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Questions and Answers
What is the primary cause of hemolytic transfusion reaction?
What is the primary cause of hemolytic transfusion reaction?
Which symptom is NOT typically associated with hemolytic transfusion reaction?
Which symptom is NOT typically associated with hemolytic transfusion reaction?
What can cause hyperkalemia during a blood transfusion?
What can cause hyperkalemia during a blood transfusion?
What is a common manifestation of anemia?
What is a common manifestation of anemia?
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What role does citrate play in blood transfusions?
What role does citrate play in blood transfusions?
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What complication can arise due to hypervolemia from massive transfusion?
What complication can arise due to hypervolemia from massive transfusion?
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What is the likely consequence of iron deficiency in relation to hemoglobin synthesis?
What is the likely consequence of iron deficiency in relation to hemoglobin synthesis?
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Which substance in the body is metabolized from released hemoglobin during a hemolytic transfusion reaction?
Which substance in the body is metabolized from released hemoglobin during a hemolytic transfusion reaction?
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Flashcards
Hemolytic Transfusion Reaction
Hemolytic Transfusion Reaction
A serious reaction to blood transfusion that occurs when the recipient's antibodies react with the donor's red blood cells. This triggers red blood cell destruction, leading to complications.
Anemia
Anemia
A condition where there is a decrease in the number of red blood cells or the amount of hemoglobin. This reduces oxygen-carrying capacity of the blood, leading to various symptoms.
Immediate complication of Blood Transfusion
Immediate complication of Blood Transfusion
A type of complication of incompatible blood transfusions that occurs due to the mismatch between the recipient's and donor's blood types.
Delayed Complications of Blood Transfusion
Delayed Complications of Blood Transfusion
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Hyperkalemia
Hyperkalemia
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Hypervolemia
Hypervolemia
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Tetany (Muscle Spasm)
Tetany (Muscle Spasm)
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Study Notes
Physiology and Pathophysiology Lecture 3
- The lecture covers physiology and pathophysiology, focusing on hypoproteinemia, blood disorders, and anemia.
- Plasma proteins are synthesized by the liver from dietary proteins.
- A normal plasma protein level is 7g/100ml of blood.
- Hypoproteinemia causes include starvation, liver disease, and renal disease (e.g., nephrotic syndrome).
- In starvation, plasma proteins decrease late in the process.
- Liver disease results in decreased plasma protein synthesis.
- Renal disease causes proteins to be lost in urine as diseased kidneys filter plasma proteins from the blood.
Consequences of Hypoproteinemia
- Fluid filtered at the arterial side of blood capillaries is reabsorbed at the venous side.
- Osmotic pressure of plasma proteins drives reabsorption, returning fluid to the blood.
- The reabsorption volume equals the volume of fluid filtered from the arterial side of the capillary.
- Decreased plasma protein levels diminish the osmotic pressure, causing less fluid to be reabsorbed.
- Reduced reabsorption leads to an increased accumulation of interstitial fluid, resulting in edema (tissue swelling).
Blood Capillary and Interstitial Fluid
- Blood hydrostatic pressure (30mmHg) pushes fluid from capillaries into interstitial space at the arterial side and (10mmHg) at the venous side.
- Osmotic pressure of plasma proteins (28mmHg) draws fluid back into capillaries at the venous side.
- Filtration occurs when hydrostatic pressure exceeds osmotic pressure, and reabsorption occurs when osmotic pressure exceeds hydrostatic pressure.
Edema
- Edema is tissue swelling due to abnormal interstitial fluid accumulation.
- It can be a consequence of decreased plasma protein levels.
Common Blood Disorders
- Common blood disorders include blood transfusion, anemia, and abnormal hemoglobin.
Red Blood Cells
- Blood transfusion, anemia, and abnormal hemoglobin are common blood issues.
Blood Transfusion Complications
- Immediate complications of blood transfusion arise from blood group incompatibility, leading to hemolytic transfusion reactions.
- Antibodies in the recipient's plasma attack donor red blood cells, causing agglutination (clumping) and hemolysis (destruction).
- This leads to histamine release and possible pain, hypotension, hemolytic jaundice (yellowing), and renal damage.
- Delayed complications include disease transmission (e.g., hepatitis, AIDS), hyperkalemia (high potassium), hypervolemia (high blood volume), tetany (muscle spasms), and others. Delayed complications can be linked to various issues like excessive blood transfusions.
Anemia
- Anemia results from reduced hemoglobin content or red blood cell count.
- Normal RBC count and hemoglobin content are maintained by equal rates of RBC production and destruction.
- Insufficient red blood cell production or increased red blood cell destruction leads to various types of anemia.
Manifestations of Anemia
- Common symptoms include headache, dizziness, lack of concentration, pallor (pale skin), and easy fatigability.
Causes of Anemia
- Anemia can result from decreased red blood cell production or increased red blood cell loss.
- Deficiency anemias arise from insufficient iron, vitamin B12, or folic acid.
- Aplastic anemia results from bone marrow depression.
- Hemolytic anemia involves increased red blood cell destruction.
Types and Causes of Anemia
- Deficiency anemias include iron, vitamin B12, folic acid, and protein deficiency anemia.
- Aplastic anemia results from bone marrow depression caused by toxins, drugs, radiation, or malignancy.
Red Blood Cell Hemolysis (Premature Destruction)
- Extracorpuscular causes include immune reactions (e.g., incompatible blood transfusions, Rh incompatibility), infections (e.g., malaria), drugs (e.g., sulfonamides), and toxins (e.g., lead, arsenic).
- Corpuscular causes involve abnormal red blood cell shapes (e.g., spherocytosis), hemoglobin defects (e.g., sickle cell anemia, thalassemia), and enzyme deficiencies (e.g., G6PD deficiency).
- Acute blood loss can also lead to anemia.
- Other causes of anemia include renal failure, liver disease, and malignancy.
Morphological Classification of Anemia
- Microcytic hypochromic anemia (e.g., iron deficiency anemia).
- Macrocytic hyperchromic anemia (e.g., vitamin B12 deficiency anemia).
- Normocytic normochromic anemia (e.g., acute blood loss).
Pathophysiology of Hemolytic Anemia
- Thalassemia (Mediterranean anemia) involves deficiencies in alpha or beta hemoglobin chains.
- Sickle cell anemia features abnormal hemoglobin (HbS) that causes red blood cells to sickle, leading to hemolysis (rupture).
Hereditary Spherocytosis
- Hereditary spherocytosis is a genetic disorder causing red blood cells to become spherical and fragile. These spherocytes are easily destroyed by the body.
Types of Abnormal Hemoglobin
- Methemoglobin, carboxyhemoglobin, and sulfhemoglobin are abnormal forms of hemoglobin.
- Methemoglobin is oxidized hemoglobin that cannot carry oxygen. Carbon monoxide-bound hemoglobin has a greater affinity for oxygen than regular hemoglobin, leading to oxygen starvation in the body. Sulfhemoglobin is bound by sulfur, leading to oxygen-carrying limitations. Hematin is hemoglobin lacking iron.
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Description
This lecture focuses on the critical aspects of hypoproteinemia, blood disorders, and anemia. Key points include the synthesis of plasma proteins by the liver, the causes of hypoproteinemia, and its impact on fluid balance in the body. Understand the complex interplay between plasma protein levels and various diseases affecting health.
