ABO System, Blood Transfusions and Components - Free MCQ Practice Test

An FFP volume of 15 mL/kg (around 4 units for a 70 kg adult) is generally adequate to counteract coagulopathy resulting from warfarin toxicity. Ideally, prothrombin complex concentrates are administered at a dosage of 50-100 units/kg intravenously at 12-hour intervals during significant bleeding incidents linked to warfarin toxicity. Additionally, recombinant factor VIIa is utilised to reverse coagulopathy within hours.

Oral vitamin K₁ is provided when there is no serious or life-threatening haemorrhage.

Group AB plasma lacks any Anti-A, Anti-B, or Anti-AB antibodies. Therefore, plasma from group AB can be administered to patients belonging to groups AB, A, B, or O. This is why they are referred to as universal FFP donors.

Massive blood transfusion involves administering blood components to the patient.

• Given the occurrence of blood loss, packed RBCs are needed as a priority.
• Platelets should be provided following packed RBCs according to the protocol outlined below. (Refer to the red box highlighted).

Platelet units can be maintained at room temperature between 20 and 24 degrees for a duration of 5 to 7 days.

The manifestation of back pain and a look of anxiety suggests the occurrence of a mismatched blood transfusion or an acute haemolytic transfusion reaction. The concerning symptom in this case is back pain or flank pain, which arises when the kidneys are affected due to immune-mediated RBC lysis.

• This typically happens because of a clerical mistake where the blood bag has been incorrectly labelled as a specific blood group.
• The transfusion should be halted immediately, and the blood bag must be sent for blood group evaluation.

The correct storage temperatures for different blood components are as follows:

• RBCs (Red Blood Cells) should be stored at 2-6°C.
• Platelets need to be kept at 20-24°C.
• FFP (Fresh Frozen Plasma) should be stored at -30°C.

Thus, the correct option reflects these storage conditions accurately.

The occurrence of respiratory distress following a blood transfusion suggests a diagnosis of Transfusion Associated Circulatory Overload (TACO), as both Central Venous Pressure (CVP) and Pulmonary Capillary Wedge Pressure (PCWP) are elevated.

The occurrence of TRALI is higher with products that contain plasma. This condition arises when donor anti-granulocyte antibodies present in the plasma target the leucocyte antigens found on neutrophils that have accumulated in the patient's lungs. The resulting acute lung injury does not respond to steroids or diuretics and requires supportive care, such as non-invasive ventilation or CPAP.

• TRALI typically manifests within 6 hours of transfusion.
• Symptoms include fever and bilateral radiographic infiltrates.
• The mortality rate ranges from 5% to 10%.
• In most instances, the condition begins to improve within 2 to 3 days rather than weeks.

Blood administration set:

• Utilise a new, sterile blood administration set with an integral 170-200 µ filter.
• Change the set at least every 12 hours during blood transfusion.
• In extremely warm climates, change the set more often, typically after every four units of blood if administered within a 12-hour timeframe.
• Use a fresh blood administration set or a specific platelet transfusion set, primed with saline.

All blood components can be slowly infused through small-bore cannulas or butterfly needles, e.g., 21 to 25 G. For rapid infusion, large-bore cannulas, e.g., 14 G, are required.

Massive blood transfusion consists of administering as much as 5 litres of blood within a 24-hour timeframe.

• To ensure rapid transfusion, the infusion of a large volume at a low temperature can result in hypothermia.
• Hypothermia is the most prevalent complication associated with massive blood transfusion.
• The occurrence of citrate toxicity can cause hypocalcaemia since citrate and calcium will chelate.
• Dilutional thrombocytopenia accounts for the coagulopathy aspect.

Whole blood during storage experiences a reduction in factors V and VIII.

• Cryoprecipitate lacks factor IX.
• Fresh frozen plasma (FFP) is the most effective source of clotting factors.

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The primary issues associated with the ingestion of copper sulphate include:

• intravascular haemolysis
• met-hemoglobinaemia
• acute kidney injury
• rhabdomyolysis

The lethal dose may be as little as 10 grams. A viper bite is mainly vasculotoxic, resulting in:

• rapidly progressing swelling at the site of the bite
• local necrosis primarily caused by ischaemia, as thrombosis obstructs local blood vessels, leading to dry gangrene

Systemic absorption occurs gradually through the lymphatic system, resulting in lymphangitis. Viper bites are characterised by:

• haemostatic abnormalities
• complications that may result in death

A persistent ooze from the bite site and the location of the IV cannula indicates an altered clotting mechanism. Additionally,:

• haemorrhage and increased capillary permeability can lead to shock and pulmonary oedema
• oliguria follows, accompanied by loin pain due to renal ischaemia

Renal failure is a common occurrence prior to death. Significant haemolysis resulting from a mismatched blood transfusion will cause hemoglobinuria.

Major blood group antigens

1. Blood group antigens are carbohydrates attached to a precursor backbone, may be found on the cellular membrane either as glycosphingolipids or glycoproteins, and are secreted into plasma and body fluids as glycoproteins.
2. H substance is the immediate precursor on which the A and B antigens are added.
3. H substance is formed by the addition of fucose to the glycolipid or glycoprotein.
4. Addition of N-acetylgalactosamine creates the A antigen, while the addition of galactose produces the B antigen.
5. Genes that determine the A and B phenotypes are found on chromosome 9p and are expressed in a Mendelian codominant manner.

• an increase in blood oozing from the surgical site
• hemoglobinuria resulting in urine discolouration, which can be observed in the urobag.

The primary blood groups in this system are A, B, AB, and O. Type O red blood cells (RBCs) do not have A or B antigens. These antigens consist of carbohydrates linked to a precursor backbone and can be located on the cellular membrane as either glycosphingolipids or glycoproteins. They are also released into plasma and body fluids as glycoproteins.

• The H substance serves as the immediate precursor to which the A and B antigens are added.
• This H substance is produced by adding fucose to the glycolipid or glycoprotein backbone.
• The addition of N-acetylgalactosamine leads to the formation of the A antigen,
• whereas the addition of galactose results in the B antigen.

• Neonates and individuals with renal failure are particularly vulnerable to hyperkalemia.
• Preventive strategies, such as employing fresh or washed RBCs, are essential for neonatal transfusions, as this complication can be life-threatening.

• Hypocalcemia, indicated by circumoral numbness and/or a tingling sensation in the fingers and toes, may occur after multiple rapid transfusions.

One unit of red blood cells is typically administered over a period of 1 to 4 hours, influenced by the volume to be transfused and the patient’s cardiovascular condition. Infusing a unit for more than 4 hours is discouraged due to the risk of bacterial growth from the opened unit being kept at room temperature.

Additionally, drugs or medications must not be injected into the bloodstream.

Hypothermia can occur if a significant volume of cold blood is administered quickly. It is among the most frequent complications of extensive transfusions and contributes to the resulting coagulopathy. This reaction is particularly pronounced in:

• Neonates
• The elderly

Hypothermia impacts the liver's ability to metabolise citrate, leading to a heightened risk of hypocalcaemia. When rapid infusions of citrated blood products are given to these patients, especially via central venous lines, it may result in arrhythmias. Additionally, hypothermia disrupts platelet function and clotting, both of which are enhanced when the patient is warmed. One method to address this issue is by using warmed intravenous fluids or blood. Devices designed for warming blood are available and can sufficiently heat the blood being infused, even during rapid and extensive transfusions.

Cryoprecipitated AHF, commonly known as cryoprecipitate, is an extract derived from FFP that is rich in high-molecular-weight plasma proteins but does not contain factor IX. It is produced by thawing one unit of FFP at a temperature between 1° and 6°C. Under these conditions, the high-molecular-weight proteins form a precipitate. The concentrated precipitated protein is obtained through centrifugation, with all but roughly 15 ml of the supernatant being discarded. Each unit of this cryoprecipitate comprises:

• Approximately 80 to 120 units of factor VIII.
• At least 150 mg of fibrinogen.
• Factor XIII and high-molecular-weight multimers of vWF.

Cryoprecipitate was originally developed for the treatment of hemophilia A. It is no longer the treatment of choice for that disorder because less infectious alternatives are available.
At the present time, cryoprecipitate is most often used for correction of hypofibrinogenemia (<100 mg/dl), particularly in patients with disseminated intravascular coagulation or in those whose fibrinogen is depleted from prolonged exposure to cardiopulmonary bypass circuits.

In non-cardiogenic pulmonary oedema caused by an immunologic blood transfusion reaction, the primary factor is:

• Donor antibody reacting with the patient's leukocytes.
• This reaction leads to inflammation and increased permeability in the lungs.
• Consequently, fluid accumulates in the lung tissues.

Understanding this mechanism is crucial for managing transfusion reactions effectively.

Management of hemolytic reactions requires immediate action once a hemolytic reaction is suspected. The transfusion must be halted without delay. Blood should be collected to:

• Detect hemoglobin in the plasma
• Repeat compatibility testing
• Conduct coagulation studies and assess platelet count

A urinary catheter should be placed, and urine should be examined for hemoglobin. Osmotic diuresis with mannitol and intravenous fluids should be initiated. If rapid blood loss occurs, administering platelets and fresh frozen plasma (FFP) is necessary.

Hemolytic transfusion reactions happen when the recipient's blood contains preformed IgM antibodies that destroy donor red cells.

Mild reactions are non-complement fixing and typically occur between 4 days and 2 weeks post-transfusion, while complement fixation takes place immediately. Symptoms of extravascular hemolysis include:

• In awake patients: chills, fever, nausea, and chest and flank pain
• In patients under general anaesthesia: an increase in temperature, unexplained tachycardia, hypotension, hemoglobinuria, and diffuse oozing in the surgical field

CPDA-I is a buffer consisting of Citrate-Phosphate-Dextrose, enhanced with adenine. It became available in the USA in 1978.

CPDA-1 is currently one of the standard solutions used as an anticoagulant-preservative in clinical settings.

• The shelf life of RBC concentrates in CPDA-1 is 35 days.
• In the CPD buffer, the lifespan is 28 days.

The Acid citrate dextrose buffer, which was introduced during World War II, also provided a shelf life of 21 days.

Complications arising from blood transfusions can include:

• Hyperkalemia - This is a condition where there is too much potassium in the blood, which can occur during transfusions.
• Citrate toxicity - Citrate is used in blood products to prevent clotting. If too much is introduced, it can lead to toxicity.
• Metabolic acidosis - This condition happens when there is an excess of acid in the body, which may be related to transfusion reactions.
• Hypothermia - Blood products can be cold, and rapid infusion may drop the body’s temperature.

Among these, metabolic acidosis is not typically considered a direct complication of blood transfusions.

Immediate intravascular haemolytic transfusion reactions arise shortly after the commencement of an incompatible transfusion. While they can sometimes be mild, they often present with a sudden clinical change. The most frequent signs of these reactions include:

• Fever, with or without chills
• Anxiety
• Chest or back pain
• Flushing
• Dyspnoea
• Tachycardia
• Hypotension

If the patient is under general anaesthesia, these symptoms may go unnoticed; only severe hypotension and signs of oozing or haemoglobinuria may indicate a haemolytic reaction. Such reactions can be life-threatening, leading to complications such as acute renal failure, shock, and intravascular coagulation. It is estimated that a fatal immediate haemolytic reaction occurs in about 1 in 600,000 red transfusions. The mortality rate for a severe immediate haemolytic transfusion reaction increases with the volume of blood transfused, reaching 44% for patients receiving over 1 L of incompatible blood.

• The most frequently detected causes of FNHTR include HLA antibodies, followed by antibodies specific to platelets and those specific to granulocytes.
• Another factor contributing to FNHTRs is the transfusion of cytokines that have formed in vitro, particularly in platelet concentrates derived from whole blood that are stored at room temperature.
• Recent research indicates that during storage, leukocytes in platelet concentrates release cytokines that might be responsible for the febrile reaction.
• The likelihood of FNHTRs occurring with platelet concentrates rises with the age of the concentrate and the concentration of leukocytes in the product.
• Additionally, the risk of bacterial contamination in the product should be considered as a potential cause of FNHTR. Symptoms resulting from the transfusion of bacteria or their toxins can range from mild to potentially fatal.
• Platelet components are more frequently implicated since they are stored at room temperature; however, certain organisms, such as Yersinia enterocolitica, can thrive in red blood cells at storage temperatures between 1° and 6°C.

Allo-immunisation to antigens on leukocytes and platelets represents one of the primary reasons for non-haemolytic febrile transfusion reactions.

Thalassemia and chronic disease-related anaemia are recognised causes of hypochromic microcytic anaemia.

• Ancyclostomiasis, a genus of hookworm, results in blood loss.
• Acute intestinal infection in tropical sprue causes damage to the jejunal and ileal mucosa; subsequently, intestinal bacterial overgrowth and heightened plasma enteroglucagon lead to a delay in small-intestinal transit.

Key to this process is folate deficiency, which likely exacerbates further mucosal damage.

Preformed ABO antibodies are found in an individual's serum when their RBCs do not have the corresponding antigen. In other blood groups, preformed antibodies are absent. The ABO blood group system is significant because nearly all individuals generate antibodies against the ABH carbohydrate antigen that they do not possess.

• The ABO system was the first blood group antigen system identified in 1900.
• It is the most critical system in transfusion medicine.
• The primary blood groups within this system are A, B, AB, and O.

Type O RBCs do not contain A or B antigens. These antigens are carbohydrates that are linked to a precursor backbone and can be located on the cellular membrane as either glycosphingolipids or glycoproteins. They are also released into plasma and bodily fluids as glycoproteins. In most individuals, A and B antigens are secreted by the cells and are detectable in circulation.