• Define terms describing blood abnormalities ("dyscrasias")
• Explain the pathophysiology of selected blood dyscrasias (anemias, clotting disorders, neoplasms)
• Describe Disseminated Intravascular Coagulation (DIC)
• Describe the pathophysiology of arterial & peripheral vascular diseases
• Core functions
– Transport: O₂, nutrients ⟶ tissues; metabolic wastes ⟶ excretory organs
– Regulatory roles: immune surveillance, inflamVenules hemostasis
• Basic flow pathway
– Heart → Arteries → Arterioles → Capillaries → Venules→ Veins → Heart → Lungs → Heart
• Structural highlights
– Valves in large veins prevent gravity-induced pooling in dependent areas - They prevent the backflow of blood
– Veins: thinner walls, less smooth muscle vs. arteries → greater capacitance
– Capillaries: single endothelial layer → ideal for diffusion
• Universal transport medium; site of cell–signal & immune interaction
• Hematopoiesis- the Production of Blood cells
– Multipotent stem cell (bone marrow) differentiates into needed element
– Dyscrasia = any disorder of blood or its cellular components
• Hematocrit- Concentration of RBC’s to water content
– Percentage of formed elements, predominantly RBCs, in whole blood
• \text{Blood} \approx 8\% of total body weight
• Plasma \approx 55\%
– Water \approx 91\%
– Proteins \approx 7\% (Albumin 57\%, Globulins 38\%, Fibrinogen 4\%, Prothrombin 1\%)
– Other solutes \approx 2\% (ions, nutrients, gases, wastes, regulators)
• Formed Elements \approx 45\%
– Erythrocytes >99\% (by number)
– “Buffy coat” <1\% → leukocytes + platelets
* Neutrophils 60!\text{–}70\% - First responders in the blood (the most watched)
* Lymphocytes 20!\text{–}25\%
* Monocytes 3!\text{–}8\%
* Eosinophils 2!\text{–}4\%
* Basophils 0.5!\text{–}1\%
* Platelets (Thrombocytes)
• Erythrocytes - Red blood cells
– Packed with hemoglobin (Hb) for O₂ transport
– Require iron (stored as ferritin), vitamins B6 and B12, folic acid
• Leukocytes
– Multiple lineages → innate & adaptive immune functions
• Thrombocytes (Platelets)
– Cytoplasmic fragments essential to coagulation
* Coagulation cascade: Prothrombin → Thrombin; Fibrinogen → Fibrin mesh Prothrombin is the one that makes the blood stick together/ Fibrogen comes from the liver
– Inadequacy → hemorrhagic risk
• Definition: ↓ functional hemoglobin (via ↓ RBC #, ↓ Hb content, or ↓ iron)
• General S/S
– Fatigue, pallor, cold intolerance
– Dyspnea, tachycardia, shortness of breath (exertional) Tachycardic due to increased effort to push blood around
– Nail & hair changes, glossitis, delayed wound healing
• Insufficient iron → inability to synthesize heme
• Epidemiology: common in menstruating women & pregnancy
• Etiologies
– Poor intake, chronic blood loss, malabsorption, liver dz
• Tx: dietary iron, oral/IV iron, treat underlying loss
• Autoimmune loss of intrinsic factor or GI malabsorption
• Patho: failure of DNA synthesis → large, fragile RBCs that hemolyze early
• Hallmark: neurological S/S, oral burning pain, glossitis
• Tx: lifelong parenteral or high-dose oral \text{B}_{12}
• Bone-marrow failure → pancytopenia
• Causes: idiopathic, drug/toxin, autoimmune, viruses (e.g.
Hep C), radiation, genetic
• Consequences: anemia, leukopenia (infection), thrombocytopenia (bleeding)
• Tx: remove cause, transfusion, bone-marrow transplant
• Autosomal-recessive mutation (HbS) → sickling when deoxygenated Both Mom and Dad have to be carriers for baby to be affected
• Patho: rigid, crescent RBCs ↓ O₂ carriage, occlude microvasculature
– Micro-clots → ischemic pain crises, organ damage - Clotting is the most common Adverse reaction
• Epidemiology: African descent 1:365 births; splenomegaly common
• Management: hydration, O₂, pain control, hydroxyurea, transfusion, gene therapy research
• Coagulation impairment etiologies: infection, vitamin K deficiency, liver failure, genetic defects
• Inherited X-linked recessive deficiency of clotting factor
– Hemophilia A = Factor VIII ↓ - Most common type of Hemophilia
• S/S: joint bleeding (hemarthrosis), hematomas, hematuria, ecchymosis
• Labs: prolonged aPTT, normal platelet count
• Tx: IV factor VIII/IX concentrates, desmopressin (mild)
• ↓ vWF → impaired platelet adhesion + ↓ factor VIII stability
• S/S similar to hemophilia but mucocutaneous emphasis (nosebleeds, menorrhagia)
• Tx: vWF concentrate, desmopressin
• \text{PTT} / \text{aPTT} ↑
• Coagulation time ↑
• Simultaneous systemic activation of coagulation & fibrinolysis
• Trigger: endothelial/tissue injury (obstetric emergency, sepsis, trauma, malignancy)
• Patho
– Widespread micro-thrombi → organ ischemia/infarcts
– Consumption of platelets & factors (\"consumptive coagulopathy\") → bleeding
• Clinical triad: petechiae/bleeding, ischemic organ signs, shock
• Lab pattern: ↑ D-dimer, ↓ fibrinogen, thrombocytopenia, prolonged PT/aPTT
• Tx: treat cause, support (cryoprecipitate, FFP, heparin in select cases)
• Arteriosclerosis: generic hardening, ↓ elasticity, lumen narrowing
• Atherosclerosis: specific plaques (lipid-rich core, fibrous cap)
• LDL (\"little devils\"): carry cholesterol to tissues; high levels → plaque risk LDL are the bad lipids
• HDL (\"heavenly darlings\"): return cholesterol to liver for excretion- HDL are the good Lipids
• Fatigue, leg weakness
• Intermittent claudication (exercise-induced pain)
• Paresthesia, ↓ leg hair, trophic nail changes
• Color change: pallor on elevation, rubor when dependent
• Ulceration, critical limb ischemia
• Revascularizationtrasound, ankle-brachial index
• LRevascularization cessation, exercise, diet, statins, antiplatelets
• Revascularization procedures if severe
• Ischemic heart disease, Myocardial infarction, Transient ischemic attack, Cerebrovascular accident, Peripheral ulcers
LDL-related complications: Myocardial infarction, Ischemic stroke, Peripheral arterial disease, Aortic aneurysm (but not anemia).
• Myeloproliferative disorder → ↑ RBCs, WBCs, platelets
• S/S: hypertension, splenomegaly, hepatomegaly, hyperviscosity-related thrombosis
• Malignant clonal proliferation of immature WBCs
– Acute vs. Chronic; Myeloid vs. Lymphoid
• Patho: marrow packed with blasts → anemia & thrombocytopenia (Low platelette)
• S/S: frequent infections, hemorrhage, bone pain, weight loss, fatigue
• Tx: chemotherapy, targeted biologics, stem-cell transplant
• Localized dilation/weakening of arterial wall (thoracic or abdominal)
• Etiologies: genetic (Marfan), atherosclerosis, hypertension, trauma, infection
• Often silent; palpable pulsatile mass (AAA)
• Rupture → massive hemorrhage, high mortality
• Tx: surgical graft or endovascular stent when \text{diameter} > 5.5\,\text{cm} or rapid growth
• Tortuous, dilated superficial veins due to valve incompetence
• Risk factors: genetics, prolonged standing, pregnancy, obesity
• Complications: edema, venous ulcer, thrombosis
• Tx: compression, sclerotherapy, vein stripping/ablation
• Virchow’s triad: venous stasis, endothelial injury, hypercoagulability
• S/S: calf warmth, erythema, edema, tenderness, positive Homan sign (controversial)
• Major complication: pulmonary embolus
• Prevention
– Early mobilization, leg exercises/ROM
– Sequential compression devices (SCDs)
– Graduated compression stockings
– Smoking cessation, treat underlying disorders
• Tx: anticoagulation (heparin, LMWH, DOACs)
Post-hip-surgery patient with suspected DVT: FIRST action → elevate the leg & notify provider (prioritize preventing embolization; do NOT massage).
• Screening & early detection (lipid panels, complete blood count) reduce morbidity
• Genetic counseling for hemophilia & sickle-cell disease
• Patient education: adherence to iron/\$\text{B}_{12}\$ therapy, anticoagulant safety, lifestyle modifications