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Thread: The Hematologist's Manual

  1. #1

    Default The Hematologist's Manual


    The process of erythropoiesis
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    The anemia evaluation process
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    Desired Outcomes/Goals

    Increase Hgb to levels that improve red cell oxygen-carrying capacity, alleviate symptoms, and prevent complication from anemia. It is important to note that continuation of a patient's therapy should be assessed primarily by resolution of clinical signs and symptoms. Patients who experience a resolution in their symptoms may not require aggressive therapy to maintain their Hgb values within normal limits. Prevention of complications owing to anemia such as hypoxia and cardiovascular sequelae can be avoided if Hgb levels are greater than 7.0 g/dL.

    General Approach to the Anemic Pateint
    The underlying cause of anemia must be determined and used to guide therapy. The mean corpuscular volume and determination of iron, ferritin, folate, and vitamin B12 levels are required to correctly determine the etiology of patient's anemia.

    Nonpharmacologic Therapy
    Transfusion of RBCs
    • Trigger for transfusion for patients without significant cardiovascular disease is 7.0 g/dL
    • Typically, only patients with acute symptoms and Hgb concentrations in the range of 7.0 to 9.0 g/dL require blood transfusions.

    Diet rich in iron, folic acid, or vitamin B12
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    Pharmacologic Therapy
    Iron-Deficiency Anemia

    • The initial treatment of IDA is oral iron therapy that provides 150 to 200 mg of elemental iron daily.
    • If treated properly, reticulocytosis should be seen in 7 to 10 days, and Hgb values should rise by about 1.0 g/dL per week. Patient should be reassessed if Hgb does not increase by 2.0 g/dL in 3 weeks.
    • The preferred dosing regimen for oral iron is to administer 50 to 65 mg of elemental iron two to three doses daily on an empty stomach (1 hour before or 2 hours after a meal, for maximal absorption). However, if patients develop intolerable GI side effects after taking iron on an empty stomach, they should be advised to take it with meals.
    • Common toxicities associated with oral iron products include abdominal pain, nausea, heartburn, constipation, and dark stools.
    • Potentially clinically significant drug interactions involving iron products include fluoroquinolone, tetracyclines, and mycophenolate mofetil. Iron decreases the absorption of these drugs. To minimize this effect, oral iron should be administered not less than 3 hours before or 2 hours after the affected drug.
    • Parenteral iron therapy is indicated when patients cannot tolerate oral formulations, are noncompliant, or fail to respond to oral iron because of malabsorption syndromes.
    • The dose of iron dextran can be calculated by the following equation: dose (mL) = 0.0442 (desired Hgb - observed Hgb) x body weight + (0.26 x body weight). The body weight that should be used is lean body weight for adults and children weighing more than 15 kg and actual body weight for children weighing 5 to 15 kg. The dose in milligrams can be calculated based on a standard concentration of 50 mg of elemental iron per milliliter. Prescribing information recommends administering iron dextran in 100-mg aliquots daily until the total dose is achieved. However, anecdotal evidence reports that the total calculated dose can be administered safely over 4 to 6 hours in 1 day.
    • Because of the risk of anaphylaxis, a test dose of iron dextran (0.5 mL over at least 30 seconds) must be administered to patients before their first dose or iron dextran. Patients should be monitor for signs of anaphylaxis for at least 1 hour before administering the total dose.
    • Other adverse effects include arthralgia, arrhythmias, hypotension, flushing, and pruritus.

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    Vitamin B12 and Folic Acid Anemia

    • Anemia from vitamin B12 or folic acid deficiency is treated effectively by replacing the missing nutrient.
    • Oral and parenteral vitamin B12 (cyanocobalamin) replacement therapies are equally effective. Vitamin B12 is absorbed completely following parenteral administration, whereas oral vitamin B12 is absorbed poorly via the GI tract. Furthermore, parenteral vitamin B12 may circumvent the need to perform a Shiling test used to diagnose a deficiency of intrinsic factor. Consequently, cyanocobalamin is commonly administered as an intramuscular injection.
    • A typical cyanocobalamin dosing regimen is 1,000 mcg/day for 1 week, followed by 1,000 mcg/week for a month or until the Hgb normalizes. Life-long maintenance therapy (1,000 mcg/month) is required for patients with pernicious anemia or surgical resection of the terminal ileum.
    • A common oral dosing regimen is from 1,000 to 2,000 mcg/day. If parenteral cyanocobalamin is used initially, oral vitamin B12 can be useful as maintenance therapy.
    • If the etiology was a dietary deficiency or reversible malabsorption syndrome, treatment can be discontinued after the underlying cause is corrected and vitamin B12 stores normalized. Typically, resolution of neurologic symptoms, disappearance of megaloblastic RBCs, and increased Hgb levels occur within a week of therapy.
    • Vitamin B12 is well tolerated. Reported adverse effects include injection-site pain, pruritus, and rash. Clinical significance of decreases in protein-bound cyanocobalamin related to proton pump inhibitor therapy has not been established.
    • The effective dose of folic acid is 1 mg/day by mouth. Absorption of folic acid generally is rapid and complete. However, patients with malabsorption syndromes may require does up to 5 mg/day.
    • Resolution of symptoms and reticulocytosis occurs within days of commencing therapy. Typically a patient's Hgb will start to rise after 2 weeks of therapy and normalize after 2 to 4 months of therapy.
    • Folic acid is well tolerated. Nonspecific adverse effects include allergic reactions, flushing, malaise, and rash.

    Anemia of Chronic Disease
    Anemia Due to Chemotherapy in Patient with Cancer
    • ESAs should only be used to prevent a transfusion and should not be initiated unless the hemoglobin is less than or equal to 10.0 g/dL.
    • A number of clinical trials and a recent meta-analysis reveal that patients administered ESAs experienced increased thrombotic events and shorter progression-free and overall survival.
    • Patients should be monitored every 4 weeks. If Hgb has not increased by 1.0 g/dL after 4 weeks and remains less than 10.0 g/dL, a one-time dose escalation of 25% is appropriate. If Hgb increases by more than 1.0 g/dL, or is more than 10.0 g/dL, the ESA should be discontinued.

    Anemia Due to CKD
    • Anemia is common in patients with CKD.
    • Early treatment of anemia in patients with CKD on dialysis has been associated with slower disease progression and lower risk of death.
    • ESA therapy is effective in treating CKD anemia.
    • The use of ESAs to achieve an Hgb greater than 11.0 g/dL resulted in increased risk of serious adverse cardiovascular events.
    • In June 2011, the FDA notified healthcare providers that the target Hgb range in patients with CKD was lowered to 11.0 g/dL in patients on hemodialysis and to 10.0 g/dL in CKD patients not on hemodialysis.
    Last edited by Janis.Y.Chen; Mon 11th July '16 at 2:20pm.
    Clinical Pharmacy Specialist - Infectious Diseases

  2. #2

    Default Re: The Hematologist's Manual

    Common Immunosuppressants

    Binding to CD80 and CD86 therefore blocking the second signal (CD28)

    gamma-Globulins derived from animals (rabbit or equine) that target against T cells (induce T cell lysis) therefore reducing the circulating number of T cells.

    Inhibiting T-cell activation, through exactly unknown mechanism.


    5.Gold sodium thiomalate

    Purine antimetabolite, converted to 6-MP; inhibits synthesis of DNA, RNA, and proteins; interferes with cellular metabolism; may inhibit mitosis.

    7.Basiliximab (cytokine blocking)
    Interleukin-2 (IL-2) receptor antagonist, blocking IL-2 binding. Basiliximab is specifically targeted against IL-2Ralpha, which is selectively expressed on the surface of activated T-lymphocytes, therefore inhibits IL-2 mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection.

    Monoclonal antibody target against CD80 and CD86, therefore blocking the second signal.

    Prodrug, with active metabolite of MPA. MPA is a potent, selective, uncompetitive, and reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH), and therefore inhibits the de novo pathway of guanosine nucleotide synthesis without incorporation into DNA. Because T- and B-lymphocytes are critically dependent for their proliferation on de novo synthesis of purines, whereas other cell types can utilize salvage pathways, MPA has potent cytostatic effects on lymphocytes.

    10.Certolizumab pegol
    Recombinant humanized anti-human TNF-alpha neutralizing antibody. Certolizumab pegol selectively neutralizes TNFα but does not neutralize lymphotoxin α (TNFβ).

    Cyclosporine has been demonstrated to suppress some humoral immunity and to a greater extent, cell-mediated immune reactions. The effectiveness of cyclosporine results from specific and reversible inhibition of immunocompetent lymphocytes in the G0- and G1-phase of the cell cycle. T-lymphocytes are preferentially inhibited. The T-helper cell is the main target, although the T-suppressor cell may also be suppressed. Cyclosporine also inhibits lymphokine production and release including interleukin-2.

    Binds and inactivates TNF, thereby preventing synovial inflammation. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind TNF molecules. Etanercept inhibits binding of TNF-α and TNF-β (lymphotoxin alpha [LT-α]) to cell surface TNFRs, rendering TNF biologically inactive. In in vitro studies, large complexes of etanercept with TNF-α were not detected and cells expressing transmembrane TNF (that binds Enbrel) are not lysed in the presence or absence of complement.

    13.Hydroxychloroquine sulfate
    Unknown; may impair complement-dependent antigen-antibody reactions; inhibits locomotion of neutrophils and chemotaxis of eosinophils.

    Recombinant humanized monoclonal anti-TNF-α antibody; prevents synovial and intestinal inflammation

    Not fully understood. Metabolite inhibits pyrimidine nucleotide synthesis; antiproliferative for T-cells

    Inhibits dihydrofolic acid reductase; inhibits purine and thymidylic acid synthesis, which in turn interferes with DNA synthesis, repair, and cellular replication; cell cycle specific for S phase of cycle

    17.Muromonab CD3
    Blocks function of CD3 in T lymphocytes (involved in Ag recognition & signal transduction)

    Sirolimus inhibits T-lymphocyte activation and proliferation that occurs in response to antigenic and cytokine (Interleukin [IL]-2, IL-4, and IL-15) stimulation by a mechanism that is distinct from that of other immunosuppressants. Sirolimus also inhibits antibody production.

    In cells, sirolimus binds to the immunophilin, FK Binding Protein-12 (FKBP-12), to generate an immunosuppressive complex. The sirolimus:FKBP-12 complex has no effect on calcineurin activity. This complex binds to and inhibits the activation of the mammalian Target Of Rapamycin (mTOR), a key regulatory kinase. This inhibition suppresses cytokine-driven T-cell proliferation, inhibiting the progression from the G1 to the S phase of the cell cycle.
    Last edited by Janis.Y.Chen; Thu 14th July '16 at 5:11pm.
    Clinical Pharmacy Specialist - Infectious Diseases

  3. #3

    Default Re: The Hematologist's Manual

    Common Hemostatics

    1.Antihemophilic factor recombinant
    Recombinant human antihemophilic factor. Temporarily replaces missing clotting factor VIII which corrects &/or prevents bleeding.

    2.Antihemophilic factor/von Willebrand factor
    Temporarily increases the plasma level of FVIII, thus minimizing the hazard of hemorrhage in patients with hemophilia A; FVIII is an essential cofactor in activation of factor X leading to formation of thrombin and fibrin.

    VWF promotes platelet aggregation and platelet adhesion on damaged vascular endothelium; it also serves as a stabilizing carrier protein for the procoagulant protein FVIII.

    3.Factor IX
    Factor IX is a vitamin K-dependent coagulation factor sythesized in the liver; purified FActor IX from human plasma temporarily replace missing clotting factor IX to correct and/or prevent bleeding

    4.Factor IX, recombinant
    Temporarily replaces missing clotting factor IX which corrects and/or prevents bleeding

    5.Anti-inhibitor coagulant complex
    Provides activated blood coagulation factors II, VII, IX and X from pooled human plasma

    6.Factor VIII, human plasma derived
    Factor VIII derived from pooled human plasma, temporarily replaces missing clotting factor VIII which corrects and/or prevents bleeding in patients with hemophilia A

    7.Vitamin K1
    Promotes hepatic synthesis of clotting factors II, VII, IX, X (exact mechanism is unknown)

    8.Fibrin sealant
    The fibrin sealant system initiates the last phase of physiological blood coagulation. Thrombin activates the conversion of fibrinogen into fibrin, which occurs by the splitting of fibrinogen into fibrin monomers and fibrinopeptides. The fibrin monomers polymerize and form a fibrin clot. Factor XIIIa, which is activated from Factor XIII (FXIII) by thrombin, crosslinks fibrin. Calcium ions are required for FXIII activation by thrombin.

    9.Factor IX complex
    Mixture of vitamin K-dependent clotting factors; temporarily increases the plasma levels of Factor IX, thus minimizing the hazards of hemorrhage in patients with hemophilia B

    10.Factor XIII A-subunit, recombinant
    Recombinant human factor XIII-A2 homodimer composed of 2 FXIII A-subunits.
    FXIII is the terminal enzyme in the blood coagulation cascade; when activated by thrombin at the site of vessel wall injury, FXIII plays an important role in the maintenance of hemostasis through cross-linking of fibrin and other proteins in the fibrin clot.

    11.Factor X, human

    Increases plasma levels of factor X and can temporarily correct the coagulation defect in these patients, as reflected by decrease in the aPTT and PT
    Factor X is the first coagulation factor of the final common pathway (thrombin pathway); it is activated into factor Xa by both factor IX and VII, along with cofactors; Xa cleaves prothrombin in 2 places, which yields the active thrombin

    12.Factor XIII concentrate, human

    Temporarily replaces missing clotting factor XIII which corrects and/or prevents bleeding
    Factor XIII is a proenzyme activated by calcium ion, by thrombin cleavage of the A-subunit to become activated factor XIII (FXIIIa); promotes cross-linking of fibrin during coagulation and is essential to the physiological protection of the clot against fibrinolysis

    13.Factor VIIa, recombinant
    Activates conversion of Factor X to Factor Xa, & Factor IX to Factor IXa

    14.Factor IX, recombinant/albumin fusion protein

    Recombinant protein that temporarily replaces missing coagulation Factor IX needed for effective hemostasis
    Comprised of genetically fused recombinant coagulation Factor IX and recombinant albumin; fusion with recombinant albumin extends the half-life of Factor IX

    Mixture of human plasma-derived fibrinogen and human plasma-derived thrombin powders that are designed to mimic the final steps in the coagulation cascade.

    Powder dissolves readily on contact with aqueous fluids (eg, blood), activating thrombin, which triggers an immediate conversion of fibrinogen into fibrin and subsequent clot formation.

    16.Prothrombin complex concentration, human
    Contains vitamin-K-dependent coagulation Factors II, VII, IX, and X, together known as prothrombin complex and the antithrombotic protein C and protein S.

    A dose-dependent acquired deficiency of vitamin K-dependent coagulation factors occurs during vitamin K antagonist treatment; vitamin K antagonists exert anticoagulant effects by blocking carboxylation of glutamic acid of vitamin K-dependent coagulation factors during hepatic synthesis, lowering both factor synthesis and function.

    Administration of prothrombin complex rapidly increases plasma levels of coagulation factors and the anti-thrombotic proteins.

    Median INR before treatment (3.0) dropped to median value of 1.2 at 30 minutes after starting infusion (in contrast to plasma which dropped to 2.4 after 30 minutes)

    Human serine protease that promotes hemostasis and acts locally when applied topically to a site of bleeding; activates platelets and catalyzes the conversion of fibrinogen to fibrin, which are steps that are essential for blood clot formation
    Last edited by Janis.Y.Chen; Thu 14th July '16 at 5:50pm.
    Clinical Pharmacy Specialist - Infectious Diseases

  4. #4

    Default Re: The Hematologist's Manual

    NHL/Non Hodgkin Lymphoma

    Pathway of Normal B-Cell Differentiation and Relationship to B-Cell Lymphocytes

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    Working Formulation for NHL
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    Negative Prognostic Factors for HL
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    Negative Prognostic Factors for NHL
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    Cotswold Staging of Classification for Hodgkin Disease
    (Also useful for NHL)
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    Desired Outcome
    Treatment of NHL depends primarily on histologic subtype (follicular low grade versus diffuse aggressive) and staging (local stage I/II versus advanced stage III/IV) to guide appropriate treatment strategy with observation, chemotherapy, radiotherapy, or chemotherapy and radiation. The Cotswold modification of the Ann Arbor staging system for HL is generally used in NHL as well.

    Treatment goals depend on the patient's specific subtype of NHL. For follicular low-grade NHL, the disease is considered to be incurable with standard therapies. There is a small prospect for cure using allogeneic SCT owing to the graft-vesus-lymphoma effect of donor T cells. Many patients with follicular low-grade NHL are older than 60 years of age, making allogeneic SCT impractical because of the high treatment-related mortality for older patients.

    The treatment goals for low-grade NHL include:

    • Observation of the disease until the patient exhibits obvious progression that limits functional capacity or is life-threatening for low-grade NHL
    • Treatment that induces the disease into remission with resolution of disease symptoms and manageable toxicity
    • Judicious selection of treatment options to avoid long-term toxicity
    • Prevention of infectious complications of treatment

    The intent of treatment for patients with aggressive histologies is cure of the malignancy. Some histologic subtypes exhibit an aggressive clinical course and are not considered to be curable. These patients are still treated with curative-intent chemotherapy or may be considered for a clinical trial.

    Nonpharmacologic Therapy
    For patients with low-grade follicular NHL, deferring initiation of therapy until progression of disease is a standard approach. The median survival time is 6 to 10 years. Some patients may be asymptomatic for several years after initial diagnosis, making observation a reasonable front-line therapy for most of these patients. Radiation therapy has a limited role in NHL relative to HL. NHL is more often a systemic disease, and radiation typically has been reserved for consolidation therapy after chemotherapy in patients presenting with a large extra oral mass. However, IFRT (involved-field radiation therapy) without systemic therapy is a treatment option for patients with stage I/II follicular lymphoma.

    For early-stage diffuse, aggressive NHL, combined-modality therapy was tested versus a longer course of chemotherapy. Overall survival favored the CHOP-radiation arm for 5 years (82% versus 72%). There was a trend toward increased toxicity, particularly hematologic and cardiac toxicity, in the CHOP alone arm. The results of this trial have established combined-modality therapy as first-line treatment for early stage NHL. Unique presentations of NHL, such as primary CNS disease, may incorporate radiation into treatment algorithms.

    Pharmacologic Therapy
    Follicular Low-Grade NHL

    The management of low-grade lymphoma is an area of controversy, especially in patients who present with early stage disease. In patients with localized disease, observation alone can be an appropriate treatment strategy. Typical indications for treatment in this population include cytopenias, recurrent infections, threatened end-organ function, disease progression over at least 6 months, or patient preference. In these patients, single-agent chemotherapy such as fludarabine or bendamustine, a unique alkylating agent with a novel chemical structure, is often offered initially. In patients in whom a more rapid response is desired, such as patients with advanced disease, multiagent chemotherapy such as CVP (cyclophosphamide, vincristine, and prednisone or prednisolone) or CHOP may be used. These regimens have not been associated with an improvement in overall survival, making it impossible to select an unequivocal first-line regimen.
    Rituximab has become an integral component in drug therapy for this disease. Rituximab is a chimeric monoclonal antibody that binds specifically to the antigen CD20 expressed on pre-B and mature B lymphocytes. NHL of B-cell origin expresses CD20 in greater than 90% of cases. CD20 is believed to play a role in early differentiation and activation of the cell cycle. Rituximab exerts its activity through antibody-dependent cytotoxicity activation of complement and induction of apoptosis. The initial clinical experience with rituximab involved 166 patients with CD20+ low-grade lymphoma treated with four doses of 375 mg/m2 of rituximab weekly. The overall response rate was 48%, with CR in 6% of patients. The median follow-up of 12 months demonstrated a median time to progression of 13 months by intent-to-treat analysis. These data established the role of rituximab as a viable treatment option in patients with indolent follicular NHL and is added to chemotherapy in most patients. Additionally, rituximab was examined as maintenance therapy administered every 8 weeks for to 2 years after rituximab-containing multiagent chemotherapy. Compared with observation, rituximab increased 3-year PFS (74.9 versus 57.6 months).

    Novel strategies for treatment of low-grade lymphomas include the combination of monoclonal antibodies directed against CD20 with a radioactive moiety attached. Two such entities - ibritumomab-yttrium 90 and tositumomab-iodine - are now approved by the FDA. The radiation component necessitates compounding both medications in a nuclear medicine pharmacy. Bendamustine has also been studied in a phase III trial of rituximab-refractory indolent lymphomas. Among 62 patients with follicular lymphoma, there was an overall response rate of 74% with a median duration of response of 9.2 months. High-dose chemotherapy is being evaluated for low-grade follicular NHL, but its role is currently limited to clinical trials.

    Diffuse, Aggressive NHL
    The mainstay of therapy for diffuse, aggressive NHL has been the administration of anthracycline-based combination chemotherapy, which generally consists of four or more drugs. Therapy options for intermediate- and high-grade NHL generally are segregated between localized (stage I/II) and advanced (stage III/IV) disease. Combined-modality therapy with an abbreviated course of CHOP and local radiation is considered a standard of care for stage I/II disease.

    The standard therapy for disseminated disease since the 1970s has been CHOP. This regimen conferred a response of 50% to 60%, with long-term survival of approximately 30%. However, the 1980s were notable for the development of newer combination chemotherapy regimens that incorporated increasing numbers of agents with varying schedules. More complex chemotherapy regimens were shown in phase II trials to have higher response rates than CHOP. The CALGB designed a phase III randomized four-arm trial to assess the impact on survival of three more intensive regimens compared with CHOP. This trial randomized 899 patients with intermediate- or high-grade NHL to CHOP or one of the three more intensive advanced-generation regimens. There were no significant differences in response rate or overall survival, which was consistent among all subgroups. Severe toxicity and death were higher in the advanced-generation treatment programs relative to CHOP. This pivotal trial has cemented CHOP as first-line chemotherapy in diffuse NHL.

    Rituximab has also come to play a vital role in treating diffuse, aggressive NHL. A French study randomized patients 60 to 80 years of age with newly diagnosed diffuse, large B-cell NHL to either CHOP for eight cycles or CHOP plus rituximab for eight cycles. Initial 2-year follow-up showed that rituximab improved CR (76% versus 63%) and median event-free survival (57% versus 38%). Long-term follow-up also showed an increase in 10-year survival (43% versus 27.6%). Similar findings in younger patients have been reported recently, making CHOP plus rituximab first-line therapy for advanced-stage diffuse, aggressive NHL.
    Last edited by CheneyHsiung; Tue 19th July '16 at 6:29pm.
    Clinical Pharmacy Specialist - Hematology

  5. #5

    Default Re: The Hematologist's Manual

    Antiemetic Agents

    1.Netupitant and Palonosetron
    Netupitant: Tachykinin NK1 receptor (substance P) antagonist

    Palonosetron: 5-hydroxytryptamine 3 (5-HT3) receptor antagonist; binds to 5-HT3 receptors both in peripheral and central nervous system, with primary effects in GI tract


    Histamine H1-receptor antagonist of effector cells in respiratory tract, blood vessels, and GI smooth muscle

    Moderate to high anticholinergic and antiemetic properties

    Antihistamine with activity against nebulized histamine; blocks vasodepressor response to histamine, with slight blocking action against acetylcholine

    Substance P/neurokinin 1 (NK1) receptor antagonist

    Cannabinoid antiemetic may act in the central nervous system by acting on cannabinoid receptors

    6.Phosphoric acid and Dextrose and Fructose
    Phosphoric acid: Antacid; phosphorated carbohydrate solution which neutralizes stomach acid

    Dextrose and fructose: Hyperosmolar carbohydrate solutions have a direct effect on the GI tract wall, resulting in reduced GI smooth muscle contraction

    Antiemetic: Antidopaminergic effect, blocking dopamine receptors in the brain, blocking vagus nerve in GI tract

    Antipsychotic: Blocking mesolimbic dopamine receptors, and blocking alpha-adrenergic receptors (D1 and D2) in brain

    8.Doxylamine and Pyridoxine

    Mechanism of action for efficacy for morning sickness is unknown

    Doxylamine: Ethanolamine derivative antihistamine

    Pyridoxine: Vitamin B6 analog


    Ethanolamine H1 antagonist containing diphenhydramine and 8-chloro-theophylline; pharmacological effects principally result from diphenhydramine moiety, has CNS depressant, anticholinergic, antiemetic, antihistamine, and local anesthetic effects

    Antiemetic action may result from inhibiting vestibular stimulation, and inhibiting acetylcholine


    Dronabinol is an orally active cannabinoid which has complex effects on the CNS, including central sympathomimetic activity

    Cannabinoid receptors have been discovered in neural tissues; these receptors may play a role in mediating the effects of dronabinol

    Has appetite stimulant effect

    Antiemetic mechanism unknown but probably involves inhibition of vomiting center in medulla oblongata


    Antiemesis: dopamine receptor blockade in brain, predominantly dopamine-2 receptor & when reuptake is prevented, a strong antidopaminergic, antiserotonic response occurs

    Droperidol reduced motor activity, anxiety, and causes sedation; also possesses adrenergic-blocking, antifibrillatory, antihistaminic, & anticonvulsive properties

    12.Phosphorated carbohydrate
    Hyperosmolar carbohydrate solution that has a direct effect on the GI tract wall; reduces GI smooth muscle contraction


    H1-receptor antagonist with low to moderate antihistaminic properties; inhibits respiratory, vascular, and GI smooth-muscle constriction

    Moderate to high anticholinergic and antiemetic properties


    Anticholinergic belladonna alkaloid

    Generally exhibits pharmacologic actions associated with other antimuscarinics

    May prevent motion-induced nausea and vomiting by blocking transmission of cholinergic impulse from vestibular nuclei

    Blocks dopamine receptors (at high dose) and serotonin receptors in chemoreceptor trigger zone of CNS; and sensitizes tissues to acetylcholine; increases upper GI motility but not secretions; increases lower esophageal sphincter tone

    16.Sodium citrate and Dextrose and Fructose

    Citric acid: Antacid; forms sodium citrate which neutralizes stomach acid

    Dextrose and fructose: Hyperosmolar carbohydrate solutions have a direct effect on the GI tract wall, resulting in reduced GI smooth muscle contraction


    Phenothiazine derivative with antidopaminergic effect: Blocker of mesolimbic dopamine receptors and alpha-adrenergic receptors in brain

    Antihistaminic effect: H1-receptor blocker


    Selective, long-acting neurokinin receptor (NK)-1 antagonist

    NK-1 receptors are highly concentrated in the vomiting center of the brain and bind a neurokinin termed substance P; activation of NK-1 receptors by substance P plays a central role in eliciting chemotherapy-induced nausea and vomiting

    Blocking the interaction of substance P at the NK-1 receptor, NK-1 receptor antagonists improve the management of nausea and vomiting

    Unclear, the drug appears to directly affect medullary chemoreceptor trigger zone by inhibiting emetic stimuli to the vomiting center
    Clinical Pharmacy Specialist - Infectious Diseases

  6. #6
    PharmD Year 1 TomHsiung's Avatar
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    Jan 2013
    Chengdu, Sichuan, China

    Default Approach to Platelet Function Disorders

    Physiology of Platelet

    History (General)
    • Bleeding location
    • Bleeding frequency
    • Bleed pattern
    • Age of onset
    • Time required for cessation
    • History of hemostatic challenges (surgery, dental procedures, trauma, and menstrual history in females)
    • Family bleeding history
    • Medication history

    Screen Tests (General)
    • Platelet count
    • RBC count
    • Prothrombin time (PT)
    • Activated partial thromboplastin time (aPTT)
    • PFA-100

    Target Tests
    • Mixing study (General)
    • Platelet aggregometry
    • Flow cytometry
    • Electron microscopy

    Prognosis and outcomes
    • Majority are associated with mild intermittent bleeding
    • Some can be associated with significant bleeding
    • Some can be so severe enough to consider bone marrow transplantation

    • ​Desmopressin
    • Antifibrinolytic agents
    • Estrogens
    • rFVIIa (recombinant FVIIa)
    • Platelet transfusion
    • Bone marrow transplantation
    Last edited by TomHsiung; Tue 22nd November '16 at 9:06am.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

  7. #7
    PharmD Year 1 TomHsiung's Avatar
    Join Date
    Jan 2013
    Chengdu, Sichuan, China

    Default Approach to von Willebrand Disease

    Physiology of von Willebrand Factor

    History (General)

    • Bleeding location
    • Bleeding frequency
    • Bleed pattern
    • Age of onset
    • Time required for cessation
    • History of hemostatic challenges (surgery, dental procedures, trauma, and menstrual history in females)
    • Family bleeding history
    • Medication history

    Screen Tests (General)

    • Platelet count
    • RBC count
    • Prothrombin time (PT)
    • Activated partial thromboplastin time (aPTT)
    • PFA-100

    Target Tests
    • Quantitative measurement of vWF (vWF:Ag)
    • Platelet-binding function (vWF:RCo, in which the agglutination of fixed platelets in response to patient plasma is measured in the presence of ristocetin)
    • FVIII coagulation (FVIII:C)
    • Genetic testing

    • Desmopressin
    • vWF-containing concentrates
    • Antifibrinolytic agents
    • Intact vWF
    Last edited by TomHsiung; Tue 22nd November '16 at 9:33am.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

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