By X. Stan. University of Denver. 2019.
Prevalence of sarcoidosis in Ireland: proceedings of the Third International Conference on Sarcoidosis cheap suhagra 100mg line. Racial differences in sarcoidosis incidence: a 5 year study in a health maintenance organization discount 100mg suhagra. A current assessment of rurally linked exposures as potential risk factors for sarcoidosis trusted suhagra 100 mg. Granulomatous pneumonitis and mediastinal lymphadenopathy due to photocopier toner dust [letter] buy suhagra 100mg. Trends and occupational associations in incidence of hospitalized pulmonary sarcoidosis and other lung diseases in Navy personnel; a 27-year historical prospective study, 1975-2001. The incidence, prevalence and severity of sarcoidosis in New-York City firefighters. In addition, there are lung diseases of unknown cause that result in pulmonary fibrosis. While epidemiologic studies have not shown an increased incidence of pulmonary fibrosis in fire fighters, this topic is of interest to fire fighters because of their potential to inhale smoke as well as industrial substances such as insulation particles and chemicals that may become airborne during fires and explosions. The key concept is that environmental exposure to potentially-fibrogenic substances can largely be prevented through the appropriate use of properly fitting respirators. In order to understand how and where pulmonary fibrosis occurs, it is necessary to describe some basic facts about the organization of the lung. The lung is composed of a number of different types of structures that serve different functions. Inhaled substances pass through the upper airway, vocal cords and larynx prior to traveling through the branching tubes that make up the bronchial tree. The airways terminate in the tiniest passages that lead into the alveoli, the gas exchanging units of the lung. In the alveoli, the pulmonary capillaries (the smallest caliber blood vessels) run directly adjacent to the alveolar air sacs, allowing for the efficient exchange of oxygen and carbon dioxide between blood and air. Scar tissue can form in the walls of the alveoli or in the airspaces of the alveoli or both. The extremely thin space in between the alveolar wall and the capillary is called the interstitium. This interstitial space becomes dramatically widened by inflammatory cells and the deposition of scar tissue, hence the broad category of this class of lung problems is termed interstitial lung disease. Major Categories of Interstitial Lung Disease and Pulmonary Fibrosis The major environmental agents that are implicated in occupational pulmonary fibrosis include inhalation of industrial dusts such as asbestos fibers, silica (from sandblasting) and coal dust from mining. The key characteristic shared by all particles that can cause pulmonary fibrosis is the size of the particles. If the particles are larger than three microns in length they tend to deposit in the nose, throat and large airways of the lung. Smaller particles are increasingly likely to be deposited in the terminal airways or alveoli, where they can cause inflammation and subsequent scarring, leading to interstitial lung disease and fibrosis. In general, single short exposures are much less likely to cause fibrosis than repeated daily exposures over years. Of asbestos workers developing asbestosis (interstitial lung disease due to asbestos) half have had >20 years of exposure. The prevalence of asbestosis in asbestos-exposed workers worldwide ranges from 3% to >20% depending upon if they were engaged in the manufacture of cement products containing asbestos, mining and milling of asbestos (highest prevalence) or manufacture of asbestos fiber or rope. Other occupational exposures included grinding brake linings, which formerly contained asbestos and may still be present in old and replacement brake pads and clutch plates. The particles must be airborne in order to cause disease, so intact insulation that is not degraded in some way does not represent a true risk of asbestos exposure until the integrity of the sealed substance is compromised during maintenance or removal activities that lead to the airborne release of asbestos fibers. Of note, fibers that are brought home on the surface of clothing can become airborne again when the clothing is handled, leading to exposure of family members. Asbestosis is of particular concern to fire fighters due to their potential exposure to insulation containing asbestos that was used in residential homes. Another common type of interstitial lung disease that can progress to pulmonary fibrosis is a condition termed hypersensitivity pneumonitis or extrinsic allergic alveolitis. This disease is mediated by an immunologic response in the lung to an inhaled organic antigen. The most common types are due to ongoing exposure to birds such as parakeets or pigeons (bird fancier s lung). The offending antigens are proteins present in the bird droppings that become aerosolized. Another common cause of hypersensitivity pneumonitis is exposure to mold, as in moldy hay (farmer s lung). There are other types of chronic inflammatory lung disease of unknown cause that sometimes lead to fibrosis such as sarcoidosis. Sarcoidosis causes a specific pattern of inflammation that the pathologist recognizes as a granuloma, composed of activated macrophages (also called epithelioid giant cells) surrounded by lymphocytes in a spherical configuration. A small minority of individuals with sarcoidosis will progress to irreversible pulmonary fibrosis. Usually the joint or skin disease is present for a long time before lung involvement occurs, but rarely, the lung disease can be the initial manifestation of these systemic disorders. These generally have a somewhat better prognosis than idiopathic pulmonary fibrosis, a condition of unknown cause. Pulmonary fibrosis can also occur as a complication of certain types of chemotherapy prescribed for cancer treatment. The best known example is bleomycin, a drug used to treat lymphoma and testicular cancer. This drug reproducibly causes pulmonary fibrosis in certain strains of laboratory mice, so is used as a standard animal model for research on pulmonary fibrosis. Another commonly-employed cancer treatment, external beam radiation therapy, can cause radiation pneumonitis and fibrosis in a minority of individuals. The acute symptoms may begin within several weeks following radiation to the chest for treatment of lung cancer, breast cancer or lymphoma. The remaining types of interstitial lung disease are termed idiopathic, meaning having no known cause. The most common types of idiopathic interstitial lung disease are termed idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia. The reason that an accurate diagnosis of the specific type of interstitial lung disease should be made is that the prognosis and potential for response to treatment as well as the dose and duration of treatment recommended is dependent upon the specific diagnosis. Cryptogenic organizing pneumonia is an inflammatory disorder that follows a viral infection and a variety of other acute insults to the lung. Its importance is that it may often be confused with bacterial pneumonia, but responds readily to treatment with systemic steroids. In contrast, idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia are generally diseases of much longer duration where symptoms may occur for months to years prior to a diagnosis. Of note, in a small minority of cases, idiopathic pulmonary fibrosis occurs in families. The genetics of the predisposition to develop idiopathic pulmonary fibrosis in both the familial and non-familial forms are only beginning to be understood. Symptoms of Pulmonary Fibrosis The main symptoms of pulmonary fibrosis are shortness of breath and frequent cough. The shortness of breath is usually only with exertion until the disease is very advanced. A minority of individuals will develop clubbing, a specific change in the soft tissue structure of the distal parts of the fingers that leads to widening of the end of the finger just after the last finger joint and a change in the angle that the nail-bed makes with surface of the finger. Swelling of the feet and legs may occur in advanced pulmonary fibrosis as explained below. Individuals with chronic interstitial lung disease and pulmonary fibrosis typically have symptoms for months to years before a diagnosis is made. Patients with this disease generally report a very gradual onset and progression of shortness of breath noted when exerting themselves. Sometime the interstitial disease is discovered accidentally when imaging of the chest is done for another reason. Often the individual is admitted to the hospital for pneumonia and only in retrospect is it apparent that interstitial lung disease is the underlying problem.
In the chronic un- cases intervention is required before decompensation of treated patient there can be hepatic cirrhosis from the the right ventricle occurs buy generic suhagra 100 mg. Echocardiography is diagnostic and is also essential to assess right ventricular function discount 100mg suhagra amex. Tricuspid regurgitation Denition Management Retrograde blood ow from the right ventricle to the Functional tricuspid regurgitation usually resolves with rightatrium during systole buy suhagra 100mg mastercard. Cardiac arrhythmias A cardiac arrhythmia is a disturbance of the nor- Aetiology mal rhythm of the heart buy discount suhagra 100 mg on line. Tachycardias are also subdivided according to their Clinical features origin: Most patients are asymptomatic but occasionally post- r Sinustachycardia. If bradycardia is episodic and severe, syncope r Ventricular tachyarrhythmias such as ventricular may occur. However, in patients with bundle branch block Most cases do not require treatment other than with- and in cases where the rapid rate of supraventricu- drawal of drugs or treatment of any underlying cause. Carotid sinus massage typically leads to a Denition sudden and sometimes prolonged sinus pause. Aetiology/pathophysiology Sinustachycardia is a physiological response to main- tain tissue perfusion and oxygenation. Clinical features Investigations Palpitations with an associated rapid, regular pulse rate. In addition anti-arrhythmic drugs may be required to Management controlanytachycardia. Atrial arrhythmias Sinus node disease Atrial ectopic beats Denition Sinusnode disease or sick sinus syndrome is a tachy- Denition cardia/bradycardia resulting from damage to the sinus Atrial ectopic beats include extrasystoles and premature node. Aetiology/pathophysiology Aetiology Sinusnode disease is relatively common in the elderly Atrial ectopics are common in normal individuals. All dueto ischaemia, infarction or degeneration of the sinus cardiac cells have intrinsic pacemaker ability. The condition is characterised by prolonged in- ually depolarise until a threshold is reached at which tervals between consecutive P waves (sinus arrest) and point rapid depolarisation occurs and a cardiac action periods of sinus bradycardia. This is most rapid in the sinoatrial may allow tachycardias (typically atrial brillation) from node, the normal pacemaker of the heart. This combination of fast and slow or group of cells the gradual depolarisation is more rapid supraventricular rhythms is known as tachy-brady syn- than usual, or if the voltage threshold for rapid depolar- drome. Clinical features Atrial utter presents with palpitations, dizziness, syn- Investigations cope or cardiac failure. Massage of the Management carotid sinus causes a transient increase in block with Atrial ectopic beats do not require treatment, although consequent slowing of the ventricular rate. If atrial ectopic beats are fre- Investigations quent they may progress to other atrial arrhythmias. Atrial utter produces a characteristic regular sawtooth utter waves at a rate of 300 bpm seen best in lead V1. Atrial utter is a rapid atrial rate between 280 and 350 bpm, most commonly 300 bpm. It may be caused by thyro- logical assessment, recurrence may be prevented by ra- toxicosis. Normally once a cardiac cell has been depolarised it is refractory to re-stimulation for a short period. This pre- vents waves of cardiac depolarisation owing in a retro- Atrial brillation grade direction. If, however, the conduction through the myocardiumisslow(usuallyduetomyocardialdamage), Denition adjacent cells may have recovered from their refractory Atrial brillation is a quivering of atrial myocardium period allowing restimulation and hence the formation resulting from disordered electrical and muscle activity. Incidence rate,inthe elderly who depend on atrial function to Common achieve sufcient ventricular lling, or if there is associ- ated signicant cardiac damage. Patients may Sex present with palpitations, acute cardiac failure or the M > F gradual onset of increasing shortness of breath. On ex- amination there is an irregularly irregular pulse with Aetiology varying pulse volume. There is also loss of the a wave of Causes may be divided into cardiac and systemic. Inacuteatrialbrillation,underlyingischaemia ease, mitral valve disease, cardiomyopathies and pul- such as a recent myocardial infarction or unstable monary disease. Thelonger the atrial brillation has been present, merous circuits have different cycle times, the result is a the less the likelihood of restoring sinus rhythm. Digoxin does not missions, but an irregularly irregular pulse of between prevent recurrence. Atrial brilla- r Control of the ventricular rate is achieved with drugs tion may be paroxysmal with attacks lasting minutes to such as digoxin, calcium channel blockers and/or - hours. Aetiology/pathophysiology The majority of junctional tachycardias are due to re- Investigations/management entry circuits. If Usually there is a slow anterograde pathway from atria the retrograde pathway is slow with delayed atrial con- to ventricles and a fast retrograde pathway back to the traction, inverted P waves appear between complexes. The re- may produce an immediate cessation of the arrhyth- entrant circuit is concealed as it slow, close to the mia. Complications Aetiology Sudden cardiac death may rarely occur if atrial brilla- Abnormalconnectionbetweenatriumandventricle(e. Pathophysiology Management r Re-entrant tachycardias are treated with drugs that NormallythefastconductionthroughthebundleofKent allows the adjacent area of ventricle to be rapidly depo- block retrograde conduction through the accessory larised (preexcitation), whilst the remainder of the ven- pathway, e. Verapamil and digoxin are contraindicated as two pathways may form a re-entry circuit with the fast they accelerate anterograde conduction through the accessory pathway causing a retrograde stimulation of accessory pathway. Clinical features Prognosis In sinus rhythm Wolff Parkinson White syndrome is With age the pathway may brose and so some patients asymptomatic. Denition Aventricular ectopic/extrasystole/premature beat is an extramyocardial depolarisation triggered by a focus in Prognosis the ventricle. Ventricular ectopics worsen the prognosis in patients with underlying ischaemic heart disease but there is no evidence that anti-arrhythmic drugs improve this. Aetiology/pathophysiology Ventricular ectopics are not uncommon in normal indi- viduals and increase in incidence with advancing age. Common causes include ischaemic heart disease and Ventricular tachycardia hypertension. Ectopic beats may arise due to any of Denition the mechanisms of arrhythmias, such as a re-entry cir- Tachycardia of ventricular origin at a rate of 120 220 cuit or due to enhanced automaticity (which may occur bpm. When ventricular ectopic beats occur regularly Ventricular tachycardia is normally associated with un- after each sinus beat, it is termed bigeminy, which is fre- derlying coronary, ischaemic or hypertensive heart dis- quently due to digoxin. Clinical features Patients are usually asymptomatic but may feel uncom- Pathophysiology fortable or beaware of an irregular heart or missed beats. The underlying mechanism is thought to be enhanced On examination the pulse may be irregular if ectopics automaticity,leadingtore-entrycircuitasinothertachy- are frequent. In ventricular tachycardia there is a small (or sometimes large) group of ischaemic or electrically non- homogeneouscells,typicallyresultingfromanacutemy- Investigations r ocardial infarction. Clinical features r Echocardiography and exercise testing may be used The condition is episodic with attacks usually lasting to look for underlying structural or ischaemic heart minutes. The presenting pic- Denition ture is dependent on the rapidity of the tachycardia and Torsades de pointes or twisting of the points is a con- the function of the left ventricle, as well as general con- dition in which there is episodic tachycardia and a pro- dition of the patient (e. Low serum potas- It is thought that the long Q T interval allows adjacent sium or magnesium may predispose to arrhythmias, so cells, which are repolarising at slightly different rates, levels should be checked. The Q T interval is prolonged by biochemical abnormalities and Complications drugs, and is also prolonged in bradycardic states. Cardiac arrest due to pulseless ventricular tachycardia or ventricular brillation. Clinical features It typically recurs in frequent short attacks, causing pre- syncope, syncope or heart failure. Management r Any underlying electrolyte disturbance should be identied and managed. It is now customary to use these in patients Denition known to have a high risk of sudden cardiac death. Chaoticelectromechanicalactivityoftheventriclescaus- ing a loss of cardiac output. Conduction disturbances Incidence The most common cause of sudden death and the most Atrioventricular block common primary arrhythmia in cardiac arrest. Atrioventricular or heart block describes an alteration in the normal pattern of transmission of action poten- Aetiology tials between the atria and the ventricles.
I try not to prescribe pseudoephedrine to avoid potential a-adrenergic stimulation of uterine vessels order suhagra 100 mg otc, although this treatment has been recommended by others ( 2 purchase suhagra 100mg on line,53) order suhagra 100 mg mastercard. Phenylpropanolamine in 726 exposures was associated with significantly greater risk of malformations (ear and eye) order suhagra 100 mg on line, whereas this risk was not detected with pseudoephedrine (39 exposures) or phenylephrine (1,249 exposures) ( 57). Phenylpropanolamine is being removed from many nonproprietary medications, and pseudoephedrine is being used instead. Hopefully, there will be no adverse pregnancy outcomes because these medications are used without prescription (or perhaps with knowledge of an existing early pregnancy). Intranasal cromolyn can be used for mild allergic rhinitis, based on experience with 296 gravidas with asthma ( 39). Tetracyclines are contraindicated because of maternal fatty liver during gestation (third trimester) and staining of teeth in the infant. Human experience with clarithromycin is not available, so azithromycin should be used if it is indicated. Allergen immunotherapy helps reduce the need for medications in cases of allergic rhinitis. This therapy can be continued in pregnancy and, if symptoms are severe and the gravida agrees, immunotherapy may be initiated during gestation. During immunotherapy in 121 pregnancies in 90 gravidas, 6 gravidas experienced anaphylaxis (42). The decision to begin immunotherapy after delivery often is made for the purpose of convenience and ability of the woman to present for injections in a timely fashion. Severe allergic rhinitis symptoms during gestation can be treated with intranasal corticosteroids and antihistamines. As stated earlier, the dose of allergen immunotherapy can be increased in the absence of large local reactions or systemic reactions. There is no evidence that the incidence of anaphylaxis from allergen immunotherapy (or skin testing) is greater during the time of gestation. Causes for urticaria and angioedema include foods, medications, infections (viral), and underlying conditions such as collagen vascular disorders. Some episodes of urticaria are attributable to dermatographism or other physical urticarias, chronic (autoimmune) urticaria, or idiopathic acute urticaria. The concentration of C1 inhibitor declines in normal pregnancy because of increased plasma volume. Some gravidas have worsening clinical symptoms and create major management problems. Stanozolol or danazol result in a fourfold to fivefold increase in the concentration of C1 inhibitor and C4. Although unavailable in the United States, a concentrate of C1 inhibitor for parenteral administration has proved effective, with onset of action in 30 to 60 minutes (66). Antifibrinolytic agents are considered unwise to use in pregnancy because of their potential thrombotic effects. Nevertheless, three pregnancies in one gravida occurred uneventfully despite use of e-amino-caproic acid ( 66). If an episode of upper airway obstruction occurs during a cesarean delivery, epinephrine, stanozolol, and intubation would be indicated. Use of C1 inhibitor concentrates, if available and of low risk, otherwise would be of value acutely. Topical corticosteroids are of value, and maternal or fetal complications are unlikely. Herpes gestationis consists of intense pruritus followed by lesions that may be bullous, papulovesicular, or pustular ( 65). Despite its long-term use, there are few data regarding the appropriateness of hydroxyzine in the first trimester, but preliminary data do not reveal teratogenic effects for its metabolite cetirizine ( 58). The established appropriateness of diphenhydramine, chlorpheniramine, or tripelennamine favors their use. Oral albuterol or terbutaline may be attempted for more difficult cases, but often prednisone 20 to 30 mg daily may be necessary to control moderate to severe urticaria or angioedema. The latter is unexpected based on current knowledge of local anesthetic reactions and may have been an untoward effect of 23 mL being used. Anaphylaxis during gestation has caused fetal distress, fetal encephalopathy, or fetal demise. Gravidas have experienced profound shock with reduced uterine blood flow during anaphylaxis in pregnancy as the fundamental insult to the fetus. As in other cases of anaphylaxis, prevention and emergency medications and therapy are needed. If the gravida is hypotensive, then usual resuscitative measures should be instituted to maintain blood pressure and the airway. Obstetric assistance should be obtained immediately should cesarean delivery be indicated. Graft ( 78) reported a successful pregnancy in a gravida treated with maintenance dosages of wasp and mixed vespid venoms. Subsequently the Committee on Insects of the American Academy of Allergy and Immunology reported 63 pregnancies in 26 gravidas with no definite systemic reactions ( 79). Five of 43 gestations resulted in spontaneous abortions, thought to be unrelated to stings or immunotherapy. Other issues should be discussed with the gravida, such as avoidance measures and personal use of epinephrine. Uncontrollable life-threatening status asthmaticus: an indication for termination of pregnant by caesarean section. Perinatal outcomes in the pregnancies of asthmatic women: a prospective controlled analysis. Fetal oxygenation, assessment of fetal well-being, and obstetric management of the pregnant patient with asthma. Effect of pregnancy on airway responsiveness and asthma severity: relationship to serum progesterone. The course of asthma during pregnancy, postpartum, and with successive pregnancies: a prospective analysis. Effects of in utero and environmental tobacco smoke exposure on lung function in boys and girls with and without asthma. Position paper of the Working Group on Immunotherapy of the European Academy of Allergy and Clinical Immunology. Drug Evaluation Annual 1994, Department of Drugs, Division of Drugs and Toxicology, 6th ed. The human respiratory nasal mucosa in pregnancy: an electron microscopic and histochemical study. Pregnancy outcome after gestational exposure to terfenadine: a multicenter, prospective controlled study. Hereditary angioneurotic oedema and pregnancy: case reports and review of the literature. Treatment of 193 episodes of laryngeal edema with C I inhibitor concentrate in patients with hereditary angioedema. Severe complication to phytomenadione after intramuscular injection in woman in labor. Renal impairment, hypertension and encephalomacia in an infant surviving severe intrauterine anoxia. These patients often reside in inner cities with low income, inadequate knowledge of asthma and its management, and no predetermined crisis plan ( 1). Physicians and nurses must address this problem, even in the acute care setting, to diminish the risk of repeated exacerbation. Instruction takes time and may not be feasible for all patients; still, reallocation of resources to allow for education in the acute setting may be cost-effective in the long run. Follow-up appointments with an asthma specialist also are recommended to reduce further the risk of subsequent hospitalization ( 6). This chapter reviews the more immediate concern of restoring the state of unlabored breathing. Proven in this regard are b-agonist bronchodilators and systemic corticosteroids, with accumulating evidence supporting the use of anticholinergic bronchodilators. For patients requiring intubation and mechanical ventilation, a strategy that avoids excessive lung inflation, mainly through prolongation of exhalation time, decreases morbidity and mortality (7).