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HEMATOLOGY AND ONCOLOGY QUESTION AND ANSWERS, Exams of Pathophysiology

HEMATOLOGY AND ONCOLOGY QUESTION AND ANSWERS

Typology: Exams

2023/2024

Available from 08/02/2024

DANTUTOR
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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 5.0
-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/mm3
◦Function: Tissue oxygenation and CO2 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 -
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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

  1. Methemoglobinemia reactions are caused by the following meds _________.
  2. How do they cause this? When do you need treatment
  3. Treatment -
    1. Nitrates, phenytoin, lidocaine, sulfonamides
  4. Increase Fe3+ in blood from Fe2+---> decreased O2 carrying capacity
  5. Tx needed if methemoglobin >
  6. 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:
  1. 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):
  1. Vaso-occlusive crises: hypoxia and infarction--> Acute chest syndrome
  2. Sequestration crisis: spleen enlarged, can lead to shock
  3. Renal failure d/t glomerular dysfx
  4. Cholecystitis d/t hemolysis, incr bili and gallstones TX: Pain mgmt, avoid triggers (cold, dehydration, etc)
  1. 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:
  1. Triggers release eosinophil chemotactic factor of anaphylaxis (ECF-A)---> attracts eosinophils
  2. Mast cells stimulate eosinophil release Infective mono: Pathophysiology -
    1. Epstein-Barr virus infects B cells
  3. B cells unaffected create antibodies
  4. 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:

  1. Uncontrolled proliferation of ________
  2. __________ causing decreased production/fx of normal blood cells
  3. Cells escape to _______ and accumulate in ______. -
    1. malignant leukocytes**
  4. Overcrowding of bone marrow
  5. Blood stream, organs Acute Lymphoblastic Leukemia: Pathophysiology - Def: rapid proliferation of immature lymphocytes Patho:
  1. Increased lymphocytes
  2. No cell differentiation
  3. increased immature stem cells
  4. 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:
  1. Cell diff stopped d/t chromosome dysfx
  2. Increased GFs--> inc. immature myeloid stem cells
  3. 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:

  1. M proteins = abnormal IgGs produced by malignant plasma cells
  2. Increased osteoclast activity
  3. Immunosuppression
  4. 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.....
  1. Leukemia
  2. Hodgkin Lymphoma
  3. Non-Hodgkin Lymphoma -
    1. BM bx
  4. CXR, BM bx for REED STERNBERG CELLS
  5. 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:

  1. Vascular injury---> vaso______ 2). _____exposure from injury causes ____to adhere 3). ______ factor released to stimulate clotting cascade -
  1. vasoconstriciton
  2. Subendothelial
  3. 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) -
  1. Adhesion 2.Activation
  2. 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

  1. 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:
  1. Heparin-PF4 complex stimulates production of heparin-PF4-IgG immune complex****
  2. Binds to PLT, activates PLT
  3. 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. -

  1. A
  2. Intrinsic
  3. Factor VIII
  4. 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. -
  5. A
  6. Intrinsic
  7. Factor IX
  8. 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)