6.1 Lecture. Understanding Anemia: Causes, Compensation, and Effects

• Anemia commonly results from four disabilities, leading to reduced oxygen-carrying capacity and tissue hypoxia.
• Compensation for anemia involves cardiovascular, respiratory, and hematologic systems.
• Hypokalemia causes fluid movement from the interstitium to intravascular spaces, expanding plasma volume and decreasing viscosity, resulting in a hyperdynamic state.
• Hypoxemia dilates arterioles, capillaries, and venules, increasing blood flow as a compensatory mechanism.
• Pulmonary compensation for anemia includes increasing the rate and depth of breathing, enhancing oxygen release from hemoglobin.
• Decreased kidney blood flow activates the renin-angiotensin system, causing sodium and water retention to increase blood volume.
• Symptoms of anemia include palpitations, dizziness, and fatigue.
• Acute blood loss primarily involves intravascular volume loss.
• Effects of acute blood loss depend on the hemorrhage rate, potentially leading to cardiovascular collapse, shock, and death.
• Significant volume loss reduces mean systemic filling pressure, decreasing venous return.
• Complete recovery from non-severe acute blood loss is possible with plasma replacement within 24 hours.
• After acute blood loss, neutrophil and platelet counts rise, with more immature cells in circulation; normal erythrocyte count returns in 4-6 weeks, hemoglobin restoration in 6-8 weeks.

Megaloblastic & Microcytic Anemia

• Megaloblastic anemias are often caused by nutritional deficiencies, such as vitamin B12 deficiency.
• Microcytic hypochromic anemia is characterized by abnormally small erythrocytes with reduced hemoglobin.
• Iron deficiency anemia is the most common nutritional disorder, affecting about one-fifth of the global population.
• Anemia of chronic disease results from decreased erythropoiesis and impaired iron utilization, associated with chronic systemic diseases, inflammation, or autoimmune conditions.
• Aplastic anemia involves hematopoietic failure and reduced production of mature cells by the bone marrow.
• Hemolytic anemia is the premature destruction of erythrocytes, either congenital or acquired.

Polycythemia Vera

• Polycythemia vera results from abnormal regulation of multipotent hematopoietic stem cells.
• This disorder involves the overproduction of one or more formed elements of the blood without a defined stimulus.
• Polycythemia vera is rare, with an incidence of 2.3 per 100,000, peaking between 60 and 80 years of age.

Platelet Disorders

• Platelet disorders are categorized into quantitative and qualitative abnormalities.
• Quantitative disorders involve an increase or decrease in circulating platelets.
• Qualitative disorders affect platelet structure or function and may coexist with quantitative disorders.
• Thrombocytopenia is defined as a platelet count less than 150,000; counts less than 30,000 can cause bleeding from minor traumas, and spontaneous bleeding can occur with counts less than 10,000.
• Heparin-induced thrombocytopenia is an immune system-mediated adverse drug reaction.
• Thrombocytosis is defined as a platelet count greater than 450,000, usually from excessive platelet production.
• Qualitative alterations in platelet function are indicated by increased bleeding time with normal platelet count.

Hemostasis & Liver Disease

• Hepatic cells produce most hemostasis factors; liver disease can affect clotting.
• Disseminated intravascular coagulation (DIC) involves widespread coagulation activation, resulting in fibrin clot formation throughout the body.
• DIC may cause consumption of platelets and clotting factors, leading to severe bleeding; it can range from acute, severe conditions to chronic, low-level states.
• Hypercoagulability or thrombophilia is primarily caused by defects in proteins involved in hemostasis.
• It can be secondarily caused by various clinical disorders.
• Acquired thrombophilia is often multifactorial.

Anemia arises from various disabilities, leading to reduced oxygen transport and tissue hypoxia. The body compensates through cardiovascular, respiratory, and hematologic adjustments. Acute blood loss mainly causes intravascular volume depletion, potentially resulting in cardiovascular collapse.