Exam 2 Blueprint - Chapter 12 Disorders of White Blood Cells PDF

Exam 2 Blueprint Chapter 12: Disorders of White Blood Cells Identity normal versus abnormal laboratory values of white blood cells on complete blood count NORMAL WBC count: 4,000-10,000 cells/mcL Neutrophils (Segs): 40%-80% Immature Neutrophils (Bands): 0%-10% Lymphocytes: 20%-40% Monocytes:...

Exam 2 Blueprint Chapter 12: Disorders of White Blood Cells Identity normal versus abnormal laboratory values of white blood cells on complete blood count NORMAL WBC count: 4,000-10,000 cells/mcL Neutrophils (Segs): 40%-80% Immature Neutrophils (Bands): 0%-10% Lymphocytes: 20%-40% Monocytes: 2%-10% Eosinophils: 1%-7% Basophils: 0%-2% ABNORMAL WBC\< 4,000/uL (Leukopenia) WBC\> 11,000/uL (Leukocytosis) Describe the synthesis and maturation of white blood cells in the bone marrow and lymph nodes Synthesis of WBC: Hematopoiesis. Formation of blood cells from HSCs in bone marrow. HSCs differentiate into WBCs. HSCs then divide into 2 linages. Myeloid linage- produces granulocytes (Neutrophils, Eosinophils, Basophils), Monocytes (become macrophages), dendritic cells Lymphoid linage- give rise to lymphocytes (B cells, T cells, Natural killer cells) Granulocytes, B cells, and monocytes mature in the bone marrow T cells mature in the thymus Discuss the basic pathological mechanisms that occur in hematologic neoplastic disease Leukemia- states of neoplastic proliferation involving WBCs Lymphoma- neoplasms of lymphocytes and are commonly solid tumors found in lymphoid tissue Myelodysplastic Syndrome (MDS)- disorders of stem cells in bone marrow. Part or all of bone marrow hematopoiesis is dysfunctional and ineffective, and differentiation of all or one category of precursor stem cells into committed cell lines in impaired. Abnormal development of one stem cell lineage within the bone marrow- RBCs, WBCs, platelets. MM- arises due to abnormal proliferation of plasma cells, which yield excessive immunoglobulin and immunoglobulin fragments. Recognize clinical manifestations of bone marrow dysfunction in hematologic neoplastic disease Leukemia & Lymphoma- bone marrow becomes overwhelmed by proliferation of neoplastic blood cells that crowd out healthy blood cells. Symptoms related to low RBC count- Anemia Low WBC count- suppressed immune system, infection highly possible Low platelet count- leads to thrombocytopenia Chapter 13: Disorders of Red Blood Cells Recognize the various etiologies of common types of anemia Causes of Anemia: loss of RBC- acutely or chronically, all blood components are lost destruction of RBCs- RBC hemolyzed (destroyed) faster than they are produced-sickle cell anemia- thalassemia Not producing enough RBCs -- iron deficiency anemia, vitamin B 12 deficiency, folic acid deficiency, aplastic anemia Pernicious Anemia (vitamin B12 deficiency)- caused by: inadequate intake, malabsorption with gastric bypass surgery, lack of intrinsic factor (required for B12 absorption) Anemia from blood loss: Acute blood loss: caused by sudden from trauma related from hemorrhage Chronic blood loss: slow from GI tract, menstrual blood loss in women Iron deficiency anemia: inadequate intake of iron, excessive blood loss in menstruation and GI blood loss. Describe the mechanisms of common types of anemia Iron deficiency Anemia: iron to synthesize hemoglobin, heme portion of hemoglobin contains iron that carries oxygen ions. Lack of iron leads to poor oxygen transport. Without enough iron, the body cannot produce adequate hemoglobin, leading to smaller and paler RBCs (microcytic, hypochromic anemia). Vitamin B12 or folate deficiency anemia: both required for DNA synthesis in production of RBC. Deficiency in either results in impaired DNA replication leading to production of abnormally large and immature RBC (megaloblast) that are ineffective in oxygen transport Hemolytic anemia: occurs when RBC are destroyed faster than they are produced (hemolysis). Premature destruction of RBC can be due to intrinsic factors (genetic defects in RBC) or extrinsic factors (external affects like antibodies or toxins) Aplastic anemia: caused by damage to bone marrow (responsible for producing RBC, WBC, and platelets) result is pancytopenia (deficiency in all blood cell types) Sickle cell anemia: genetic disorder that causes production of abnormal hemoglobin. Under low oxygen conditions defective hemoglobin causes RBC to assume sickle shape. Misshapen cells are less flexible and cause get stuck in blood vessels leading to blockages, and early destruction of RBC Thalassemia: inherited disorder characterized by reduced production of one or more globin chains that make up hemoglobin. Leads to ineffective RBC production and increased RBC destruction. List the sign and symptoms of disorders of RBC, including anemias and polycythemia Most anemias: excessive fatigue, SOB w/ activity, red swollen tongue, pica (eat dirt, crave ice) Anemia from Acute blood loss: depend on volume of blood lost, hypotension, tachycardia, tachypnea, pallor (cool clammy skin), loss of consciousness as bleeding worsens Anemia from Chronic blood loss: pallor, weakness, exercise intolerance, fatigue may not develop in obvious manner. Not as dramatic as acute blood loss. Hemolytic anemia: general signs of anemia: pallor, fatigue, SOB, tachycardia. Signs related to hemolysis: chills, jaundice ( caused by increased bilirubin levels produced by breakdown of RBCs), dark urine (caused by increased urobilinogen), and enlarged spleen. Sickle cell: common signs of anemia present, particularly fatigue and exercise intolerance. Jaundice and bile concentration in gall bladder. Leads to gallstones. Chest pain with tachypnea, fever, cough and low arterial saturation Thalassemia: common signs of anemia: fatigue, weakness, pallor, exercise intolerance Iron deficiency anemia: common signs of anemia: fatigue, weakness, and exercise intolerance. If caused by GI blood loss, patient may have Melena. Women of childbearing age may have menorrhagia. Specific to Iron deficiency: hair loss, pica Pernicious anemia (results from vitamin B12 deficiency): fatigue, exercise intolerance, dyspnea, weakness, tachycardia, pt may also have glossitis Aplastic Anemia: High output heart failure can occur, increased susceptibility to infections caused by WBC deficiency, increased bleeding risk caused by platelet deficiency. Polycythemia: headache, dizziness, weakness, SOB especially when lying down, feeling of fullness on left side of abdomen, may have abdominal pain and angina. Chapter 14: Disorders of Platelets, Hemostasis, and Coagulation Explain the process of hemostasis, including platelet aggregation and activation, and the coagulation cascade Hemostasis: physiological process that stops bleeding at the sight of injury. Primary hemostasis is when the platelets aggregate to form a platelet plug and adhere to the site of injury. In secondary hemostasis, the deposition of fibrin occurs, which is generated by the coagulation cascade. These 2 processes happen simultaneously and interweave to create a durable blood clot or thrombus, that will stop the bleeding at a site of injury. Describe pathological disorders caused by excessive clotting Thrombocytosis (enhanced platelet activity) can occur with disturbances in blood flow and endothelial damage. **Deep vein thrombosis (DVT)** in the femoral vein can travel into the inferior vena cava and flow into the right atrium and ventricle. Then into the pulmonary artery can cause a **pulmonary embolism. Heart failure** which causes weakened pumping of blood can also lead to venous stasis in lower extremities, which predisposes to thrombus formation. **Atrial fibrillation** causes quivering, noncontracting atrium, leads to stagnation of arterial blood in the left atrium. **Ischemic stroke** Antiphospholipid syndrome- associated w formation of multiple clots. Describe disorders of defective hemostasis or coagulation that cause excessive bleeding Defective coagulation- ( inherited disorders) hemophilia A, hemophilia B, and von Willebrand disease (vWD), common acquired deficiency - occurs in liver disease, like alcohol related cirrhosis. Prolonged bleeding is provoked by injury or trauma. Large bruises, hematomas, or prolonged bleeding into GI or urinary tract or joins are common. **DIC** Defective hemostasis- **Vitamin K deficiency** can cause liver to produce dysfunctional clotting factors Chapter 11: Disorders of the Immune System Differentiate between innate and adaptive immunity Innate immunity- give right at birth, immediate and non specific response. Examples- natural killer cells, skin & GI tract Adaptive immunity- antigen/ toxin has to have been in body one time already, so the body can recognize and remember for quicker response. Examples- B lymphocyte (antibody mediated/ humoral immunity). T lymphocyte ( cell mediated immunity) Compare and contrast the mechanisms of B lymphocyte (also called antibody-mediated or humoral) immunity verses T lymphocyte (also called cell-mediated) immunity. B lymphocyte- mature in bone marrow, spleen, and lymph nodes, they mature into plasma cells which can produce antibodies (igs). On the 1sr exposure to antigen primary immune response occurs, on 2^nd^ exposure secondary immune response occurs, immune system recognizes it and quickly produces antibodies against it. T lymphocytes- mature in thymus gland, after maturation, mature T cells are in blood and lymph nodes. Become one of 2 types of cells: CD4 cells ( T helper cells), CD8 cells (cytotoxic T cells) Describe the different mechanisms of four hypersensitivity reactions Type I immediate hypersensitivity- rapidly developing immune reaction when exposed to a specific antigen ( ex allergic reactions), cells involved: CD4 cells, IgE antibodies, eosinophils, mast cells Type II Cytotoxic Hypersensitivity- immunoglobulins (antibodies) target cells coated w antigen, causing cell destruction and phagocytosis ( ex blood transfusion reaction) Type III Immune Complex Hypersensitivity- antigen combines with Ig in circulation and these complexes are then deposited in tissues. ( ex system- wide: systemic lupus erythematosus) , localized: Rheumatioid arthritis) Type IV Delayed Hypersensitivity- T lymphocytes attack antigen days after the exposure (delayed) ( ex: exposure to poison ivy, organ transplant rejection) Discuss the mechanisms of significant autoimmune diseases Autoimmune means immune reactions to self antigens, result from the loss of self tolerance. SLE (Lupus)- SLE production of autoantibodies against a wide range of self-antigens, including DNA, RNA, and nuclear proteins. This leads to the formation of immune complexes (antigen-antibody complexes) that deposit in various tissues, triggering inflammation and tissue damage. Symptoms- classic butterfly rash, joint inflammation and musculoskeletal symptoms, splenic enlargements, pleural effusion, vasculitis, pericarditis, anemia, and thrombocytopenia. Rheumatoid arthritis- chronic autoimmune inflammatory disorder that affects joints and may have systemic effects. RA is driven by an autoimmune response targeting synovial joints. Autoantibodies such as rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA) form immune complexes in the joints, activating macrophages and synovial fibroblasts. Type 1 diabetes- T1DM is caused by the autoimmune destruction of insulin-producing beta cells in the pancreas. Cytotoxic T cells (CD8+ T cells) recognize self-antigens presented by pancreatic beta cells and destroy them, leading to a loss of insulin production. Multiple Sclerosis- immune system attacks the myelin sheath surrounding nerve fibers in the central nervous system (CNS). T cells, particularly CD4+ Th1 and Th17 cells, recognize myelin antigens and initiate an inflammatory response that damages oligodendrocytes (myelin-producing cells). Discuss the mechanisms of immunodeficiency disorders Primary (congenital) deficiencies- genetic, usually manifesting infancy to 2 years Secondary (acquired) deficiencies- acquired because of loss of immune function from various problems (infection, malnutrition, splenectomy, HIV/AIDS, immunosuppression for treatment. Signs of immunodeficiency- reoccurring infections, persistent lymphadenopathy (enlarged lymph nodes) Identify the three stages of HIV infection and clinical presentation of each stage 1 stage- acute retroviral syndrome, last about 2 weeks then resolves , flu/mono like symptoms, pt may not seek care 2 stage- lies dormant w no symptoms, person has viral particles in blood, can transmit virus to others. 3 stage- Chronic HIV infection, if untreated, viral load increases and CD4 count decreases over time. Can last 6-10 months. Person has immune deficiency, multiple body defects. Define the significant laboratory test involved in diagnosis in HIV infection and AIDS CD4 count, HIV viral load (most accurate) (also called HIV RNA assay), HIV antibody, and HIV drug resistance testing AIDS- person with HIV must have AIDS- defining condition or CD4 count less than 200 cells/mm3 Chapter 40: Cancer Identify common risk factors and etiologies that can lead to cancer Chemical carcinogens- smoking, tobacco use, alcohol consumption. Inherited gene mutations, family history of cancer. Environmental/work place exposure- asbestos, Radiation/ UV exposure. Infections (HPV, HIV), diet, immunosupression, aging chronic inflammation. Differentiate among the characteristics of benign versus malignant neoplasia Benign- not cancerous, well differentiated, remains localized, cohesive, well- demarcated from surrounding tissue (slower to grow) Malignant tumors (cancerous), invasive and destructive to surrounding cells. Cells easily metastasize ( easily travels) Recognize the pathological mechanisms involved in the development of cancer in the body Genetic mutations of bad oncogenes, loss of tumor suppressor genes, epigenetic changes, genomic instability and DNA repair defects. Recognize the most common types of cancer and their symptoms and clinical manifestations Lung cancer- cough, hemoptysis ( blood in sputum) , chest pain, dyspnea, wheezing, productive cough Brest cancer- singular, nontender, firm mass, Nipple discharge, nipple or skin retraction, adherence to skin or chest wall, pagers ( redness, crusting of nipple), peau d'orange ( thickness of skin that resembles an orange peel Prostate cancer- early- no symptoms, obstructed urine flow: decreased force of stream, incomplete emptying of the bladder, straining, late stage symptoms: hematuria ( blood in urine), azotemia ( nitrogen in urine) , anemia, anorexia, back pain: vertebral bone metastasis Colorectal cancer- fatigue, weakness, weight loss, iron deficiency anemia, changes in bowel habits ( diarrhea/ constipation), Melena ( blood in the stool) Chapter 22: Renal Disorders Describe the various activities of the kidney and how these actions are affected in renal dysfunction Identify causes of prerenal, intrarenal, and postrenal dysfunction of the kidney Explain the signs and symptoms of major types of kidney dysfunction Recognize assessment modalities and laboratory test used to diagnose kidney dysfunction Differentiate between acute kidney injury and chronic renal failure Chapter 23: Urological Disorders Differentiate between acute kidney injury and chronic renal failure Recognize the common etiologies of urological dysfunction Identify signs, symptoms, and clinical manifestations of urological disorders