The importance of race in medical student performance of an AIDS risk assessment interview with simulated patients.

INTRODUCTION: This study was done to ascertain the effect of race on medical student-patient communication. The primary hypothesis was that interviewing performance scores would be higher when race of student and race of simulated patient instructor (SPI) were concordant than when they were discordant. METHODS: Data obtained from student interactions with four Caucasian and four African American female SPIs participating in a case involving an AIDS risk assessment interview were analysed. Performance was assessed using two instruments: an 8-item behaviourally anchored interviewing skills scale and a 14-item checklist reflecting content relevant to sexual behaviour and AIDS risk. SPI groups were comparable and SPIs were trained to a high level of inter-rater reliability. Students (24 African American and 180 non-African American) were assigned to SPIs based on the spelling of the student's name. Performance was scored independently at the conclusion of each interview by both the SPI and the student her/himself. RESULTS: African American students had lower scale scores than non-African American students in interactions with Caucasian (but not African American) SPIs; and all student scores, both on the skills scale and the content checklist, were higher with African American than with Caucasian SPIs (as assessed by both SPI and student). Women students had higher scores than men. CONCLUSIONS: Race of SPI has an influence on student performance of an AIDS risk assessment interview. Further studies focusing on racial interactions in the medical interview are required. It appears that race of SPI may need to be accounted for in the development and interpretation of SPI-based clinical competence exams.

Training students in education of the hypertensive patient: enhanced performance after a simulated patient instructor (SPI)-based exercise.

The process whereby a physician explains to the ill patient what has gone wrong and what can be done about it can be taught and evaluated by simulated patients (SPIs). This study was designed to determine whether a training experience in educating a diabetic SPI improves subsequent performance with a hypertensive SPI. Competence in educating a hypertensive SPI by students who had no prior training experience (n = 26) was compared to that of an experimental group (n = 20) that had a prior training session. Performance was assessed with a counseling skills scale and a case-specific content checklist (1 = poor to 5 = excellent). Students in the experimental group performed better than controls in both counseling skills (4.46 v 3.86, P < .01) and completeness of coverage of content (3.28 v 2.65, P < .01). Students in both groups focused more on clinical features and treatment than on laboratory testing and follow-up. The ability to counsel "patients" with hypertension can be enhanced by a prior learning experience with a diabetic SPI. Clinical application of knowledge about hypertension can be assessed by SPIs.

Teaching smoking-cessation counseling to medical students using simulated patients.

OBJECTIVE: Our objective was to evaluate the effectiveness of using simulated patient instructors and the Ockene method to instruct third-year medical students in smoking-cessation counseling techniques. DESIGN: We used a clinical exercise with self-study preparation and simulated patient instructors. METHODS: One hundred fifty-nine students participated in a smoking-cessation counseling session in which cognitive and behavioral endpoints were assessed by simulated patient instructors and the students themselves. RESULTS: Student performance in the cognitive and behavioral components of model smoking-cessation counseling was acceptable. Specific areas of weakness, such as the tendency of students to underemphasize the personal and social benefits of smoking cessation, and to overestimate their competence on a number of skill items, were identified. Student evaluation of the exercise was positive. CONCLUSIONS: Smoking-cessation counseling can be taught effectively to third-year medical students by simulated patient instructors during a clinical clerkship.

The effect of a standardized patient instructor experience on students' anxiety and confidence levels performing the male genitorectal examination.

BACKGROUND: Standardized patient instruction (SPI) is recommended as a nonthreatening method for teaching the male genitorectal examination. The article's purpose is to describe the method's effectiveness in reducing anxiety and increasing confidence among men and women students from diverse cultures. DESCRIPTION: We implemented an SPI program in 1993 to teach the examination to 2nd-year students. Students performed their examinations in mixed gender groups of three; a man student was responsible for disrobing the SPI and performing the first exam. During the 45-min session, each of the three students performed the examination in turn, and each received immediate feedback on their technique and interpersonal approach to the patient. EVALUATION: All students (n = 190) evaluated their SPI encounter immediately after the session had ended. CONCLUSIONS: Men and women students from all ethnic groups reported decreased anxiety and increased confidence levels after the SPI session. These findings indicate that a carefully orchestrated SPI session is effective in reducing students' anxiety about crossing personal space boundaries, overcoming a variety of proscriptions on gender-appropriate interactions, and increasing their confidence to perform this sensitive examination.

Effect of circulating epinephrine on platelet function and hematocrit.

We investigated the effect of raising arterial plasma epinephrine within the lower pathophysiological concentration range on various indicators of blood platelet function and hematocrit. Epinephrine was raised over 60 minutes by a stepwise increasing intravenous infusion in 40 healthy men aged 20 to 40 years. Platelet count increased progressively with increasing arterial epinephrine to a maximal change of 69 +/- 6 x 10(9)/L in EDTA-anticoagulated blood and a maximal change of 42 +/- 6 x 10(9)/L in acid-citrate-dextrose (ACD)-anticoagulated blood, and the weight of circulating platelets increased by 29% (P < .001). Platelet size increased significantly in EDTA and decreased in ACD, and the difference between EDTA and ACD was significant (P < .0001) for both count and size, suggesting that epinephrine not only recruits platelets into the circulation but also induces some microaggregation in vivo or adhesion ex vivo. Aggregation of platelets in vitro induced by epinephrine decreased (P < .003 for delta optical density and P = .038 for maximal optical density) after epinephrine infusion compared with saline but did not change when stimulated with ADP or collagen. These findings suggest a selective downregulation of the epinephrine-activating mechanisms concomitant with a rise in the platelet content of epinephrine by 81% (P < .001) and no change in the platelet sodium-proton membrane exchange. The release of granular content (beta-thromboglobulin and platelet factor 4) to the circulation in response to epinephrine was not significant. Thus, under acute conditions it seems that the platelets may protect themselves against inappropriate overstimulation by epinephrine. The importance of platelet epinephrine uptake is still unknown, but sodium-proton exchange does not seem to be involved in regulating the effects of circulating epinephrine on platelet function. Epinephrine has a pronounced effect on raising hematocrit (maximal change of 1.74 +/- 0.13 x 10(-2), P < .0001).

Sympathetic nervous system involvement in essential hypertension: increased platelet noradrenaline coincides with decreased beta-adrenoreceptor responsiveness.

Platelet catecholamine content may reflect integrated plasma catecholamine concentrations over time. The present study aimed at examining sympathetic nervous system (SNS) involvement in essential hypertension by assessing platelet noradrenaline (NA) and typically beta-adrenoreceptor mediated responses to adrenaline (A) infusion as indices of sympathetic tone. Healthy white men were recruited by public advertising and screening (mean +/- SD): Hypertensives (n = 13, sitting blood pressure [BP] 153 +/- 13/106 +/- 7 mmHg, age 34 +/- 5 years, weight 83 +/- 10 kg) were compared to normotensives (n = 13, sitting BP 114 +/- 9/75 +/- 9 mmHg, age 30 +/- 6 years [n.s.], weight 82 +/- 9 kg [n.s.]). Loss of platelet granular contents (including NA) prior to analysis was minimized by studying young subjects (age range 20-40 years, minimal atherosclerosis), using arterial blood sampling, and processing blood immediately. These procedures resulted in plasma beta-thromboglobulin and platelet factor 4 levels which were not significantly different between groups. Sympathetic activation resulting from stress was minimized by not labelling subjects as either hypertensive or normotensive. Mean arterial platelet NA content was significantly higher in hypertensives (64 +/- 31 pg/mg of platelet weight) compared to normotensives (43 +/- 20 pg/mg, p < 0.05) both at baseline and following 35% expansion of the circulating platelet pool by A infusion (p < 0.05) and correlated with arterial NA in the hypertensives (r = 0.79, p < 0.002) but not in the normotensives (r = 0.04, n.s.). Similar increases in platelet and plasma A during infusion in both groups suggest unchanged platelet uptake capacity and plasma clearance in the hypertensive group.(ABSTRACT TRUNCATED AT 250 WORDS)

Ketanserin's sympatholytic and serotonin2-receptor blocking actions precede the hypotensive effects.

The hypotensive action of ketanserin in humans remains incompletely defined but may be mediated by factors unrelated to vascular alpha 1 or serotonin2-receptor blockade. We examined the effects of ketanserin on indices of sympathetic drive, alpha 1- and serotonin2-receptor responses, and sympathetic tone in 13 elderly men with mild hypertension. Studies were performed after ten days and six weeks of double-blind assignment to placebo and ketanserin 40 mg twice daily. An eight week long single-blind, placebo washout period separated the double-blind phases. In the entire group, ketanserin lowered BP and heart rate significantly after six weeks but not at ten days. In contrast, plasma noradrenaline, an index of sympathetic drive, and platelet aggregation in response to 1 microM serotonin, an index of serotonin2-receptor antagonism, declined significantly after both ten days and six weeks (P < 0.05) on ketanserin versus placebo. Mean BP after six weeks on ketanserin fell to > 10% in seven patients (responders) and to < 10% in six subjects (nonresponders). Responders had higher baseline SBPs and heart rates compared with nonresponders. Even in responders, BP was reduced at six weeks but not after ten days on ketanserin versus placebo. Plasma and platelet noradrenaline, plasma renin activity, and platelet responses to serotonin at baseline and during ketanserin did not distinguish between responders and nonresponders. Ketanserin reduces sympathetic drive and antagonizes serotonin2-receptors in the short term. The relationship of these actions to the hypotensive effect of ketanserin, which is delayed and dependent on the initial BP, is unclear.

Evaluation of self-measured home vs. clinic intra-arterial blood pressure.

Home blood pressure (BP) monitoring is useful in the clinical management of patients with hypertension and the identification of those with "white-coat" hypertension; i.e. high readings in the clinic but normal BP at home. In the process of evaluating this technique, we compared self-measured home BP with intra-arterial BP. Healthy white men (n = 40) of 20-40 years of age and body weight below 95 kg were recruited by advertising in the local newspaper. Following a standardized procedure, performed within 2-4 weeks of a response to the advertisement, BP was measured by a physician at a clinic screening, by the subject at home (14 readings in 7 days) and finally in the clinic concomitantly intra-arterially and oscillometrically. The correlation coefficient for mean (M) home BP (r = 0.73) and oscillometric BP (r = 0.74) against intra-arterial BP were slightly higher than for screening BP (r = 0.65). However, in plots of the differences for individual MBP between the methods against the average of the methods, it appears that at levels of average MBP above 100 mmHg, screening BP overestimates the BP level, while this was not the case for home BP or oscillometric BP. Thus, by using intra-arterial measurement as standard of comparison, subject self-measured home BP is a reliable method of estimating blood pressure level in young men. Home BP measured shortly after screening and recruitment provides useful information of resting BP in subjects who potentially may have initial anxiety about BP measurement.

Effects of lovastatin treatment on red blood cell and platelet cation transport.

Hypercholesterolemia frequently accompanies hypertension, and it has been suggested that by affecting membrane lipid composition, hypercholesterolemia may cause or accentuate abnormalities in several red blood cell transports associated with hypertension. Such an effect might obfuscate the relation of membrane markers to hypertension and decrease their usefulness in genetic studies of the heritable basis of hypertension. To determine if changing plasma lipids affects membrane transport, we studied the effects of the cholesterol-lowering agent lovastatin on red blood cell lithium-sodium countertransport and sodium-potassium-chloride cotransport, red blood cell sodium and water content, and platelet amiloride-sensitive volume responsiveness to cytoplasmic acidification, an indirect measure of sodium-proton exchange that has been proposed as a new membrane marker for hypertension. In a 24-week, placebo-controlled, double-blinded, randomized trial, lovastatin significantly lowered total and low density lipoprotein cholesterol and raised high density lipoprotein cholesterol. Red blood cell lithium-sodium countertransport and sodium-potassium-chloride cotransport were not significantly altered. Red blood cell sodium content decreased significantly in the lovastatin-treated group, probably as a result of an increase in red blood cell sodium-potassium pump activity. Platelet amiloride-sensitive responses to cytoplasmic acidification were significantly depressed by lovastatin treatment, suggesting that lowering plasma cholesterol may suppress platelet sodium-proton exchange. It has been hypothesized that the hyperlipidemias frequently observed in essential hypertensive patients may alter membrane lipid composition and affect membrane cation transport activities.(ABSTRACT TRUNCATED AT 250 WORDS)

Platelet function during antihypertensive treatment with quinapril, a novel angiotensin converting enzyme inhibitor.

The effect of various antihypertensive medications on platelet function is of increasing interest. Conflicting effects of captopril on platelet function are reported and the impact of angiotensin converting enzyme (ACE) inhibitors not containing a sulfhydryl group such as enalapril, lisinopril, and quinapril on platelet function remains unstudied. Therefore, the aim of the present study was to examine the effect of antihypertensive treatment with quinapril, a novel ACE inhibitor not containing a sulfhydryl group, on platelet function. Ten white men (age range of 32-61 years) with untreated mild-to-moderate essential hypertension (supine diastolic blood pressure greater than 95 mm Hg) were treated with 4 weeks each of placebo and quinapril in a double-blind, randomized, crossover design. Quinapril (20 mg twice a day) significantly lowered systolic (p less than 0.01) and diastolic blood pressure (p less than 0.01) without any significant effect on heart rate or plasma catecholamines. No significant change was noted for in vitro platelet aggregation induced by epinephrine, ADP, or collagen. Plasma concentrations of the platelet release factors beta-thromboglobulin and platelet factor 4 did not change, nor did the platelet content of norepinephrine, platelet weight (mg/10 ml of blood), circulating platelet count, or platelet size. Thus, as assessed by a broad spectrum of platelet parameters, we found that antihypertensive treatment with quinapril has no significant effect on platelet function in patients with mild-to-moderate essential hypertension. These "platelet-neutral" properties of quinapril suggest that quinapril, both from a thromboembolic and a hemostatic point of view, may be a rather safe agent for treatment of hypertension.

Artefacts in measurement of blood pressure and lack of target organ involvement in the assessment of patients with treatment-resistant hypertension.

OBJECTIVE: To determine the relative importance of factors known to cause therapy-resistant hypertension, and to derive an efficient approach to the evaluation of this problem in clinical practice. DESIGN: Consecutive sample. SETTING: University hospital hypertension clinic and clinical research center. PATIENTS: Fifteen patients referred for management of refractory hypertension and found to have a seated diastolic blood pressure greater than 95 mm Hg while taking a standard dose of hydrochlorothiazide, propranolol, and hydralazine or its equivalent for at least 4 weeks. MEASUREMENTS AND MAIN RESULTS: Seven patients (group 1) had normal, resting mean intra-arterial blood pressure (mean pressure less than 107 mm Hg) and eight had elevated pressure (group 2). Patients in group 1 had minimal or not target organ involvement whereas those in group 2 had higher minimum vascular resistance by forearm plethysmography and greater interventricular septal wall thickness. Factors contributing to resistant hypertension, particularly in group 1, were "office hypertension" (clinic systolic blood pressure at least 20 mm Hg higher than home systolic blood pressure), pseudohypertension (cuff diastolic blood pressure at least 15 mm Hg higher than simultaneously determined intra-arterial pressure), and "cuff-inflation hypertension" (intra-arterial diastolic blood pressure rise of at least 15 mm Hg during cuff inflation). CONCLUSION: Home blood pressure monitoring and echocardiography are recommended as initial steps in the evaluation of patients with resistant hypertension. Intra-arterial blood pressure measurement is particularly helpful in patients with resistant hypertension who do not have office hypertension yet have normal septal thickness on echocardiography.