Hematologic System Pathophysiology Quiz

Hematologic System Pathophysiology

• Blood elements include plasma, blood cells, plasma clotting factors, and serum
• Lymphoid organs such as the spleen and bone marrow are part of the hematopoietic system.

Blood Components

• Plasma comprises 55% of total blood volume.
• Plasma is mostly water (91%), soluble blood proteins (7%), hormones, nutrients, and electrolytes (2%).
• Blood elements (45% of total blood volume) consist of red blood cells, white blood cells, and blood platelets.

Plasma

• Plasma is the liquid component of blood, pale yellow, and comprises 91% water and 9% other substances.
• It's a colloid, meaning it contains suspended substances that don't settle out.
• Important constituents include albumin (water regulation and tissue movement), globulins (immune system and transport), and fibrinogen (blood cell formation).

Blood Cells

• Erythrocytes (RBCs)
• Leukocytes (WBCs):
  • Neutrophils
  • Monocytes
  • Eosinophils
  • Basophils
  • Lymphocytes: T lymphocytes and B lymphocytes
• Thrombocytes (Platelets)

Functions of the Hematologic System

• Transport Medium: RBCs and plasma transport gases, nutrients, vitamins, hormones, and waste products.
• Defensive Function: White blood cells (through phagocytosis) and antibody/T-lymphocyte formation combat pathogens.
• Hemostatic Function: Platelets and clotting factors stop bleeding after vessel injury.
• Homeostatic Function: The whole blood system maintains a constant internal environment.

Fate of Erythrocytes (RBCs)

• RBCs cannot divide, grow, or synthesize proteins.
• Their lifespan is 100-120 days.
• They are removed by phagocytosis in the spleen or liver.
• New RBCs are produced in bone marrow, with production increasing when oxygen levels are low or during pregnancy.

Hemoglobin

• Hemoglobin is the protein in RBCs that carries oxygen from the lungs to tissues and carbon dioxide back to the lungs.
• It's made up of four globulin chains.

Types of Hemoglobin

• HbA1: The major hemoglobin in humans, appearing 12 weeks after birth.
• HbF: Synthesized during fetal development and replaced by HbA in the first few months of life.
• HbA1c: Contains glucose residues; levels are used to monitor blood sugar control in diabetics.

HBS and Sickle Cell Anemia

• HBS contains two mutant beta-globin chains.
• Glutamate at position 6 is replaced with valine, causing RBCs to have a shorter lifespan (less than 20 days).
• Sickle cell anemia is a consequence of this mutation.

Normal Values Related to RBCs

• Red blood cell count: 4.0-5.5 million/mL blood
• Hemoglobin: 14.0-17.5 g/100 mL (males); 12.0-16.0 g/100 mL (females)
• Hematocrit: 42%-52% (males); 36%-48% (females)

Normal Values Related to WBCs

• Total leukocyte count: 4000-11,000/mm³
• Differential leukocyte count:
  • Neutrophils: 60-70%
  • Eosinophils: 2-4%
  • Basophils: 0-1%
  • Lymphocytes: 20-30%
  • Monocytes: 2-8%

Normal Values Related to Platelets and Coagulation

• Platelet count: 1/4-1/2 million/mm³ (average 300,000/mm³)
• Bleeding Time: 1-6 minutes.
• Whole Blood Coagulation Time: 6-10 minutes.
• Activated Partial Thromboplastin Time: 30-40 seconds
• Prothrombin Time: 10-14 seconds

Anemia

• Anemia results from decreased RBC count or hemoglobin, leading to reduced oxygen transport to tissues.
• Manifestations include pale or yellowish skin, fatigue, cold hands/feet, headache, shortness of breath, and irregular heartbeat.

Types of Anemia

• Microcytic: small RBCs, low hemoglobin content.
• Macrocytic: larger RBCs.
• Hypochromic: decreased hemoglobin content per RBC.

Normocytic Normochromic Anemia

• Results from decreased RBC production (bone marrow depression, aplastic anemia) or rapid RBC loss (hemorrhage, hemolysis).
• Causes include radiation, chemotherapy, chemicals, certain antibiotics, toxins, infections, massive hemorrhage, and hemolysis.

Hemolytic Anemia

• Hemolysis is the premature destruction of RBCs.
• Causes include acquired causes such as chemical toxins, bacterial toxins, drugs, snake venom, autoimmune issues, cancers, and certain viral/parasitic infections (malaria).
• Some inherited forms include hereditary spherocytosis, sickle cell anemia, and thalassemia.
• Manifestations include jaundice (yellowing of skin and mucous membranes), increased blood viscosity, decreased blood flow to tissues (hypoxia), pain, and splenomegally.

Microcytic Hypochromic Anemia

• Small, pale RBCs caused by iron deficiency.
• Causes include decreased iron intake (vegetarians, infants, females), decreased iron absorption, and chronic blood loss (bleeding, neoplasia).

Macrocytic Anemia

• Larger RBCs commonly associated with insufficient cell and hemoglobin content, often caused by vitamin B12 or folic acid deficiency.

Polycythemia

• Increased RBC count.
• Relative: Decreased plasma volume, increased RBC concentration.
• Primary: Bone marrow produces excessive RBCs and possibly other blood cells, leading to blood thickening and complications like clots or bleeding.
• Secondary: Caused by chronic hypoxia; e.g., high altitudes.

Manifestations of Polycythemia

• Increased blood volume.
• Increased blood viscosity.
• Risk of thrombosis.
• Occlusion of small blood vessels.
• Impaired blood flow to tissues (ischemia).
• Hepatosplenomegally.

Pathophysiology of Hemostasis

• Hemostasis stops bleeding when a blood vessel is injured.
• Steps include vessel vasoconstriction, platelet plug formation, blood clot formation, and fibrous tissue growth.

Abnormalities in Coagulation Process

• Increased bleeding tendency due to abnormalities in coagulation processes.
• Causes include genetic disorders (hemophilia), acquired disorders (vitamin K deficiency, liver disease), and drug-induced issues.
• Characteristics include increased coagulation time.

Hemophilia

• Rare bleeding disorder due to clotting factor deficiencies.
• Ranges from mild to severe bleeding episodes.
• Manifested by excessive bleeding with trauma or surgery, or bleeding into muscles and joints.
• Treatment involves injury avoidance, prevention of bleeding, and replacement of deficient clotting factors.

Vitamin K Deficiency

• Vitamin K is essential for synthesizing clotting factors II, VII, IX, and X.
• Sources include exogenous (dietary) and endogenous (intestinal bacteria).
• Deficiency may stem from intestinal malabsorption or antibiotic-induced bacterial flora destruction.
• Treatment involves Vitamin K administration and supplementation of deficient clotting factors.

Liver Diseases

• Liver synthesizes clotting factors.
• Liver diseases decrease clotting factor production, leading to blood coagulation defects and increased bleeding tendencies.
• Examples include hepatitis, cirrhosis, liver cancer, and liver failure.

Drug-Induced Coagulation Problems

• Anticoagulants (e.g., Warfarin, heparin) can interfere with blood clotting.

Abnormalities in Blood Platelets

• Decreased platelet count or impaired platelet function result in increased bleeding tendencies.
• Characterized by prolonged bleeding time.

Increased Blood Coagulability

• Increased blood coagulability signifies a higher risk of thrombosis.
• Causes include inherited coagulation disorders, obesity, cancer, sepsis, polycythemia, prolonged bed rest, venous stasis, trauma, and surgery.