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Patho exam 2
pathophsyiology
| Question | Answer |
|---|---|
| RBC role | Transport oxygen through hemoglobin. |
| Microcytic RBC | Small RBCs. Main causes: iron deficiency anemia and thalassemia. |
| Macrocytic RBC | Large RBCs. Main causes: vitamin B12 deficiency and folate deficiency. |
| Iron deficiency anemia | Microcytic anemia. Fatigue, pallor, and koilonychia (spoon nails). Treat with iron supplementation. |
| Pernicious anemia | Vitamin B12 deficiency causing megaloblastic anemia with neurological problems such as neuropathy, paresthesia, and impaired balance. Treat with vitamin B12, often intramuscularly. |
| Folate deficiency anemia | Megaloblastic anemia caused by folate deficiency WITHOUT neurological deficits. Treat with folate replacement. Leafy greens are a good source. |
| Aplastic anemia | Bone marrow failure causing pancytopenia: ↓ RBCs → fatigue, ↓ WBCs → infections, ↓ platelets → bleeding/petechiae. Treatment may include bone marrow transplantation. |
| Hemolytic anemia | RBCs are destroyed faster than they can be replaced. Hemoglobin breaks down → ↑ bilirubin → jaundice and possibly dark urine. Treat by removing the cause and supportive therapy. |
| Thalassemia | Inherited mutation, ↓ globin chain production → ↓Hg/ microcytic anemia w ineffective erythropoiesis. Treat: transfusions, iron chelation, bone marrow transplantation. iron is NOT necessarily ↓ because the problem is globin production, not iron deficiency. |
| RBC Sickle Cell Disease | Mutation in HbS causes RBCs to sickle → vaso-occlusion → severe pain and tissue ischemia + shortened RBC lifespan → hemolytic anemia. |
| Sickle Cell Disease triggers | Hypoxia, cold temperatures, dehydration, physical exertion, and infection. |
| Erythropoietin (EPO) | Kidneys detect tissue hypoxia → release EPO → stimulates bone marrow to produce RBCs/reticulocytes. |
| Chronic Kidney Disease (CKD) and anemia | Kidney damage causes ↓ EPO production → ↓ RBC production → anemia. |
| Hemostasis | Process that stops bleeding after blood vessel injury. |
| Stages of hemostasis | 1. Vascular spasm → 2. Platelet plug formation → 3. Coagulation cascade → 4. Clot retraction → 5. Fibrinolysis. |
| Stages of hemostasis 1: Vascular spasm | Immediate vasoconstriction of the injured vessel → ↓ blood flow → ↓ blood loss. |
| Stages of hemostasis 2: Platelet Plug Formation (Primary Hemostasis) | Injury exposes collagen → von Willebrand factor (vWF) helps platelets adhere to collagen → platelets activate and release chemicals → more platelets are recruited → unstable platelet plug forms. |
| von Willebrand factor (vWF) | Helps platelets stick to exposed collagen at the site of vessel injury. |
| Stages of hemostasis 3: Coagulation Cascade (Secondary Hemostasis) | Intrinsic and extrinsic pathways converge at Factor X → prothrombin is converted to thrombin → thrombin converts fibrinogen into fibrin → fibrin forms a strong mesh that stabilizes the platelet plug. Requires calcium. |
| Stages of hemostasis 4: Clot Retraction | Actin and myosin inside platelets contract → squeeze out serum and pull the edges of the injured vessel closer together. |
| Stages of hemostasis 5: Fibrinolysis | tPA activates plasminogen into plasmin → plasmin breaks down the fibrin mesh after the vessel has healed. |
| Primary vs Secondary Hemostasis | Primary hemostasis = platelet plug formation. Secondary hemostasis = coagulation cascade and fibrin stabilization. |
| Coagulation cascade pathway | Intrinsic pathway + Extrinsic pathway → Common pathway → stable fibrin clot. |
| Intrinsic pathway | Triggered by endothelial injury. Involves Factors XII, XI, IX, and VIII. Activates Factor X. Monitored by PTT/aPTT and associated with heparin therapy. |
| Extrinsic pathway | Triggered by tissue factor released by damaged tissue. Primarily involves Factor VII. Activates Factor X. Monitored by PT/INR and associated with warfarin therapy. |
| Common pathway | Both intrinsic and extrinsic pathways activate Factor X → Factor X with Factor V helps convert prothrombin to thrombin → thrombin converts fibrinogen to fibrin → stable clot forms. |
| Thrombin | Converts fibrinogen into fibrin. |
| Fibrin | Forms a strong protein mesh that stabilizes the platelet plug and creates a stable clot. |
| Calcium in coagulation | Calcium is required for multiple steps of the coagulation cascade. |
| Intrinsic pathway memory | Intrinsic = XII, XI, IX, VIII → PTT/aPTT → Heparin. |
| Extrinsic pathway memory | Extrinsic = VII → PT/INR → Warfarin. |
| Clotting / platelet disorders | Disorders involving platelets, clotting factors, or abnormal clot formation. |
| Hemophilia | Factor VIII or IX deficiency → impaired coagulation and prolonged bleeding. |
| Von Willebrand disease | Deficiency or dysfunction of von Willebrand factor → impaired platelet adhesion and abnormal bleeding. |
| Immune Thrombocytopenic Purpura (ITP) | Autoimmune destruction of platelets by IgG antibodies → severe thrombocytopenia → petechiae, purpura, and mucosal bleeding. |
| Deep Vein Thrombosis (DVT) | Blood clot forms in a deep vein, usually because of factors such as venous stasis or hypercoagulability. |
| Pulmonary Embolism (PE) | A clot, usually from a DVT, travels to the lungs and blocks pulmonary blood flow. |
| Venous Thromboembolism (VTE) | Includes both deep vein thrombosis (DVT) and pulmonary embolism (PE). |
| Disseminated Intravascular Coagulation (DIC) | Consumptive coagulopathy causing widespread abnormal clotting → platelets and clotting factors are consumed → patient can develop BOTH thrombosis and hemorrhage. |
| DIC key idea | Widespread clotting → clotting factors and platelets get consumed → severe bleeding can occur. |
| Mediators of inflammation | Chemical signals that trigger and control the body's inflammatory response to injury or infection. Main sources include cells, plasma, and proteins. |
| Mediators of inflammation: Cell | Made locally and ready to act. Important sources include WBCs, platelets, and mast cells. |
| Mediators of inflammation: Plasma | Plasma-derived mediators are mainly produced by the liver and become activated after injury. |
| Mediators of inflammation: Proteins | Important protein mediators include cytokines, chemokines, complement, and kinins. |
| Cytokines | Chemical messengers that regulate and coordinate immune and inflammatory responses. |
| Chemokines | Chemical signals that direct WBC movement toward the site of injury through chemotaxis. |
| Complement | Proteins that help the immune system destroy and clear pathogens. |
| Kinins | Inflammatory mediators such as bradykinin that increase vascular permeability and contribute to pain. |
| Bradykinin | Kinin that increases vascular permeability and causes pain |
| Vascular phase of inflammation | Vasodilation → ↑ blood flow → redness and warmth. ↑ vascular permeability → fluid leaves blood vessels → edema/swelling. |
| Vasodilation | Blood vessels widen → ↑ blood flow → redness and warmth. |
| Increased vascular permeability | Fluid and proteins leave blood vessels and enter tissues → edema/swelling. |
| Cellular phase of inflammation | WBCs leave the blood vessel and enter injured tissue. Sequence: margination → adhesion → diapedesis/transmigration → chemotaxis → phagocytosis → activation. |
| Margination | WBCs move toward the inner wall of the blood vessel. |
| Adhesion | WBCs stick to the endothelial wall of the blood vessel. |
| Transmigration / Diapedesis | WBCs squeeze between endothelial cells and leave the blood vessel to enter injured tissue. |
| Chemotaxis | WBCs follow chemical signals toward the site of injury. |
| Phagocytosis | WBCs engulf and remove pathogens, damaged cells, and cellular debris. |
| Activation | WBCs become activated and release inflammatory mediators to help fight injury or infection. |
| Assessment of acute inflammation | ↑ WBCs/leukocytosis, ↑ immature neutrophils/bandemia or left shift, ↑ ESR, ↑ CRP, and ↑ fibrinogen. |
| Cardinal signs of inflammation | Redness, heat, swelling, pain, and loss of function. |
| Types of WBC and what they indicate | Neutrophils → bacterial infection/acute inflammation. Lymphocytes → viral infection/adaptive immunity. Eosinophils → parasites/allergies. Basophils → allergic inflammation. Monocytes/macrophages → chronic inflammation and antigen presentation. |
| Neutrophils | First responders in acute inflammation. Rapidly phagocytose pathogens. ↑ neutrophils commonly indicate acute bacterial infection. |
| Bandemia / Left Shift | ↑ immature band neutrophils in circulation because the bone marrow is rapidly releasing neutrophils. Commonly indicates an active bacterial infection or significant acute inflammation. |
| Lymphocytes | Associated with viral infections and adaptive immunity. Includes B cells and T cells. |
| Eosinophils | Associated with parasitic infections and allergic reactions/type I hypersensitivity. |
| Basophils | Associated with allergic inflammation. Release histamine and heparin. |
| Monocytes and macrophages | Associated with chronic inflammation. Macrophages phagocytose debris and pathogens and participate in antigen presentation. |
| Histamine | Released by mast cells and basophils. Promotes vasodilation and increased vascular permeability. |
| Heparin | Anticoagulant released by basophils and mast cells. |
| Wound healing stages | 1. Hemostasis/inflammation → 2. Proliferative phase → 3. Remodeling phase. |
| Wound healing stage 1: Hemostasis/inflammation | Injury activates platelets and clot formation. WBCs arrive and produce an inflammatory response to remove pathogens and damaged tissue. |
| Wound healing stage 2: Proliferative | Rebuilding phase. Includes fibroblasts, angiogenesis, granulation tissue formation, and epithelialization. |
| Wound healing stage 3: Remodeling | Scar tissue forms and collagen is reorganized and strengthened over time. |
| Fibroblasts | Cells that produce collagen and other extracellular matrix components during wound healing. |
| Angiogenesis | Formation of new blood vessels that supply oxygen and nutrients to healing tissue. |
| Granulation tissue | New fragile pink/red tissue containing new blood vessels, fibroblasts, and extracellular matrix that fills a healing wound during the proliferative phase. |
| Epithelialization | New epithelial cells grow across the wound surface to restore the skin barrier. |
| Types of healing: Primary intention | Clean wound with minimal tissue loss and well-approximated edges, usually closed with sutures or staples. Heals rapidly with minimal scarring. |
| Types of healing: Secondary intention | Large open wound with extensive tissue loss. Edges cannot be brought together. Heals from the bottom up with granulation tissue. Takes longer, causes more scarring, and has higher infection risk. |
| Types of healing: Tertiary intention | Also called delayed primary closure. Deep, contaminated, infected, or swollen wound is left open initially to allow drainage and healing, then closed surgically later. |
| Primary vs Secondary vs Tertiary | Primary = clean edges together. Secondary = large tissue loss and wound stays open. Tertiary = wound left open initially and closed later. |
| Risk factors for ↓ wound healing | Poor nutrition, impaired blood flow, ↓ oxygen, inflammation, impaired immune response, infection, wound separation/dehiscence, older age, and foreign bodies. |
| Factors/diet that assist in wound healing | ↑ protein supports tissue repair. Vitamin A supports epithelialization. Vitamin C supports collagen synthesis. Carbohydrates provide energy. Fats help maintain cell membranes. |
| Protein and wound healing | Supports tissue repair and rebuilding. |
| Vitamin A and wound healing | Supports epithelialization. |
| Vitamin C and wound healing | Required for collagen synthesis. |
| Carbohydrates and wound healing | Provide energy needed for healing. |
| Fats and wound healing | Help maintain cell membranes. |
| Complications of wound healing | Poor healing can lead to infection, wound separation/dehiscence, excessive scar formation, and abnormal granulation tissue. |
| Keloids | Excessive scar tissue formation that extends beyond the original wound margins. |
| Healing in older adults | ↓ dermal thickness, ↓ collagen content, ↓ elasticity, and ↑ vulnerability to wounds. |
| Wound dehiscence | Separation of previously closed wound edges. It is a complication of wound healing and can occur when healing is impaired. |
| Infectious process and stages | Incubation → prodromal → acute → convalescence. |
| Incubation | Pathogen is present but there are no symptoms yet. |
| Prodromal | Early stage with nonspecific symptoms. |
| Acute stage | Peak stage of infection with more characteristic symptoms. |
| Convalescence | Recovery stage where symptoms decline. |
| Innate immunity | Immunity present from birth. Immediate, nonspecific, and has no memory. Includes skin, mucous membranes, neutrophils, macrophages, NK cells, inflammation, and complement. |
| Adaptive immunity | Specific immunity that responds to particular antigens. Slower during first exposure but creates memory, allowing a faster and stronger response during later exposure. |
| Humoral mediated immunity | B cells → plasma cells → antibodies → primarily protects against extracellular pathogens. |
| Cell mediated immunity | T cells, especially CD4 helper T cells and CD8 cytotoxic T cells. CD8 cells kill infected or abnormal cells. |
| Humoral vs Cell mediated immunity | Humoral = B cells and antibodies. Cell-mediated = T cells and direct cellular immune responses. |
| Active immunity | Host makes its own antibodies and develops immune memory. Examples: natural infection and vaccination. Slower to develop but long-lasting. |
| Passive immunity | Host receives pre-made antibodies. Examples: placenta, breast milk, IVIG/HBIG. Immediate but temporary and does not create immune memory. |
| Primary immune response | First exposure to an antigen. Has a lag period while the immune system develops a response. IgM is produced first and memory cells are formed. |
| Secondary Immune Response: Mechanism | Occurs upon re-exposure to a previously encountered antigen. |
| Secondary Immune Response: Key Players | Driven by long-lived Memory B Cells and Memory T Cells created during the primary exposure. |
| Secondary Immune Response: Key Features | Faster, stronger, and longer-lasting than the primary response. Produces higher antibody levels with little or no lag period. |
| Secondary Immune Response: What dominates | IgG is the dominant antibody. IgM is the first antibody produced during the primary response. |
| IgG | Most abundant immunoglobulin. Only major antibody class that crosses the placenta. Dominant antibody in the secondary immune response. |
| IgA | Protects mucosal surfaces. Found in breast milk, tears, and saliva. |
| IgM | First antibody produced during the primary immune response. Also associated with ABO blood group antibodies. |
| IgE | Binds mast cells and basophils → type I hypersensitivity, allergies, and anaphylaxis. |
| Memory cells | Memory B and T cells remain after the primary immune response and allow the body to respond faster during a later exposure to the same antigen. |
| Hypersensitivity Type I | IgE-mediated and immediate. Associated with allergies, asthma, and anaphylaxis. Mast cells release histamine. |
| Hypersensitivity Type II | IgG or IgM antibodies attack antigens on cells. Examples include incompatible blood transfusion reactions and some hemolytic anemias. |
| Hypersensitivity Type III | Antigen-antibody immune complexes deposit in tissues → inflammation and tissue damage. |
| Hypersensitivity Type IV | T-cell mediated and delayed. No antibodies are involved. Examples include poison ivy/contact dermatitis and TB skin reaction. |
| Hypersensitivity memory | Type I = IgE/immediate. Type II = IgG/IgM attack cells. Type III = immune complexes. Type IV = T cells/delayed. |
| Autoimmune diseases | Breakdown of self-tolerance causes the immune system to attack self-antigens → inflammation and tissue destruction. |
| Autoimmune disease examples | Systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes mellitus, and multiple sclerosis. |
| Self-tolerance | The immune system normally recognizes the body's own cells as "self" and does not attack them. |
| CD4 cells | Helper T lymphocytes. Regulate the immune response and activate B lymphocytes and cytotoxic T lymphocytes. Primary target of HIV. |
| HIV/AIDS acute stage | Primary infection phase. Can cause systemic infection symptoms. Seroconversion occurs when the immune system produces antibodies against HIV. |
| HIV/AIDS chronic stage | Latency/chronic phase. HIV continues replicating while the CD4 T-cell count gradually decreases. Can last many years. |
| Overt AIDS phase | CD4 count <200 cells/µL OR an AIDS-defining illness. Can involve opportunistic infections, Kaposi sarcoma, non-Hodgkin lymphoma, wasting syndrome, and metabolic disorders. |
| Tumor cells: Benign presentation | Usually encapsulated, localized, slow-growing, and non-invasive. |
| Tumor cells: Malignant presentation | Often unencapsulated, irregular, invasive, and capable of spreading to distant sites. |
| Tumor cells: Metastasis presentation | Malignant cells spread from the original tumor to distant sites through blood/hematogenous spread or lymphatics. |
| Anaplasia | Loss of normal cell differentiation. Hallmark of malignant cells. |
| TP53 gene | Tumor suppressor gene known as the "guardian of the genome." Promotes DNA repair or apoptosis when DNA is damaged. Mutation can allow damaged cells to divide uncontrollably. |
| VEGF in cancer | Tumor cells can secrete VEGF → stimulates angiogenesis → creates new blood vessels that supply tumors with oxygen and nutrients and support tumor growth. |
| TNM staging | T = primary Tumor size/extent. N = regional lymph Node involvement. M = distant Metastasis. |
| Paraneoplastic syndromes | Disorders caused by substances produced by a tumor rather than direct invasion of the tumor. Examples include SIADH with small-cell lung carcinoma, hypercalcemia with squamous cell carcinoma, and Cushing syndrome from ectopic ACTH production. |
| Susceptibility of cancer: Heredity | Inherited mutations in tumor suppressor or DNA repair genes such as TP53 or BRCA1/2 can increase cancer susceptibility. |
| Susceptibility of cancer: Immunocompetence / Immune Surveillance | Decreased immune function can reduce the ability of NK cells and cytotoxic T cells to identify and destroy abnormal cells. Examples include aging, HIV/AIDS, and immunosuppressive drugs. |
| Susceptibility of cancer: Environmental & Chemical Carcinogens | Tobacco smoke, asbestos, alcohol, and radiation such as UV light and X-rays can damage DNA and contribute to cancer development. |
| Potential cancers / Oncogenic Viruses | HPV → cervical cancer. HBV/HCV → hepatocellular carcinoma. EBV → Burkitt lymphoma. |
| Hemostasis sequence | Vascular spasm → platelet plug → coagulation → clot retraction → fibrinolysis. |
| Primary vs Secondary Hemostasis | Primary = platelets make the plug. Secondary = coagulation cascade adds fibrin to stabilize the plug. |
| Coagulation pathway | Intrinsic + Extrinsic → Factor X → thrombin → fibrinogen → fibrin. |
| Intrinsic vs Extrinsic | Intrinsic → PTT/aPTT → heparin. Extrinsic → PT/INR → warfarin. |
| Inflammation cellular sequence | Margination → adhesion → diapedesis → chemotaxis → phagocytosis → activation. |
| Acute inflammation WBC | Neutrophils are first responders and are strongly associated with acute bacterial infection. |
| Bandemia / Left shift | ↑ immature neutrophils in circulation → bone marrow is rapidly releasing neutrophils → commonly indicates active bacterial infection/significant acute inflammation. |
| Wound healing sequence | Hemostasis/inflammation → proliferation → remodeling. |
| Hypersensitivity types | I = IgE/immediate. II = IgG/IgM against cells. III = immune complexes. IV = T cells/delayed. |
| Antibody sequence | IgM = first in primary response. IgG = most abundant + crosses placenta + dominates secondary response. IgA = mucosa. IgE = allergies/anaphylaxis |
| Bone marrow — role | Produces RBCs, WBCs, and platelets through hematopoiesis. |
| Bone marrow — RBC production | Produces RBCs in response to erythropoietin (EPO) stimulation. |
| Bone marrow — WBC production | Produces different WBCs that defend against infection and coordinate immunity. |
| Bone marrow — platelet production | Megakaryocytes in bone marrow produce platelets for hemostasis. |
| Neutrophils — main role | First responders; phagocytize bacteria and debris during acute inflammation. |
| Basophils — main role | Release histamine and heparin; mainly involved in allergic inflammation. |
| Eosinophils — main role | Fight parasites and participate in allergic reactions. |
| B cells — role | Adaptive immune cells that become plasma cells and produce antibodies. |
| T cells — role | Coordinate immunity and kill infected or abnormal cells. |
| Macrophages — role | Phagocytize pathogens and debris, present antigens, and help regulate inflammation. |
| Hemoglobin (Hgb) | Protein inside RBCs that carries oxygen and some carbon dioxide. |
| Hematocrit (Hct) | Percentage of blood volume made up of RBCs. |
| Erythropoietin (EPO) | Kidney hormone that stimulates bone marrow to make RBCs when oxygen is low. |
| Platelets — role | Cell fragments that adhere to injured vessels and form the initial platelet plug. |
| Iron deficiency anemia — treatment | Iron replacement and treatment of the underlying cause of blood loss. |
| B12 deficiency anemia — treatment | Vitamin B12 replacement, often IM when absorption is impaired. |
| Sickle cell anemia — treatment | Hydration, pain control, oxygen when needed, hydroxyurea, and transfusions when indicated. |
| Aplastic anemia — treatment | Remove the cause and provide supportive care; severe cases may require stem cell transplant. |
| Thalassemia — treatment | Transfusions for severe disease, iron chelation for iron overload, and possible stem cell transplant. |
| Hgb vs Hct | Hgb measures the oxygen-carrying protein; Hct measures the percentage of blood that is RBCs. |
Created by:
mahak
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