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Theonlyexceptionisdobutamine diabetes blindness prevention discount 50mg acarbose, which can be used up to 24 hours after the solution was made diabetes test no prick trusted 25 mg acarbose, even if discolorationappears diabetes type 2 kidney pain order acarbose 50mg with visa. Asaresult diabetes symptoms in type 1 discount acarbose 25mg visa,thehalflives of noncatecholamines are much longer than those of catecholamines. Third, noncatecholamines are considerably less polar than catecholamines and hence aremoreabletocrosstheblood-brainbarrier. ReceptorSpecificity To understand the actions of individual adrenergic agonists, we need to know theirreceptorspecificity. Variabilityinreceptorspecificityamongtheadrenergic agonists can be illustrated with three drugs: albuterol, isoproterenol, and epinephrine. Epinephrine is even less selective, acting at all four adrenergic receptor subtypes:alpha1,alpha2,beta1,andbeta2. In the upper part of the table, receptor specificity is presented in tabular form. By learning this content, you will be well on your way to understanding the pharmacologyofthesympathomimeticdrugs. The ability of a drug to selectively activate certain receptors to the exclusion of others depends on the dosage: at low doses, selectivity is maximal; as dosage increases, selectivity declines. For example, when albuterol is administered in low to moderate doses, the drug is highly selective for beta2-adrenergic receptors. So-called selective agents will activate additional adrenergic receptorsifthedosageisabnormallyhigh. TherapeuticApplicationsandAdverseEffectsof AdrenergicReceptorActivation Inthissectionwediscusstheresponses-boththerapeuticandadverse-thatcan be elicited with sympathomimetic drugs. Because many adrenergic agonists activate more than one type of receptor (see Table 13. Consequently, rather than attempting to structurethispresentationaroundrepresentativedrugs,wediscusstheactionsof theadrenergicagonistsonereceptoratatime. Ourdiscussionbeginswithalpha1 receptors, and then moves to alpha2 receptors, beta1 receptors, beta2 receptors, and finally dopamine receptors. For each receptor type, we discuss both the therapeuticandadverseresponsesthatcanresultfromreceptoractivation. This is the same approach to understanding neuropharmacologic agents that we discussed in Chapter10. TherapeuticApplicationsofAlpha1Activation Activation of alpha1 receptors elicits two responses that can be of therapeutic use: (1) vasoconstriction (in blood vessels of the skin, viscera, and mucous membranes);and(2)mydriasis. Hemostasis Hemostasis is defined as the arrest of bleeding, which alpha1 agonists support throughvasoconstriction. Specific alpha1-activating agents employed as nasal decongestants include phenylephrine (administered topically) and pseudoephedrine(administeredorally). Themechanismisalpha1-mediatedvasoconstriction,whichreduces blood flow to the site of anesthetic administration. Because keeping the drug at the local site of action prolongs anesthesia, allows a reduction in anesthetic dosage, and reduces the systemic effectsthatalocalanestheticmightproduce. ElevationofBloodPressure Because of their ability to cause vasoconstriction, alpha1 agonists can elevate bloodpressureinhypotensivepatients. Pleasenote,however,thatalpha1agonists are not the primary therapy for hypotension. Rather, they are reserved for situations in which fluid replacement and other measures either are contraindicatedorhavefailedtorestorebloodpressuretoasatisfactorylevel. Hypertension Alpha1 agonists can produce hypertension by causing widespread vasoconstriction. The cause is lack of blood flow to the affected area secondary to intense local vasoconstriction. If extravasation occurs, the area should be infiltrated with an alpha1-blocking agent. The mechanism is this: alpha1-mediated vasoconstriction elevates blood pressure, which triggers the baroreceptor reflex, causing heart rate to decline. However, their ability to activate alpha2 receptors in the periphery has little clinical significance because there are no therapeutic applications related to activation of peripheral alpha2 receptors. Furthermore, activation of these receptors rarely causes significant adverse effects. By activating central alpha2 receptors, we can producetwousefuleffects:(1)reductionofsympatheticoutflowtotheheartand bloodvesselsand(2)reliefofseverepain. Thecentralalpha2agonistsusedfor effects on the heart and blood vessels, and the agents used to relieve pain, are discussedinChapters15and22,respectively. TherapeuticApplicationsofBeta1Activation HeartFailure Heart failure is characterized by a reduction in the force of myocardial contraction,resultingininsufficientcardiacoutput. Shock this condition is characterized by profound hypotension and greatly reduced tissueperfusion. By increasing heart rate and force of contraction, beta1 stimulants can increasecardiacoutputandcantherebyimprovetissueperfusion. CardiacArrest Byactivatingcardiacbeta1receptors,drugshavearoleininitiatingcontraction in asystole or pulseless ventricular rhythms. Initial management focuses on cardiopulmonary resuscitation, external pacing, or defibrillation (whichever is applicable), and identification and treatment of the underlying cause. When a beta1 agonist is indicated, epinephrine,administeredintravenously,isthepreferreddrug.
Methyldopa Tablets:250mg signs having diabetes order genuine acarbose, 500mg Initialdose: 250mg2-3 timesaday Maintenance does:0 diabetes diet harvard order 25 mg acarbose amex. Studies regarding methyldopa use in pregnant patients have shown improved outcomes without fetal harm diabetes mellitus type 2 health education purchase acarbose 50 mg free shipping, so the American Congress of Obstetricians and Gynecologists has designated methyldopa as a preferred drug in management of hypertension duringpregnancy managing diabetes guideline purchase acarbose visa. AdverseEffects PositiveCoombsTestandHemolyticAnemia A positive Coombs testa develops in 10% to 20% of patients who take methyldopa chronically. Blood counts (hematocrit, hemoglobin, or red cell count)shouldalsobeobtainedbeforetreatmentandperiodicallythereafter. Of the patients who have a positive Coombs test, about 5% develop hemolytic anemia. Coombs-positive patients who do not develop hemolytic anemia may continue methyldopa treatment. However, if hemolytic anemia does develop, methyldopa should be withdrawn immediately. Hepatotoxicity Methyldopa has been associated with hepatitis, jaundice, and, rarely, fatal hepatic necrosis. These drugs have little or no effect on the release of epinephrine from the adrenal medulla. Reserpine is a naturallyoccurringcompoundpreparedfromtherootofRauwolfiaserpentina,a shrub indigenous to India. Hence, the effects of reserpine closely resemble those produced by a combinationofalpha-andbeta-adrenergicblockade. TherapeuticUses Hypertension the principal indication for reserpine is hypertension. AdverseEffects Depression Reserpine can produce severe depression that may persist for months after the drugiswithdrawn. Patientsshouldbeinformedthatorthostatichypotension,themost serious cardiovascular effect, can be minimized by moving slowly when changing from a seated or supine position to an upright position. In addition, patients should be advised to sit or lie down if lightheadedness or dizziness occurs. Pregnantwomen Breastfeeding women Olderadults PrescribingandMonitoringConsiderations Clonidine TherapeuticGoal Clonidineisusedtoreducebloodpressureinhypertensivepatients. OngoingMonitoringandInterventions EvaluatingTherapeuticEffects Monitor blood pressure and heart rate before each dose. This can be relieved by taking frequent sips of fluids, chewingsugarlessgum,andsuckingonhardcandy. If hemolysis occurs, withdraw methyldopa immediately; hemolytic anemia usually resolves quickly. Obtain blood counts (hematocrit, hemoglobin, or red cell count) beforetreatmentandperiodicallythereafter. Medical applications include relief of pain, suppression of seizures, production of anesthesia, and treatment of psychiatric disorders. Much of our ignorance stems from the anatomic and neurochemical complexityofthebrainandspinalcord. Passageacross the barrier is limited to lipid-soluble agents and to drugs that cross by way of specifictransportsystems. Keep in mind,however,thatthesemechanismsaretentative,representingourbestguess based on available data. As we learn more, it is almost certain that these conceptswillbemodified,ifnotdiscarded. These altered effects are the result of adaptive changes that occur in the brain in response to prolonged drug exposure. IncreasedTherapeuticEffects Certaindrugsusedinpsychiatry-antipsychoticsandantidepressants-mustbe taken for several weeks before full therapeutic effects develop. For example, phenobarbital(anantiseizuredrug)producessedationduringtheinitialphaseof therapy; however, with continued treatment, sedation declines while full protectionfromseizuresisretained. Physical dependence is a state in which abrupt discontinuationofdrugusewillprecipitateawithdrawalsyndrome. Thekindsof adaptivechangesthatunderlietoleranceanddependencearesuchthat,afterthey have taken place, continued drug use is required for the brain to function "normally. DevelopmentofNewPsychotherapeuticDrugs Becauseofdeficienciesinourknowledgeoftheneurochemicalandphysiologic changesthatunderliementaldisease,itisimpossibletotakearationalapproach to the development of truly new (nonderivative) psychotherapeutic agents. History bears this out: virtually all of the major advances in psychopharmacologyhavebeenserendipitous. Inadditiontoourrelativeignoranceabouttheneurochemicalandphysiologic correlates of mental illness, two other factors contribute to the difficulty in generating truly new psychotherapeutic agents. First, in contrast to many other diseases,welackadequateanimalmodelsofmentalillness. Second, mentally healthy individuals cannot be used as subjects to assess potential psychotherapeutic agents because most psychotherapeutic drugs either have no effectonhealthyindividualsorproduceparadoxicaleffects. After a new drug has been found, variations on that agent can be developed systematically:(1)structuralanalogsofthenewagentaresynthesized;(2)these analogs are run through biochemical and physiologic screening tests to determinewhethertheypossessactivitysimilartothatoftheparentcompound; and(3)afterserioustoxicityhasbeenruledout,promisingagentsaretestedin humans for possible psychotherapeutic activity. Using this procedure, it is possibletodevelopdrugsthathavefewersideeffectsthantheoriginaldrugand perhapsevensuperiortherapeuticeffects. However,althoughthisproceduremay produce small advances, it is not likely to yield a major therapeutic breakthrough. When we studiedthepharmacologyoftheperipheralnervoussystem,weemphasizedthe importance of understanding transmitters and their receptors before embarking onastudyofdrugs. Cardinal symptoms are tremor, rigidity, postural instability, and slowed movement. In addition to these motor symptoms, most patients also experience nonmotor symptoms, especially autonomic disturbances, sleep disturbances, depression, psychosis,anddementia.
BiochemistryandPhysiologyofIron To understand the consequences of iron deficiency as well as the rationale behind iron therapy diabetes prevention articles discount acarbose 25mg online, we must first understand the biochemistry and physiology ofiron diabetes 911 best purchase acarbose. MetabolicFunctions Iron is essential to the function of hemoglobin metabolic disease pathology cheap acarbose 50mg otc, myoglobin (the oxygen-storing molecule of muscle) blood sugar 300 symptoms buy acarbose 25mg otc, and a variety of iron-containing enzymes. In the discussion that follows, the numbers in parentheses refer to the circled numbersinthefigure. UptakeandDistribution the life cycle of iron begins with (1) uptake of iron into mucosal cells of the small intestine. Afteruptake,ironcaneither(2a)undergostoragewithinmucosalcellsinthe formofferritin(acomplexconsistingofironplusaproteinusedtostoreiron)or (2b) undergo binding to transferrin (the iron transport protein) for distribution throughoutthebody. Lastly(3c),someoftheironinplasmaistakenupbymuscle (for production of myoglobin) and some is taken up by all other tissues (for productionofiron-containingenzymes). After hemoglobin is made in bone marrow, iron reenters the circulation (4) as a component of hemoglobin in erythrocytes. RegulationofBodyIronContent the amount of iron in the body is regulated through control of intestinal absorption. If all dietary iron were readily absorbed, body iron content would rapidly accumulate to a toxic level. However, excessive buildup is prevented through controlofironuptake:asbodystoresrise,uptakeofirondeclines;conversely,as bodystoresbecomedepleted,uptakeincreases. Forexample,whenbodystores of iron are high, only 2% to 3% of dietary iron is absorbed. DailyRequirements Requirements for iron are determined largely by the rate of erythrocyte production. In most cases, the iron needs of pregnant women are too great to be met by diet alone. Consequently, iron supplements (about 27mg/day) are recommended duringpregnancyandfor2to3monthsafterdelivery. Therefore, if physiologic requirements are to be met, the diet must contain10timesmoreironthanweneed. Otherfoodswithahighiron content include muscle meats, fish, fowl, cereal grains, beans, and green leafy vegetables. Exceptforindividualswhohaveveryhigh iron requirements (infants, pregnant patients, those undergoing chronic blood loss),theaveragedietissufficienttomeetironneeds. The reduced oxygen-carrying capacity of blood resultsinlistlessness,fatigue,andpalloroftheskinandmucousmembranes. If tissue oxygenation is severely compromised, tachycardia, dyspnea, and angina may result. In addition to causing anemia, iron deficiency impairs myoglobin production and synthesis of iron-containing enzymes. Diagnosis the hallmarks of iron deficiency anemia are (1) the presence of microcytic, hypochromic erythrocytes and (2) the absence of hemosiderin (aggregated ferritin) in bone marrow (Table45. Of these, the ferrous salts (especially ferrous sulfate) and carbonyl iron are used most often. Fourferrousironsalts are available: ferrous sulfate, ferrous gluconate, ferrous fumarate, and ferrous aspartate. It is also thepreferreddrugforpreventingdeficiencywhenironneedscannotbemetby diet alone. Ferrous sulfate costs less than ferrous gluconate or ferrous fumarate but has equal efficacy and tolerability. These effects, which are dose dependent, include nausea, heartburn, bloating, constipation, and diarrhea. Gastrointestinal reactions are most intense during initial therapy and becomelessdisturbingwithcontinueddruguse. PatientEducation PreventingToothStaining Liquid iron preparations can stain the teeth. This can be prevented by (1) diluting liquid preparations with juice or water, (2) administering the iron through a straw or with a dropper, and (3) rinsing the mouth after administration. By contrast, in young children, iron-containing products remain oneoftheleadingcausesofpoisoningfatalities. Serum iron should be measured and the intestine x-rayed to determine whether unabsorbed tablets are present. Gastric lavage may be considered in patients with intentional ingestionoflargeamountsofiron. Interaction of iron with other drugs can alter the absorption of iron, the other drug,orboth. Ascorbic acid (vitamin C) promotes iron absorption but also increases its adverse effects. Ferrous sulfate is available in standard tablets and in enteric-coated and sustained-release formulations. The enteric-coated and sustained-release products are designed to reduce gastric disturbances. Unfortunately, although side effects may be lowered, these special formulations have disadvantages. Unfortunately,theamountinmostproductsistoolowtohelp:more than 200mg of vitamin C is needed to enhance the absorption of 30mg of elementaliron.
- Activated charcoal
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- "Water pills" (diuretics )
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- Next, the doctor examines the entire knee joint. If there is damage to more than one part of your knee, you may need a total knee replacement. Most of the time, however, this is not needed.
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Specificimmuneresponsesarepossible becausecertaincellsoftheimmunesystem(TlymphocytesandBlymphocytes) possess receptors that can recognize individual antigens diabetes mellitus definicion cheap acarbose 50mg on-line. Cell-mediated immunity refers to immune responses in which targets areattackeddirectlybyimmunesystemcells-specifically diabetic diet examples order acarbose 25mg on-line,cytolyticTcellsand macrophages diabetes symptoms after eating sugar generic 25 mg acarbose visa. Themajoractorsarethelymphocytes(Bcells diabetes mellitus type 2 labs purchase acarbose 50 mg amex,cytolytic T cells, helper T cells), macrophages, and dendritic cells. Asdiscussedlater,antibodyspecificityisdeterminedbythe structure of highly specific receptors found on the surface of B cells. B cells are so named because in chickens, where B cells were discovered, these cells are produced in the bursa of Fabricius, a structure not found in mammals. Specificity of attack is determined by the presence of antigen molecules on the surface of thetargetcellandspecificreceptorsforthatantigenonthesurfaceoftheTcell. Specificity of helper T cells is achieved through highly specific cellsurface receptors that recognize individual antigens. The term helper is somewhat misleading in that it connotes a useful but dispensable role. Helper T cells are not simplynicetohavearound,theyareabsolutelyrequiredforaneffectiveimmune response. Macrophages Macrophages begin their existence in the bone marrow, enter the blood as monocytes, and then infiltrate tissues, where they evolve into macrophages. Althoughtheirmajorjob is phagocytosis, macrophages also have an important role in specific acquired immunity,naturalimmunity,andinflammation. Becauseantigenpresentation is an absolute requirement for specific immune responses (see later), you can appreciatehowimportantmacrophagesare. DendriticCells Dendritic cells perform the same antigen-presenting task as do macrophages. Mastcells,whichare derived from basophils, are concentrated in the skin and other soft tissues. Bothcelltypesreleasehistamine,heparin,and other compounds that cause the symptoms of immediate hypersensitivity. The role of mast cells and basophils in allergic reactions is discussedinChapter61. As discussed later, neutrophils avidly devour cells that have been tagged with antibodies of the immunoglobulin G (IgG) class. Accordingly, neutrophils can be viewed as important effectors in humoral immunity. Eosinophils Eosinophils attack and destroy foreign particles that have been coated with antibodies of the IgE class. Eosinophils also contribute to tissue injury and inflammation associated with immediatehypersensitivityreactions. Antibodies Antibodies are a family of structurally related glycoproteins that mediate humoralimmunity. Themostcharacteristicfeatureofantibodiesistheirability to recognize and bind with specific antigens. SomeoftheantibodiesthatB cellsproduceareretainedonthesurfaceoftheBcell,wheretheyserveasthe receptors whereby B cells recognize specific antigens. However, most of the antibodiesthatBcellsproducearesecretedfromthecell,afterwhichtheybind to their specific antigen, thereby initiating the effector phase of humoral immunity. Because antigens are big, the antigenbinding region of the resultant antibodies cannot recognize and bind the entire antigen molecule. Rather, the antibodies recognize and bind selected small portions of the antigen, referred to as epitopes or antigenic determinants. In research and in clinical practice, we may want to generate antibodies to molecules that are too small to induce an immune response. CharacteristicFeaturesofImmuneResponses Cell-mediated immunity and humoral immunity share five characteristic features: specificity, diversity, memory, time limitation, and selectivity for antigens of nonself origin. ThisispossiblebecauseourimmunesystemshavemillionsofclonesofBandT lymphocytes-each of which is preprogrammed to recognize a different antigenicdeterminant. However, some of the new cells become memory cells, therebyincreasingthepoolofantigen-specificcellsavailabletorespondinthe future. Thereasonsare twofold:First,astheimmuneresponseproceeds,itgreatlydecreasesthelevelof antigen that initiated the response, thereby attenuating the stimulus for continuing. SelectivityforAntigensofNonselfOrigin Under normal conditions, our immune systems target only foreign antigens, leavingpotentiallyantigenicmoleculesonourowncellsuntouched. Sparingof selfispossiblebecause,asTcellsdevelopinthethymus,cellsthatareableto react with antigens of self origin are eliminated. Thereare many diseases of autoimmune origin, including psoriasis, multiple sclerosis, rheumatoid arthritis, myasthenia gravis, type 1 diabetes, systemic lupus erythematosus, two inflammatory bowel diseases (ulcerative colitis and Crohn disease),andtwothyroiddiseases(GravesdiseaseandHashimotothyroiditis). PhasesoftheImmuneResponse Specific immune responses can be viewed as having three main phases: recognition,activation,andeffector. RecognitionPhase the recognition phase occurs when a mature lymphocyte encounters its matchingantigen. Antigen recognition is possible because of antigenspecificreceptorsonthelymphocytesurface. ActivationPhase Antigen recognition activates the lymphocyte, which then undergoes proliferation and differentiation. Some of the daughter cells differentiate into cellsthatactivelyparticipateintheimmuneresponse,attackingthesourceofthe antigen. With cell-mediated or antibody-mediated immunity, several effector mechanisms can be involved. In cell-mediated immunity, antigen-bearing target cells can be lysed by cytolytic T cells, or they can be ingested by macrophages.
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