key differentiator: BNP levels (↑ in TACO, normal/low in TRALI).

Delayed Reactions (Days to weeks)
- Delayed Hemolytic Transfusion Reaction (DHTR)
  - Onset: 3-10 days
  - Symptoms/Signs: Jaundice, fever, unexpected ↓Hb.
  - Pathophysiology: Anamnestic response to non-ABO antigens (e.g., Kidd, Duffy); extravascular hemolysis (IgG).
  - Prevention: Antibody screening.
  - Management: Usually supportive.

Alternatives & Special Situations - Beyond the Donor

Pharmacological Alternatives:
- Erythropoiesis-Stimulating Agents (ESAs): E.g., Epoetin, Darbepoetin; stimulate RBC production.
- Iron Therapy: Oral/IV for iron deficiency anemia.
Non-Pharmacological Alternatives:
- Autologous Transfusion: Patient's pre-donated blood.
- Intraoperative Cell Salvage: Collects & reinfuses shed surgical blood.
- Acute Normovolemic Hemodilution: Pre-op blood removal, volume replacement, later reinfusion.
Massive Transfusion Protocol (MTP):
- For major hemorrhage (e.g., >10 units PRBCs/24h).
- Components: PRBC:FFP:Platelets, typically 1:1:1 ratio.
- Aims: Correct lethal triad (acidosis, hypothermia, coagulopathy).
- Adjuncts: Calcium, Tranexamic Acid (TXA).

⭐ Tranexamic acid (TXA) inhibits fibrinolysis; used in trauma and MTPs to ↓ bleeding. Dose: 1g IV loading, then 1g over 8 hours.

High‑Yield Points - ⚡ Biggest Takeaways

Universal RBC donor: O RhD negative; Universal RBC recipient: AB RhD positive.

Universal plasma donor: AB group; Universal plasma recipient: O group.

Massive transfusion: >10 units PRBCs in 24h or >4 units in 1h; risks hypothermia, coagulopathy, hypocalcemia.

FNHTR: Most common reaction; due to cytokines; prevent with leukoreduction.

TRALI: Leading mortality cause; donor antibodies vs recipient leukocytes.

Blood storage lesion: ↓ 2,3-DPG, ↓ pH, ↑ K+; RBCs viable 35-42 days.

Alternatives: Erythropoietin, iron, autologous transfusion, cell salvage.

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Blood Transfusion and Alternatives