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• The following are study notes on blood-related tests and conditions.

Mean Corpuscular Volume (MCV)

• Measures the average volume/size of a single red blood cell
• Calculation: MCV = (Hematocrit % × 10) / RBC count (in millions/μL)
• Unit: Femtoliters (fL)
• Microcytic Anemia (Low MCV < 80 fL): Indicates smaller than normal RBCs; common in iron deficiency anemia, thalassemia, and anemia of chronic disease
• Normocytic Anemia (Normal MCV 80-100 fL): Indicates normal-sized RBCs; associated with acute blood loss, hemolytic anemia, anemia of chronic disease, and aplastic anemia
• Macrocytic Anemia (High MCV > 100 fL): Indicates larger than normal RBCs; can be seen in vitamin B12 deficiency, folate deficiency, certain types of liver disease, or hypothyroidism

Mean Corpuscular Hemoglobin Concentration (MCHC)

• Measures the average concentration of hemoglobin in a given volume of packed red blood cells
• Calculation: MCHC = (Hemoglobin (g/dL) × 100) / Hematocrit (%)
• Unit: Grams per deciliter (g/dL)
• Hypochromic (Low MCHC < 32 g/dL): Indicates RBCs with less hemoglobin (paler color); common in iron deficiency anemia and thalassemia
• Normochromic (Normal MCHC 32-36 g/dL): Indicates normal hemoglobin concentration; seen in normocytic anemias like anemia of chronic disease or acute blood loss
• Hyperchromic (High MCHC > 36 g/dL): Rare; indicates spherocytosis or other RBC membrane disorders where cells are densely packed with hemoglobin

Red Cell Distribution Width (RDW)

• Measures the variation in the size (volume) of red blood cells
• Calculation: RDW = (Standard Deviation of MCV / Mean MCV) × 100
• Unit: Percentage (%)
• High RDW (> 14.5%): Indicates a larger variation in RBC size (anisocytosis); often seen in mixed anemias (e.g., iron deficiency anemia combined with vitamin B12 or folate deficiency) and conditions where RBCs are being created and destroyed at uneven rates
• Normal RDW (11.5%-14.5%): Indicates uniform size of RBCs; typical in chronic anemias without a significant variation in cell size

Summary of Interpretation

• Microcytic, Hypochromic Anemia:
  • MCV: Low
  • MCHC: Low
  • RDW: Can be high if the anemia is combined with another type
  • Common Causes: Iron deficiency, thalassemia
• Normocytic, Normochromic Anemia:
  • MCV: Normal
  • MCHC: Normal
  • RDW: Can be normal or high
  • Common Causes: Acute blood loss, hemolytic anemia, anemia of chronic disease, aplastic anemia
• Macrocytic Anemia:
  • MCV: High
  • MCHC: Can be normal or elevated
  • RDW: Often high
  • Common Causes: Vitamin B12 deficiency, folate deficiency, liver disease, hypothyroidism

Tests Measuring Iron Levels

• Serum Iron: Measures the amount of circulating iron bound to transferrin
  • Low Serum Iron: Indicates potential iron deficiency anemia, chronic blood loss, or anemia of chronic disease
  • High Serum Iron: May indicate hemochromatosis, hemolytic anemia, or iron poisoning
• Ferritin: Measures the amount of stored iron in the body; also an acute-phase reactant
  • Low Ferritin: Strongly suggests iron deficiency, as it reflects depleted iron stores
  • High Ferritin: Can indicate iron overload (hemochromatosis) or be elevated due to inflammation, infection, or malignancy, as it acts as an acute-phase reactant
• Transferrin: A protein that transports iron in the bloodstream
  • Low Transferrin: May indicate malnutrition, chronic liver disease, or inflammation
  • High Transferrin: Typically indicates iron deficiency as the body produces more transferrin in an attempt to increase iron transport
• Total Iron-Binding Capacity (TIBC): Measures the blood's capacity to bind and transport iron
  • High TIBC: Common in iron deficiency anemia, reflecting the body's increased need for iron
  • Low TIBC: Often seen in chronic inflammatory conditions, malignancies, or liver disease, as the body's iron-binding capacity is reduced
• Transferrin Saturation: The percentage of transferrin that is saturated with iron; calculated as (Serum Iron / TIBC) × 100
  • Low Transferrin Saturation: Indicates iron deficiency anemia
  • High Transferrin Saturation: May indicate iron overload disorders like hemochromatosis
• Occult Blood Testing: Detects hidden blood loss in the gastrointestinal tract, which can be a cause of iron deficiency anemia
  • Positive Occult Blood: Indicates gastrointestinal bleeding, which can lead to chronic iron loss and resultant anemia

Specific Types of Anemia

• Anemia of Chronic Illness: The second most common type of anemia, often seen in chronic infections, inflammatory conditions, and chronic diseases
  • Mechanism:
    • Proinflammatory cytokines inhibit erythropoietin production
    • They destroy immature erythroblasts
    • Stimulate the release of hepcidin, which controls iron absorption and blocks iron release, thereby reducing iron availability despite normal or increased iron stores
  • Pattern in Iron Studies:
    • Serum Iron: Low
    • Ferritin: Normal or high (due to inflammation)
    • TIBC: Low or normal
    • Transferrin Saturation: Low
• Hemolytic Anemia: Anemia caused by the destruction of red blood cells
  • Causes: Genetic disorders, autoimmune diseases (e.g., lupus, rheumatoid arthritis), drug reactions (e.g., NSAIDs, penicillin, cephalosporins), and neonatal hyperbilirubinemia
  • Pattern in Iron Studies:
    • Serum Iron: Can be normal or high due to increased iron release from destroyed RBCs
    • Ferritin: Can be normal or high
    • TIBC: Typically normal
    • Transferrin Saturation: Can be high
    • Other: Elevated bilirubin and hemoglobinuria, decreased haptoglobin
• Aplastic Anemia: A stem cell disorder leading to pancytopenia (reduction of all blood cell types)
  • Causes: Congenital, chemotherapy, viral infections, autoimmune diseases
  • Diagnosis: Bone marrow biopsy showing hypocellular marrow
  • Pattern in Iron Studies:
    • Serum Iron: Can be normal
    • Ferritin: Can be normal
    • TIBC: Typically normal
    • Other: All cell lines (RBCs, WBCs, platelets) are decreased
• Sickle Cell Anemia: A genetic, autosomal recessive hemolytic anemia characterized by the presence of hemoglobin S (HbS)
  • Prevalence: Affects approximately 1 in 500 African Americans
  • Pattern in Iron Studies:
    • Serum Iron: Typically normal
    • Ferritin: Typically normal
    • TIBC: Typically normal
    • Other: HbS is identified, low oxygen capacity, crises can be triggered by infection, dehydration, hypoxia, leading to vaso-occlusive events and an increased risk of complications like myocardial infarction, stroke, and pulmonary injury
• Vitamin B12 Deficiency (Pernicious Anemia): Anemia due to impaired DNA synthesis and shortened RBC lifespan, not due to hemolysis
  • Causes: Inability to absorb B12 (lack of intrinsic factor), dietary deficiency, autoimmune destruction of gastric mucosal cells
  • Pattern in Iron Studies:
    • Serum Iron: Normal
    • Ferritin: Normal
    • TIBC: Normal
    • Other: Elevated homocysteine, symptoms like paresthesias, balance issues, and oral pain
• Folate Deficiency: Anemia due to impaired RNA/DNA synthesis, leading to ineffective erythropoiesis
  • Causes: Dietary deficiency (lack of fruits and vegetables), poor absorption, drug interference (e.g., aspirin), maternal deficiency leading to fetal neural tube defects
  • Pattern in Iron Studies:
    • Serum Iron: Normal
    • Ferritin: Normal
    • TIBC: Normal
    • Other: Megaloblastic anemia noted on blood smears

Summary of Iron Studies

• Includes serum iron, ferritin, transferrin, TIBC, and transferrin sat.
• Provide vital insights into iron metabolism and help diagnose various forms of anemia
• Abnormal results can indicate specific deficiencies or disorders:
  • Iron Deficiency Anemia: Low serum iron, low ferritin, high TIBC, low transferrin saturation
  • Anemia of Chronic Illness: Low serum iron, normal/high ferritin, low/normal TIBC, low transferrin saturation
  • Hemolytic Anemia: Variable serum iron, high bilirubin, normal TIBC, potentially decreased haptoglobin
  • Aplastic Anemia: Pancytopenia, normal iron studies
  • Sickle Cell Anemia: Identified HbS, normal iron studies, potential crises based on stressors
  • Vitamin B12 and Folate Deficiencies: Normal iron studies, associated with macrocytic red blood cells and megaloblastic anemia

Details on Specific Types of Anemia

• Iron Deficiency Anemia:
  • Cause: Insufficient iron intake, chronic blood loss (e.g., gastrointestinal bleeding, heavy menstruation), poor iron absorption.
  • Symptoms: Fatigue, pallor, shortness of breath, dizziness, brittle nails
  • Diagnosis: Low hemoglobin, hematocrit, serum ferritin levels, and elevated total iron-binding capacity (TIBC)
  • Treatment: Iron supplements, dietary changes, treating the underlying cause of iron loss
• Vitamin B12 Deficiency Anemia (Pernicious Anemia):
  • Cause: Poor absorption due to lack of intrinsic factor, dietary deficiency
  • Symptoms: Fatigue, weakness, pallor, shortness of breath, neurological symptoms (e.g., numbness, tingling), cognitive disturbances
  • Diagnosis: Low serum vitamin B12 levels, elevated methylmalonic acid and homocysteine levels
  • Treatment: Vitamin B12 injections or high-dose oral supplements
• Folate Deficiency Anemia
  • Cause: Inadequate dietary intake, malabsorption, excessive alcohol intake, increased demand (e.g., pregnancy)
  • Symptoms: Similar to B12 deficiency anemia but without neurological symptoms.
  • Diagnosis: Low serum folate levels, elevated homocysteine levels
  • Treatment: Oral folic acid supplements, dietary adjustments
• Aplastic Anemia:
  • Cause: Bone marrow failure (can be due to autoimmune disease, toxins, medications, infections)
  • Symptoms: Fatigue, frequent infections, uncontrolled bleeding, pallor
  • Diagnosis: Pancytopenia (low counts of all blood cells), bone marrow biopsy showing hypocellularity
  • Treatment: Immunosuppressive therapy, bone marrow transplant, supportive care (e.g., blood transfusions)
• Sickle Cell Anemia:
  • Cause: Genetic mutation causing abnormal hemoglobin (HbS) leading to sickle-shaped RBCs.
  • Symptoms: Painful crises, fatigue, swelling in hands/feet, frequent infections, delayed growth, vision problems
  • Diagnosis: Hemoglobin electrophoresis, blood smear showing sickle cells
  • Treatment: Pain management, hydroxyurea, blood transfusions, possible bone marrow transplant
• Hemolytic Anemia:
  • Cause: Premature destruction of RBCs (autoimmune disease, genetic conditions, infections, drug reactions)
  • Symptoms: Fatigue, jaundice, dark urine, fever, abdominal pain, splenomegaly
  • Diagnosis: Elevated reticulocyte count, low haptoglobin, increased indirect bilirubin, positive Coombs test (if autoimmune)
  • Treatment: Depends on the cause—corticosteroids, immunosuppressants, possibly splenectomy for hereditary conditions
• Anemia of Chronic Disease
  • Cause: Inflammatory, infectious, or neoplastic diseases (e.g., chronic kidney disease, rheumatoid arthritis, cancer)
  • Symptoms: Typically mild symptoms compared to other anemias, such as fatigue and pallor
  • Diagnosis: Normal or high ferritin (body's reserve of iron), low serum iron and TIBC, normal-to-low transferrin saturation
  • Treatment: Managing the underlying chronic disease, sometimes erythropoiesis-stimulating agents
• Acute Blood Loss Anemia:
  • Cause: Sudden hemorrhage (e.g., trauma, surgical blood loss, gastrointestinal bleeding)
  • Symptoms: Rapid onset of symptoms like dizziness, weakness, shortness of breath, pallor, rapid heartbeat, low blood pressure
  • Diagnosis: A significant drop in hemoglobin and hematocrit, physical signs of acute blood loss
  • Treatment: Immediate control of bleeding source, fluid resuscitation, blood transfusions

Hodgkin Lymphoma (HL)

• Characterized by the presence of Reed-Sternberg cells, large abnormal cells usually found in lymph nodes
• Typically arises in a single lymph node or chain of nodes before spreading to adjacent lymph nodes
• Subtypes:
  • Classical Hodgkin Lymphoma:
    • Nodular sclerosis Hodgkin lymphoma (most common subtype)
    • Mixed cellularity Hodgkin lymphoma
    • Lymphocyte-rich Hodgkin lymphoma
    • Lymphocyte-depleted Hodgkin lymphoma
  • Nodular Lymphocyte-Predominant Hodgkin Lymphoma:
    • Contains popcorn cells (lymphocyte-predominant cells) instead of Reed-Sternberg cells
• Treatment:
  • Combination chemotherapy (ABVD regimen), radiation therapy, targeted therapy, stem cell transplant in advanced cases

Non-Hodgkin Lymphoma (NHL)

• More common than Hodgkin lymphoma.
• Encompasses a diverse group of lymphomas with varying behaviors and treatment responses
• Arises from B-cells, T-cells, or natural killer (NK) cells in the lymphatic system
• Subtypes:
  • B-Cell Lymphomas:
    • Diffuse Large B-Cell Lymphoma (DLBCL): The most common type of NHL
    • Follicular Lymphoma (FL): Low-grade, indolent lymphoma
    • Mantle Cell Lymphoma (MCL): Aggressive type involving the mantle zone of lymph nodes
    • Burkitt Lymphoma: Fast-growing NHL more common in children
  • T-Cell Lymphomas:
    • Peripheral T-Cell Lymphoma: Various types of aggressive T-cell lymphomas
    • Cutaneous T-Cell Lymphomas: Skin-associated lymphomas like mycosis fungoides
• Other NHL Subtypes:
  • Marginal Zone Lymphoma, Waldenström Macroglobulinemia, Extranodal NK/T-Cell Lymphoma, Angioimmunoblastic T-Cell Lymphoma, Intravascular Large B-Cell Lymphoma, etc. Treatment: Varies based on the subtype; approaches may include chemotherapy, immunotherapy, radiation therapy, and stem cell transplant. Primary Mediastinal B-Cell Lymphoma (PMBCL) and Primary CNS Lymphoma Rare subtype involving the thymus and mediastinal lymph nodes More common in young women Treated with chemotherapy (e.g., R-CHOP) Primary CNS Lymphoma: Arises in the brain, spinal cord, or eyes Treatment: Chemotherapy, immunotherapy, and Targeted Therapy: Commonly used to kill cancer cells Radiation Therapy: Used to target localized lymphomas Stem Cell Transplant: Employed in advanced or refractory cases

Intrinsic Pathway

• Initiation: Factor XII Activation:
  • Initiated by the activation of Factor XII (Hageman factor) when it contacts exposed collagen from a damaged blood vessel wall or a negatively charged surface
• Activation of Factor XI:
  • Factor XII to XIla Conversion: Factor Xlla activates Factor XI by cleaving it to form Factor Xla
• Activation of Factor IX:
  • Factor Xla Activation of Factor IX: Factor Xla, in the presence of calcium ions (Ca²+), cleaves Factor IX to form Factor IXa
• Formation of Tenase Complex
  • Factor IXa's Role: Factor IXa, along with the Factor VIIla cofactor (activated by thrombin) and calcium ions, form the tenase complex on the platelet surface
• Conversion of Factor X:
  • The tenase complex activates Factor X to form Factor Xa, a pivotal enzyme in the coagulation cascade
• Role in Clotting
  • Significance: Factor Xa plays a central role in the common pathway of the coagulation cascade by converting Prothrombin (Factor II) into its active form, Thrombin (Factor lla)
• Inhibitors and Regulation:
  • Anticoagulant Mechanisms:
    • Tissue Factor Pathway Inhibitor (TFPI): Regulation of TF-VIla complex
    • Antithrombin III: Inhibition of Factors IXa and Xa
    • Protein C and S: Degrades Factors Va and VIIIa, limiting clot formation
• Clinical Relevance:
  • Deficiencies in any of the intrinsic pathway factors can lead to bleeding disorders such as Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency)
  • Activation of the intrinsic pathway is essential for maintaining hemostasis and preventing excessive bleeding when blood vessels are damaged
• In brief
  • Initiation: Factor XII activation upon contact with surfaces like collagen.
  • Activation of Factor XI: Factor XIla activates Factor XI, leading to Factor Xla.
  • Activation of Factor IX: Factor Xla further activates Factor IX to Factor IXa.
  • Formation of Tenase Complex: Factor IXa, Factor VIlla, and calcium ions form the tenase complex.
  • Conversion of Factor X: Tenase complex activates Factor X to Factor Xa, continuing the clotting cascade.

Extrinsic Pathway

• Typically triggered by external trauma that causes blood to exit the vascular system
• Initiation:
  • Tissue Factor Exposure: Initiated by exposure to Tissue Factor (TF), also known as Factor III, which is present outside the bloodstream
  • TF is exposed upon tissue injury, such as trauma to the blood vessel, and it binds to Factor VII
• Activation of Factor VII:
  • Factor VII Activation: The TF-Factor VII interaction forms the active enzyme Factor Vlla, often referred to as the initial trigger for the clotting cascade in response to tissue damage
• Generation of Xa:
  • Activation of Factor X: The TF-VIla complex activates Factor X by cleaving it to its active form, Factor Xa, in the presence of calcium ions (Ca2+)
• Common Pathway Initiation:
  • Convergence at the Common Pathway:
    • Active Factor Xa generated by the extrinsic pathway converges at the common pathway of the clotting cascade, where Factor Xa plays a central role in the activation of the common pathway factors
• Role in Coagulation
  • Thrombin Generation: Factor Xa's role includes converting Prothrombin (Factor II) to its active form, Thrombin (Factor Ila), which is a key enzyme that plays multiple roles in the coagulation cascade
• Regulation and Inhibitors:
  • Anticoagulant Mechanisms:
    • Tissue Factor Pathway Inhibitor (TFPI): Controls TF-VIla complex activity
    • Antithrombin III: Inhibits Factors IXa and Xa
    • Protein C and S: Regulate Factors Va and VIlla and the overall clotting process
• Clinical Relevance:
  • Tissue Factor (TF) serves as an essential initiator of the extrinsic pathway in response to external injury
  • Factor VIla plays a significant role in activating Factor X to Xa, thereby connecting the extrinsic pathway to the common pathway in the clotting cascade
  • Dysregulation in the extrinsic pathway can result in bleeding disorders or thrombotic conditions, requiring careful management and treatment
• In brief
  • Initiation: Tissue Factor (TF) exposure upon vessel injury
  • Activation of Factor VII: TF forms a complex with Factor VII to generate Factor Vlla
  • Generation of Factor Xa: Factor VIla activates Factor X to Xa
  • Common Pathway: Factor Xa feeds into the common pathway, supporting further clotting steps
  • Thrombin Generation: Thrombin is crucial for converting Fibrinogen to Fibrin, stabilizing the clot

The common pathway

• Final series of events in the blood coagulation process that leads to the formation of a stable blood clot
• The point where intrinsic and extrinsic pathways converge, ultimately resulting in the conversion of fibrinogen to fibrin, which solidifies the clot
• Initiation: - Activation of Factor X: - After activation by both the intrinsic and extrinsic pathways, Factor X is converted to its active form, Factor Xa
  • Prothrombinase Complex Formation
    • Prothrombinase Complex:
    • Factor Xa interacts with Factor Va (also activated by thrombin) and calcium ions (Ca2+) to create the prothrombinase complex
    • Accelerates the conversion of Prothrombin (Factor II) to its active form, Thrombin (Factor Ila)
  • Thrombin Generation
    • Thrombin Production:
    • Thrombin is a central enzyme in the coagulation cascade with multiple critical functions in hemostasis
    • Catalyzes the conversion of Fibrinogen (Factor I) into Fibrin, a mesh-like protein that forms the structural framework of a blood clot
  • Fibrin Formation
    • Fibrinogen to Fibrin Conversion:
    • Fibrinogen - a soluble plasma protein circulating in the blood
    • Thrombin cleaves specific peptide bonds in fibrinogen to form Fibrin Monomers
  • Fibrin Polymerization:
    • Fibrin monomers aggregate and crosslink to form a stable fibrin mesh, which entraps platelets and forms a stable blood clot at the site of injury Stabilization and Clot Formation -Fibrin Stabilization:
    • Factor XIIIa (activated by thrombin) crosslinks the fibrin strands to form a stable, insoluble clot, preventing further bleeding
• Inhibition and Regulation
  • Antithrombotic Mechanisms:
    • Tissue Factor Pathway Inhibitor (TFPI): Limits the TF-VIIa complex activity
    • Antithrombin III: Inactivates thrombin, Factors IXa, Xa, Xla, and Xlla
    • Protein C and S: Degrade Factors Va and VIIIa, downregulating clotting
• Clinical Relevance
  • Thrombin: Essential for the conversion of fibrinogen to fibrin, the polymerization process, and initiation of secondary hemostasis
  • Fibrin: Forms a stable clot, preventing further blood loss and facilitating the healing process
• In brief
• Activation of Factor X: Leads to the formation of the prothrombinase complex
• Formation of Thrombin: Key enzyme in the common pathway, catalyzing the conversion of fibrinogen to fibrin
• Fibrin Formation: Fibrinogen cleavage and polymerization into a stable clot structure
• Fibrin Stabilization: Crosslinking by Factor XIIIa for clot stability

Additional Key definitions in the coagulation cascades

• Tissue Factor (TF): Initiates the extrinsic pathway of coagulation by binding to Factor Vlla, triggering the activation of Factor X
• Factor VII: Activated by Tissue Factor (TF), initiates the extrinsic pathway by activating Factor X in the presence of calcium
• Factor X: Activated by both the intrinsic and extrinsic pathways, converts prothrombin to thrombin
• Prothrombinase Complex: A complex formed by Factors Va, Xa, and calcium, catalyzes the conversion of prothrombin to thrombin
• Prothrombin: A precursor protein that is converted to thrombin by the prothrombinase complex
• Thrombin: A key enzyme in the coagulation cascade that: 1) converts fibrinogen to fibrin; 2) activates Factors V, VIII, and XI; 3) activates platelets; 4) stimulates the release of Factor VIII from Weibel-Palade bodies in endothelial cells; and 5) activates protein C
• Fibrinogen: A soluble plasma protein that is converted by thrombin into insoluble fibrin, forming the meshwork of the blood clot
• Fibrin: The insoluble protein that forms the meshwork of the blood clot, trapping platelets and red blood cells
• Factor XIII: Cross-links fibrin monomers into a stable fibrin meshwork, strengthening the clot
• Factor XII Initiates the intrinsic pathway of coagulation by activating Factor XI upon contact with negatively charged surfaces like collagen
• Factor VIII: Co-factor for the activation of Factor X by the tenase complex (Factors VIlla, IXa, and Ca2+), part of the intrinsic pathway
• Factor IX Activated by Factor Xla, participates in the intrinsic pathway by activating Factor X in the presence of Factor VIIIa and calcium
• Antithrombin: A naturally occurring anticoagulant that inhibits thrombin and other coagulation factors like Factor Xa, IXa, and Xla
• Protein C: An anticoagulant protein that inactivates Factors Va and VIIIa, helping to regulate the coagulation cascade
• Protein S: A cofactor for protein C, enhancing its ability to inactivate Factors Va and Villa
• t-PA (tissue plasminogen activator): A thrombolytic agent that converts plasminogen to plasmin, which breaks down fibrin and dissolves blood clots

Hemostasis

• A finely tuned physiological process essential for preventing blood loss following vascular injury while preserving the fluidity of blood within the vascular system
• Vascular Spasm (Vasoconstriction):
  • Initiation: When a blood vessel is damaged, it immediately constricts (vasoconstriction) to reduce blood flow to the injured area
  • A reflex response involving the smooth muscle of the vessel wall

Thromboembolic Disorders

• A group of conditions where blood clots form in the blood vessels and can potentially travel to other parts of the body, causing blockages and serious health issues
• Basics:
  • Thrombus: A blood clot that forms inside a blood vessel
  • Embolus: A thrombus or other debris that breaks free and travels through the bloodstream
  • Thromboembolism: A general term for conditions involving blood clots that travel
• Types:
  • Deep Vein Thrombosis (DVT): Blood clots form in the deep veins, typically in the legs
  • Pulmonary Embolism (PE): A blood clot travels from the legs (or sometimes arms) to the lungs, blocking blood flow
• Risk Factors:
  • Virchow's Triad: Venous stasis (slow blood flow), endothelial injury (damage to the lining of blood vessels), and hypercoagulability
  • Age, obesity, pregnancy, cancer, surgery, trauma, prolonged immobilization
• Inherited hypercoagulable states (like Factor V Leiden, protein C/S deficiencies)
• Certain medications (oral contraceptives, hormone replacement therapy)
• Causes:
  • Immobility: Prolonged bed rest, long flights, or sitting for extended periods increases the risk of blood clots
  • Surgery: Major surgery can increase the risk, especially in the legs or abdomen
  • Cancer: Cancer cells can release substances that promote clotting
  • Inherited clotting disorders: Some people are born with a higher risk of blood clots Hormone therapy: Estrogen-containing medications, including birth control pills, can increase the risk.
• Symptoms:
  • DVT: Pain, swelling, redness, warmth, and tenderness in the affected leg
  • PE: Shortness of breath, chest pain, cough, rapid heart rate, and dizziness
• Diagnosis:
  • Physical examination: To assess for symptoms like swelling and tenderness
  • Imaging tests: Ultrasound, CT scan, or MRI to visualize the blood clot
  • Blood tests To check for markers of clotting and inflammation
• Treatment:
  • Anticoagulants (blood thinners): To prevent clots from growing and to reduce the risk of new clots forming
  • Thrombolytics: Drugs that dissolve existing blood clots
  • Compression stockings: To help prevent swelling and promote blood flow
  • Lifestyle changes: Including regular exercise, staying hydrated, and avoiding long periods of sitting or standing
• Complications:
  • Pulmonary embolism: Can be life-threatening if it blocks a major artery in the lungs
  • Stroke: If a clot travels to the brain
  • Deep vein thrombosis: Can cause pain, swelling, and even leg ulcers

Proximal DVT

• More dangerous than DVT in smaller veins of the calf (distal DVT)
• Risk Factors:
  • Larger size: the femoral and iliac veins are significantly larger than the calf veins
  • Higher risk of complications: proximal DVT has a higher risk of developing serious complications like:
    • Pulmonary embolism (PE): A blood clot from the DVT can travel to the lungs, blocking blood flow and causing potentially fatal respiratory problems
    • Post-thrombotic syndrome: causes long-term damage to the veins, leading to swelling, pain, and skin discoloration in the affected leg
  • Increased risk of recurrence: Proximal DVT has a higher chance of recurring compared to distal DVT
• Symptoms :
  • Marked swelling in the thigh or groin
  • Severe pain, often described as a throbbing or aching sensation
  • The skin above the affected vein may become red and warm
  • The affected area may be tender to the touch
  • The skin may appear bluish or dark
• Diagnosis:
  • Ultrasound
  • D-dimer test
  • Venography
• Treatment:
  • Anticoagulation therapy: Medications -compression therapy
  • Inferior vena cava filter
• Surgery and Risk Factors:
  • Knee replacements. Pelvic and spine surgeries
  • Abdominal surgeries
  • Bowel resection
  • Trauma surgeries
• Mitigation Factors:
  • Employed assessment
  • Fluid managements
  • Use tournaquets
  • Enable mobilization

Other hypercoagulable states

• Protein C Deficiency
• Family History of Thrombosis, Pregnancy, Oral Contraceptives and Cancer-inherited mutations
• Deep Vein Thrombosis
• Caused by lack of Protein C in activity

Protein S Deficiency

• Similar to Protein C Deficiency
• Decreased level in Protein C

Factor Five Leiden

• Caused by point mutations
• Creates stroke/Thrombosis

Primary Immune

Purpura (ITP): Antibodies target and destroy Platelets

Thromobotic

deficiency in ADAMS13 enzyme can cause microthrombi

Hemophillia A and B

• Disrupt intrinsic pathways
• Have prolonged bleeding

Disseminated Coagulation

• Widespread Activation cascade causing bleeding.
• Excessive clotting and bleeding

Several factors can shift the oxygen

• Increase Body Temps
• High Carbon Dioxide
• Decrease PH levels

Leukopenia

Definition-Lower counts of white blood cells. viral/autoimmune related

Leukocytosis

High White Blood cells infections, immune disorders

Valvular Heart Disorder

• Can affect aortic/mitral valves
• Classified by murmurs, and patho

Aortic Stenosis

• Narrowing heart valve
• Caused by heart disease
• Causes shortness of breath

Valvular Regurgitation

• Diastolic murmor during aortic conditions
• Increases pressure

Myocardial Ischemia

• Oxygen deprivation to heart
• Caused by reduction of blood flow
• Chest pains that rotate through the shoulders

Atherosclerosis

Fatigue, and Diaphrosis

Acute Coronary Syndromes

• Reduction of Heart levels

Myocardial Infacrtion

• Blood blockage to heart levels
• High pressure in arteries

P.A.D

Lower extremities affected causes fatigue in legs

Atrial Filbrilation

Rapid chaotic activity in heart caused by smoking