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Advanced Pathophysiology: Hematology and
Oncology
_____ is the aqueous component of blood - Plasma Components important to know in plasma - Albumin Gamma globulins Fibrinogen Clotting factors Normal value and function of the following: Albumin -
- 3.5 to 5.
- Carrier molecule
- Fluid balance--> oncotic pressure to pull H2O into vessels (hydrophilic) Function of the following: Gamma globulins -
- Aka immunoglobulins
- Immune response "G A M E-D" --every type of immuneglobulins Function of the following: Fibrinogen -
- Clotting factor
- Hemostasis (precursor to fibrin clot) _______ produce lymphocytes (B, T, NK cells) - Lymphoid progenitors _______ other cell types - Myeloid progenitors Normal value and function of the following: Erythrocytes - ◦4.2 - 6.2 million/mm ◦Function: Tissue oxygenation and CO 2 removal via hemoglobin _______ results in RBC development in _________ - Erythropoiesis, bone marrow Erythropoiesis requires the substances______ - Vit. B12 and Folate Process of erythropoiesis into RBC and how this occurs -
Erythroid progenitor → proerythroblast → erythroblast → reticulocyte → erythrocyte via DIFFERENTIATION ________ promotes release of erythropoietin from peritubular cells in kidney - Tissue hypoxia What does erythropoietin do? - Stimulate erythropoiesis (increase # of proerythroblasts) _____ is a molecule that carries O2. It contains the following: 2 pairs of polypeptide chains + 4 iron/protoporyphin complexes - Hemoglobin How many O2 molecules can heme carry? - FOUR ( It is "saturated" if all hemes are bound with O2.) _______ results from the binding of O2 to Fe2+ (oxidize to Fe3+) - Oxyhemoglobin _______ results from release of O2 to tissue (reduce to Fe2+) - Deoxyhemoglobin ______ is made from a rx oxidizing to Fe3+; this does not transport O2 efficiently - methemoglobin
- Methemoglobinemia reactions are caused by the following meds _________.
- How do they cause this? When do you need treatment
- Treatment -
- Nitrates, phenytoin, lidocaine, sulfonamides
- Increase Fe3+ in blood from Fe2+---> decreased O2 carrying capacity
- Tx needed if methemoglobin >
- TX: Methylene blue _______ competes with O2 for binding with deoxyhemoglobin, due its high affinity with Hgb. What am I? - Carbon monoxide Fill in the blanks for the process of RBC destruction:
S/S and treatment of iron deficiency anemia/microcytic hypochromic anemia - S/S:
- Fatigue/weakness, pale
- SOB (ineffective gas exchange)
- Thin, brittle fingernails
- Burning mouth syndrome
- Neuromuscular S/S (parasthesias, gait issues, H/A) TX: Iron supplements, stop bleeding source Normocytic normochromic anemia: causes and patho - Def: Anemia of chronic disease (can become microcytic over time) Causes:
- 2nd inflammatory mediators--> dec RBC lifespan, dec erythropoietin, and dec bone marrow response Normocytic normochromic anemia: clinical S/S and treatment - S/S: Mild Fe deficiency anemia TX: Erythropoietin, ID and treat cause B-12 deficiency macrocytic anemia: causes and patho - Def: Large cells Patho: ◦DNA and RNA synthesis depends on B12---> Deficiency--->Cytoplasm increases RBC size but slow nuclei-->Defective RBCs die prematurely (hemolysis) Causes:
- Vegans: poor PO intake of B
- Pernicious anemia: lack intrinsic factor (d/t dyfx proton pump that make it)= cannot absorb B
- EtOH abuse: poor absorption B-12 deficiency macrocytic anemia: clinical manifestation and treatment - S/S: ◦Vague GI, cardiac and renal S/S early on ◦Fatigue ◦Red, beefy tongue ◦Severe neuro S/S d/t demyelination TX: B12 replacement, monitor reticulocyte count Folic acid deficiency macrocytic anemia: causes and patho - Patho: Folic acid deficient--> apoptosis/hemolysis (necessary for DNA+RNA synthesis and cytoplasm enlarge cell)
Causes: ◦Poor dietary intake of folic acid ◦ETOH abuse - contributes to ↓ of folate stores in liver Folic acid deficiency macrocytic anemia: clinical S/S and treatment - S/S:
- Neuro s/s uncommon
- Scaling on lips, corners of mouth
- Neural tube defects in developing embryo TX: Folate replacement Aplastic anemia: pathophysiology - Hematopoietic failure: immune-mediated destruction of hematopoietic stem cells Trigger: meds, chemicals, env't that alters stem cells in bone marrow, increased abnormal cytotoxic T cells that destroy stem cells Aplastic anemia: S/S, treatment - **Pancytopenia: (fatigue, infections risk, bleeding) TX: radiation, chemo (destroy T-lymphocytes), BM/stem cell transplant, immunosuppression Sickle Cell Disease: Pathophysiology - Def: abnormal Hgb S in RBCs Patho:
- Autosomal recessive
- Point mutation =glutamic acid replaced by valine
- Cycles of dexygenation/oxygenation= abnormal Hgb stiffens--> sickling
- Acidosis dec O2 affinity for Hgb--> de-O2 of RBC--> sickling Causes ischemia/hypoxic injury and hemolysis Sickle Cell Disease: S/S, treatment - S/S (think microthrombi everywhere):
- Vaso-occlusive crises: hypoxia and infarction--> Acute chest syndrome
- Sequestration crisis: spleen enlarged, can lead to shock
- Renal failure d/t glomerular dysfx
- Cholecystitis d/t hemolysis, incr bili and gallstones TX: Pain mgmt, avoid triggers (cold, dehydration, etc)
- B cells _______ are agranulocytes from the lymphoid progenitor family. They function to ingest foreign material and pathogens and act as "antigen presenting cells" - Monocytes/macrophages Monocytes mature into macrophages ____ are paid assassins out to kill tumor/viral-infected cells without prior exposure. They also activate T cells+phagocytes. - Natural killer (NK) cells Neutrophilia: Lab value, Causes, S/S -
- Increased in neutrophils to > 7500/uL
- Causes: inflammation, cancer, stress Complications:
- Viscous blood, risk thrombosis/ occlusion
- L shift: increased bands (in severe infections) Neutropenia: Lab value, Causes, complication - Decrease in neutrophils (ANC<2000/ uL) Causes:
- Severe infection, chemo/radiation, aplastic anemia Complication: Fatal infections Eosinophilia - Increase in the number of circulating eosinophils (Absolute eosinophilc count > 450/μL) Causes: Allergies, asthma, eczema, parasites Patho:
- Triggers release eosinophil chemotactic factor of anaphylaxis (ECF-A)---> attracts eosinophils
- Mast cells stimulate eosinophil release Infective mono: Pathophysiology -
- Epstein-Barr virus infects B cells
- B cells unaffected create antibodies
- Cytotoxic T cells destroy infected cells Lasts 1-3 weeks Infective mono: S/S, TX - ◦Classic triad: Fever, painful pharyngitis, lymphadenopathy TX: Supportive, antivirals (if severe)
___________ is associated with EBV. It's pathophysiology is the _______ of a proto-oncogene, causing increased cell growth. S/S include jaw deformity, GI S/S Treatment includes ______ and __________. - Burkitt's Lymphoma Overexpression of proto-oncogene TX: Chemo and monoclonal antibodies The following are the characteristics of leukemia:
- Uncontrolled proliferation of ________
- __________ causing decreased production/fx of normal blood cells
- Cells escape to _______ and accumulate in ______. -
- malignant leukocytes**
- Overcrowding of bone marrow
- Blood stream, organs Acute Lymphoblastic Leukemia: Pathophysiology - Def: rapid proliferation of immature lymphocytes Patho:
- Increased lymphocytes
- No cell differentiation
- increased immature stem cells
- overcrowding in BM and dec production/fx of normal blood cells Acute Lymphoblastic Leukemia (ALL): S/S and TX - S/S:
- Bone pain, CNS effects
- Anemia, infection, bleeding
- Enlargement of organs w/ lots of RBC flow TX: Chemo Acute Myeloblastic Leukemia: Pathophysiology S/S, TX - Def: lots of immature neutrophils in blood/BM Patho:
- Cell diff stopped d/t chromosome dysfx
- Increased GFs--> inc. immature myeloid stem cells
- Overcrowding in BM S/S: similar to other leukemias (abrupt) TX: Chemo
High grade: Aggressive adenopathy, organ involvement (GI/GU, skin, bone) Multiple myeloma: Pathophysiology, DX, S/S, TX - Def: Plasma cell cancer (masses in BM, lytic bone lesions) Patho:
- M proteins = abnormal IgGs produced by malignant plasma cells
- Increased osteoclast activity
- Immunosuppression
- Bence-Jones protein DX: M protein/Bence-Jones protein in blood/urine S/S:
- Bone pain, Hypercalcemia
- Proteinuria, renal failure
- Viscous blood TX: chemo/rad, biphosphonates (high PO4 decreases Ca conc), stem cell transplant How to diagnose.....
- Leukemia
- Hodgkin Lymphoma
- Non-Hodgkin Lymphoma -
- BM bx
- CXR, BM bx for REED STERNBERG CELLS
- Node bx Main difference between acute and chronic leukemia - Acute: Abrupt, precursor cells Chronic: Fully differentiated (poorly fxning) and SLOW What are the leukocytes? - neutrophils, lymphocytes, monocytes, eosinophils, basophils "Nobody Likes My Educational Background"---> you doing okay pal? _______ are also called platelets. They are made up of cytoplasmic fragments and function in hemostasis and involved in inflammation. - Thrombocytes ________ is the process of creating more platelets. ______ produced by the ________ stimulates fragmentation from megakaryocytic, creating more platelets. - Thrombopoiesis Liver thrombopoietin
What are the three components of hemostasis? - Blood vessel response Platelet response Clotting factor response Blood vessel response in hemostasis:
- Vascular injury---> vaso______ 2). _____exposure from injury causes ____to adhere 3). ______ factor released to stimulate clotting cascade -
- vasoconstriciton
- Subendothelial
- von Willebrand factor Platelet response to vascular injury: Step 1: __________
- Damage to epithelium, exposure of subendothelium
- Epithelial cells release vWF---> PLT adhere to vWF Step 2: __________
- PLT release chemicals--> fx to recruit other PLT, aggregation, clotting factors
- ADP, Ca, clotting factors, PLT factor 4 Thromboxane (TXA): vasoconstriction, aggregation Step 3: ____________
- Initiated by ADP, TXA
- ADP changes glycoprotein shape to inc fibrinogen affinity
- Fibrinogen binds---> hemostatic plug (need Ca) -
- Adhesion 2.Activation
- Aggregation Describe the two pathways of clotting factor response and the result -
- Extrinsic (tissue factor) - initiated when there is vascular injury, tissue factor released by endothelial cells Shorter, faster Measure: PT
Trigger releases TF-->activate extrinsic pathway-->prothrombin creates thrombin---> promotes fibrinogen to create fibrin--> thrombosis
- Hemorrhage
- Bleeding-->consumes clotting factors and platelets
- Slow fibrinolysis while plasminogen creates plasmin (can't keep up with widespread clotting)
- FDPs formed which inhibit clot formation End result: Thrombosis and bleeding cycle S/S and TX of DIC -
- Hemorrhage: oozing from IV sites, scleral bleed, epistaxis
- Thrombosis: CV, pulm, CNS
- Labs: FDPs/D-dimer present TX:
- eliminate trigger, control thrombosis, maintain organ function
- Transfuse PLT, cryo, FFP Immune Thrombocytopenic Purpura (ITP): Patho, S/S, TX - Patho: IgG produced against antigens on surface of PLT ---> macrophages destroy plts S/S: Mild-moderate bleeding, petechiae, bruises TX: IVIG, glucocorticoids Thrombotic Thombocytopenic Purpura (TTP): Patho, S/S, TX - Patho: Too small/absent enzyme --> vWF very long, PLT aggregate on vWF--> obstruction of blood vessels S/S: Thrombocytopenia, schistocytes, stroke, renal failure, fever TX: Plasma exchange Heparin-induced thrombocytopenia (HIT): Patho, S/S, - Immune-mediated drug rx Patho:
- Heparin-PF4 complex stimulates production of heparin-PF4-IgG immune complex****
- Binds to PLT, activates PLT
- Release more PF4, recruit more PLT--> plt aggregation, activate coag. cascade
S/S: Thrombocytopenia, DVT/PE TX: Switch anticoagulation ________ are genetic mutation of clotting factors - Hereditary thrombophillias In _________, nucleotide mutation alters protein C, so factor ___ is unable to be inactivated - Factor V Leiden Factor V A mutation in ________ --> excess fibrin-->excess clotting - Prothrombin Hemophillia _____ impact the ______pathway, causing life-threatening bleeding. It is caused by a deficiency in ________. It is_____-linked ___ trait. -
- A
- Intrinsic
- Factor VIII
- X-linked recessive Hemophillia _____ (also known as Christmas Disease) impact the ______pathway, causing life- threatening bleeding. It is caused by a deficiency in ________. It is_____-linked ___ trait. -
- A
- Intrinsic
- Factor IX
- X-linked recessive TX for hemophilia A and B; Labs to monitor in both - Hemophilia A: Factor VIII Hemophilia B: Factor IX Labs: PT and aPTT Von Willebrand Disease is a _______ trait. It is caused by a deficiency in ________, so platelets can't adhere to site of injury - autosomal dominant, von Willebrand Factor (vWF)
