Its action bears more resemblance to amphetamine than to fluoxetine in that its primary mode of therapeutic action involves norepinephrine and to a lesser degree dopamine, but it also releases some serotonin from presynaptic clefts. It should not be used with ephedrine, as it may increase the likelihood of side effects. Ephedrine should be used with caution in patients with inadequate fluid replacement, impaired adrenal function, hypoxia, hypercapnia, acidosis, hypertension, hyperthyroidism, prostatic hypertrophy, diabetes mellitus, cardiovascular disease, during delivery if maternal blood pressure is >130/80 mmHg, and during lactation.Contraindications for the use of ephedrine include: closed-angle glaucoma, phaeochromocytoma, asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis), concomitant or recent (previous 14 days) monoamine oxidase inhibitor (MAOI) therapy, general anaesthesia with halogenated hydrocarbons (particularly halothane), tachyarrhythmias or ventricular fibrillation, or hypersensitivity to ephedrine or other stimulants. Ephedrine should not be used at any time during pregnancy unless specifically indicated by a qualified physician and only when other options are unavailable. Adverse effects
Ephedrine is a potentially dangerous natural compound; as of 2004 the US Food and Drug Administration had received over 18,000 reports of adverse effects in people using it.Adverse drug reactions (ADRs) are more common with systemic administration (e.g. injection or oral administration) compared to topical administration (e.g. nasal instillations).
Acquired hemolytic anemia can be divided into immune and non-immune mediated forms of hemolytic anemia. Immune
Immune mediated hemolytic anaemia (direct Coombs test is positive)
Autoimmune hemolytic anemia
Warm antibody autoimmune hemolytic anemia
Idiopathic
Systemic lupus erythematosus (SLE)
Evans syndrome (antiplatelet antibodies and hemolytic antibodies)
Cold antibody autoimmune hemolytic anemia
Idiopathic cold hemagglutinin syndrome
Infectious mononucleosis and mycoplasma (atypical) pneumonia
Paroxysmal cold hemoglobinuria (rare)
Alloimmune hemolytic anemia
Hemolytic disease of the newborn (HDN)
Rh disease (Rh D)
ABO hemolytic disease of the newborn
Anti-Kell hemolytic disease of the newborn
Rhesus c hemolytic disease of the newborn
Rhesus E hemolytic disease of the newborn
Other blood group incompatibility (RhC, Rhe, Kidd, Duffy, MN, P and others)
Alloimmune hemolytic blood transfusion reactions (i.e., from a non-compatible blood type)
Drug induced immune mediated hemolytic anemia
Penicillin (high dose)
Methyldopa

Non-immune
Non-immune mediated hemolytic anemia (direct Coombs test is negative)

Drugs (i.e., some drugs and other ingested substances lead to hemolysis by direct action on RBCs, e.g., ribavirin )
Toxins (e.g., snake venom; plant poisons such as aesculin)
Trauma
Mechanical (from heart valves, extensive vascular surgery, microvascular disease, repeated mechanical vascular trauma)
Microangiopathic hemolytic anemia (a specific subtype with causes such as TTP, HUS, DIC and HELLP syndrome)
Infections (Note: Direct Coombs test is sometimes positive in hemolytic anemia due to infection)
Malaria
Babesiosis
Sepsis
Membrane disorders
Paroxysmal nocturnal hemoglobinuria (rare acquired clonal disorder of red blood cell surface proteins)
Liver disease

Drug induced hemolysis
Drug induced hemolysis has large clinical relevance. It occurs when drugs actively provoke red blood cell destruction. It can be divided in the following manner:
Drug-induced autoimmune hemolytic anemia
Drug-induced nonautoimmune hemolytic anemiaA total of four mechanisms are usually described, but there is some evidence that these mechanisms may overlap. References


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