Going before the board: how to prepare yourself.
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Biomedical subjects
Publications and source records attributed to S Daum.
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Pulmonary circulation has become possible only by right heart catheterisation. The point of increased pressure in relation to pulmonary capillary wedge pressure is divided into postcapillary (passive), capillary and precapillary (active) pulmonary hypertension (PH). We assume that reduction of alveolar oxygen partial pressure leads to a growth of mast cells not only peribronchially, but also especially perivascularly, causing pulmonary arteriolo-vasoconstriction during release of eicosanoids (mediators). The individual components (vasoconstrictive, obliterative, obstructive, reactive, nutritive, primary, porto-pulmonary) are discussed. Long-term elevated pulmonary artery pressure (increased arterial vasoconstriction) results in right heart hypertrophy, which begins particularly in the right heart ejection tract. Depending on the underlying parenchymal or vascular diseases, we must differentiate between chronic cor pulmonale parenchymal or vascular. Right ventricular catheterisation may be differentiated into compensated or decompensated situation. Timely normalisation of pulmonary artery pressure may even lead to regression of the right ventricular hypertrophy. Right ventricular contractility on hypoxia is basically different in adapted and non-adapted patients (important for therapy and prognosis). Progression of right ventricular muscle mass and constant myocardial vasculature will cause stenocardias; in that case, permanent oxygen insufflation is indicated. Right ventricular hypertrophy affects the left heart, conducting alteration in pulmonary circulation (pulmo cardialis).
Asthma bronchiale (a.b.) is defined as paroxysmal or permanent, partly or completely reversible dyspnoea due to a bronchospasm resulting from pathological hyperreactivity of the bronchial system. In the pathogenesis participate allergic, immuno-infiltrative and genetic factors, irritating substances (environment) and infectious. The allergic constituent acts via sensitization and allergization of the mast cell, to its degranulation with release of mediators (histamine, serotonin, leukotrienes, thromboxane, PAF) with subsequent bronchoconstriction and production of viscous mucus. As to adrenergic factors, a block of beta-adrenergic receptors and reduced adrenal function is involved. As to non-adrenergic factors an increased sensitivity of the parasympathetic--vagus is involved which conditions bronchoconstriction and hyperkrinia. From the clinical aspect extrinsic (atopic) and intrinsic (cryptogenic) asthma bronchiale can be differentiated. The former is encountered more frequently in childhood and adolescence, in subjects with a positive family-history, high IgE and positive skin tests and a known allergen. The latter type of a.b. is found in adolescence, in subjects with a negative family-history, with eosinophilia; it is conditioned by infection (e.g. chronic bronchitis), strain, cold and takes a dangerous course (aspirin). As to the course, attacks of a.b. are involved with a symptom-free interval (extrinsic a.) easily controlled by treatment. Then there is the chronic form with a variable course and the necessity of permanent treatment. Status asthmaticus is in recent years with increasing frequency the cause of death and thus calls for maximal treatment. It is the third most serious form of a.b. Assessment of arterial blood gases is very important as a check of treatment as well as from the prognostic aspect (cross-over intubation). From the differential diagnostic aspect we must consider the asthmoid component in chronic bronchitis, pulmonary embolism, left-sided cardiac failure, tracheal or bronchial compression by an aortal aneurysm, tumour. The differential diagnosis is not always easy.
Intestinal intraepithelial lymphocytes (IEL) appear to represent a peculiar set of immune cells compartmentalized at the interface between the organism and the external environment. In previous studies we observed that within human IEL TCR-tau/delta T cells represent a major fraction that predominantly express the CD8 molecule and preferentially uses the V-delta-1 gene segment. Thus these data suggested a preferential accumulation/homing of CD8+ V-delta-1+ IEL within the human intestinal epithelium. However, to date the functional role of these cells with regard to immune regulation at this most critical immunological site is poorly understood. In this study, the cytotoxic potential and proliferative capacity of human IEL in response to mitogenic stimuli has been characterized with respect to IEL T cell receptor type and TCR-tau/delta variable gene segment usage as determined by flowmetry. The frequency of TCR-1+ IEL expressing both CD56 and CD16 which are considered to be NK-cell markers was found to be much higher (38.9 +/- 12.4%) than within intestinal lamina propria lymphocytes (LPL) (9.1 +/- 4.8%) or peripheral blood lymphocytes (PBL) (6.4 +/- 3.3%). In contrast, the fractions of CD16-CD56+ cells within IEL, LPL and PBL were comparable. Surprisingly, IEL mediated NK-cell activity (K562 lysis) was virtually absent whereas within PBL it was within the normal range. Furthermore, in cytotoxicity assays employing 51Cr-labeled OKT3 hybridoma cells and P815 cells as targets, the cytotoxic potential of IEL was much lower than that of PBL.(ABSTRACT TRUNCATED AT 250 WORDS)
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Over a period of 3 years, 224 laser treatments were performed on 105 patients. 84% were carried out under local anesthesia and 16% under general anesthesia. A neodymium-YAG laser (MBB-AT) was used. In 74% of the cases complete or partial tumor removal was possible. 72% of the successfully recanalized stenoses were still open after 4-6 months. In 19% of the cases low-grade complications occurred. The mortality was below 1%. The chief indications for endobronchial laser treatment are exophytic endobronchial tumors in the area of the trachea and primary bronchi. Endobronchial laser coagulation is indicated when surgery is no longer possible. It serves primarily to improve ventilation and bronchial drainage and in particular to prevent retention pneumonia.
Several studies have shown that the capability for exercise can be increased in patients with pacemakers by means of adjusting the rate. Respiration is one of the parameters considered for rate control. The aim of our study was to determine how respiratory parameters such as ventilation, tidal volume, and respiratory rate are capable of controlling the pacemaker rate, especially when measured indirectly by means of impedance plethysmography. We examined four volunteers and eight patients with implanted cardiac pacemakers using bicycle ergometry at increasing work loads. We recorded heart rate, uptake of oxygen, and ventilation directly (by pneumotachygraphy) and indirectly (by chest wall impedance plethysmography). A good correlation of directly to indirectly measured ventilation (r = 0.8687) was found. Our study suggests that respiratory minute volume is more appropriate for rate control of physiologic pacemakers than tidal volume or respiratory rate alone. Measurement by means of impedance plethysmography is sufficiently precise to be used for this purpose. Further studies must be conducted as to the optimum realization within an implantable device.
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Glycerol trinitrate in patches (DEPONIT 10) resulted in a statistically significant pressure drop in the pulmonary artery, the pulmonary capillaries, and the right atrium within 24 hours following drug application. This pressure reduction was recorded also after 4 weeks of continuous therapy. The reduction of pulmonary artery pressure and pulmonary vascular resistance is not only a consequence of improved pre- and afterload, but in addition also of a decrease in airways resistance and direct influence on arteriolar constriction in the pulmonary vascular bed. The beneficial effects upon pulmonary haemodynamics were equally recorded several months later.
In 10 patients with pulmonary hypertension, glycerol trinitrate in patch form (DEPONIT 10) effected a statistically significant drop in pulmonary artery pressure, pulmonary capillary pressure and right atrial pressure within 24 hours following drug application. This pressure reduction was also recorded after 4 weeks of continuous therapy. The reduction of pulmonary artery pressure and pulmonary vascular resistance is not only a consequence of improved pre- and afterload, but also of a decrease in respiratory tract resistance and a direct influence on arteriolar constriction in the pulmonary vascular bed. Beneficial effects upon pulmonary haemodynamics were also recorded several months later.
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During a period of 15 months we performed a laser therapy of bronchi stenosis due to malignant tumors in 28 patients. We used a Neodym-YAG-Laser (MBB-AT, Munich), guided through a fiberbronchoscope (Olympus BF-1 TR). 59% of total-stenoses and 83% of the partly occluded bronchi could be opened sufficiently. During a follow-up period of 12 months (mean 4.7 m) 83% of the bronchi remained open. According to our experience, fractional tissue removal is the method of choice rather than all-at-once coagulation since tissue edema may cause bronchial occlusion 1 to 3 days after treatment. We think, if surgical treatment is ruled out, intrabronchial laser coagulation is an alternative with little impairment of the patient to prevent hypoventilation and repair functional conditions.
In 28 patients PO2 and PCO2 were measured continuously during diagnostic fiberbronchoscopy by means of transcutaneous electrodes (PtcO2 and Ptc CO2 System TCM Radiometer Copenhagen). A mean decrease in PtcO2 of 31% (s +/- 16.5%) was found. This effect can be prohibited by using oxygen insufflation at a rate of 0.5 liters per minute by nasal tube. The positive effect of fiberbronchoscopic lavage in cases of severe dyscrinism is documented. A mean increase in PtcO2 of 42% was found after the procedure, but there is a time lag of 20-30 minutes until the maximal increase is reached. In patients with known but not acute bronchial asthma the irritation of the bronchial system by fiberbronchoscopy induces a histamine release. There is no relation between the release of histamine and the decrease in arterial oxygen tension.