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Pharmacy版 - 散尽家财 求心率衰竭特效药!谢谢!
相关主题
请教考过NAPLEX的同学恳请大家帮忙几个翻译
宝宝9个月回国,小儿麻痹疫苗要不要在当地吃求关于治疗MRSA的药
上过学的请帮看看P1第二学期中间生娃可以不,这是我们的curriculum问问,NAPLEX的PK部分
rotation小感-the last lecture请问: 抗生素那一章要掌握到什么程度
Residency 面试 SOAP note 考题 (答案48小时后登出)OMG,上了贼船了。。。
包子求推荐:入门级的cancer therapy相关书籍 (转载)dose and dose strength
问个也是关于可达龙和心脏大家帮我看要选哪个Specialty track?
血压控制的目标是什么???strep throat 用amoxicillin的dosage regimen应该是怎样的?
相关话题的讨论汇总
话题: hf话题: patients话题: heart话题: digoxin
进入Pharmacy版参与讨论
1 (共1页)
s*********i
发帖数: 916
1
不好意思麻烦大家
我外婆86岁 现在高烧在医院 说是得了感冒 但实际上一直都有心率衰竭的病
现在日渐严重 有时候全身浮肿 全身乏力 说话都没有劲
我是菜鸟一个 不知道什么药理病理 到专业药版来求求大家
谁好心告诉我 在美国这边 有没有心率衰竭的特效药 或者是急救药什么的
我也知道老人年岁大了 到时候了 但是外婆对我的疼爱 使我不能就这么轻易说放弃
总要尽最大努力和最大孝心
麻烦大伙告知药名 什么途径才能买到 我知道在美国这类处方药不是轻易能到手的
回帖的都发包子 谢谢大伙费心帮忙了!
c*******n
发帖数: 1214
2
At the moment, use furosemide to reduce the edema and work load of heart may
be OK. For a 86 year old heart failure patient, use digoxin may help the
quality of life.
f****o
发帖数: 2770
3
这个病没得治的,能活到86岁不错了。
如果她平时没有吃什么beta-blocker和其他一些maintenance的药的话,现在都住院了
,那很有可能就不行了。
不是什么病都有特效药的,特别是到了现在这个地步。
而且就算能买到药,你知道吃什么strength,dose,frequency么?这种事情不是你写在
网上我们就能做出therapeutic regimen recommendation的。
你还是告诉医院让他们治疗吧。如果不行了也没办法。而且会死的很突然。
你要是想尽最大努力和最大孝心,如果真要死,还是开始准备后事吧。
r****e
发帖数: 148
4
楼上朋友的话听得让人难受,更何况是对一位想尽力尽点小心的人.
楼主不要伤心, 目前这种情况医院肯定是会紧急处理的,而且现代医学都有成熟的常规
处理方案, 国内外差别应该不会很大.我想如果是在国内几个大城市,特别是省会城市,
医疗设施和条件都不会太差, 要相信此时正在为你外婆尽力抢救的医生和护士.
而且就象普通看病, 必须要医生看到病人,亲自检查诊断才能做出合适的处理. 任何医
生都不能仅凭几页纸的检查报告为病人提供诊疗的建议.这是对保护患者应尽的职业规
范.
而药师本来就不具处方权,更不能随便给您提出治疗药用药建议.这也是为了对您外婆负
责.请见谅!
愿您外婆能顺利脱离险境,转危为安.
f****o
发帖数: 2770
5
我讲话难听由于家庭遗传,真不好意思。
我吧书本上的东西全部贴出来,你能看懂多少算多少吧。
Heart Failure
DEFINITION
Heart failure (HF) is a clinical syndrome caused by the inability of the
heart to pump sufficient blood to meet the metabolic needs of the body.
Heart failure can result from any disorder that reduces ventricular filling
(diastolic dysfunction) and/or myocardial contractility (systolic
dysfunction).
PATHOPHYSIOLOGY
Causes of systolic dysfunction (decreased contractility) are reduction in
muscle mass (e.g., myocardial infarctio
f****o
发帖数: 2770
6
GENERAL PRINCIPLES
The first step in managing chronic HF is to determine the etiology or
precipitating factors. Treatment of underlying disorders (e.g., anemia,
hyperthyroidism) may obviate the need for treatment of HF.
Nonpharmacologic interventions include cardiac rehabilitation and
restriction of fluid intake (maximum 2 L/day from all sources) and dietary
sodium (approximately 1.5 to 2 g of sodium per day).
Stage A: The emphasis is on identifying and modifying risk factors to
prevent developm
f****o
发帖数: 2770
7
heart failure的药美国有的国内基本上也都有,其实没有必要从美国弄的。
现在已经住院了就让医院处理吧。maintenance med和emergency treatment都是不一样
的。
现在这个阶段你可以看看你外婆有什么未完成的愿望,可以让她生前实现,如果突然去
了不会有遗憾。heart failure prognosis是很难断定的,很多临终的病人都会死的很
突然。
如果这次能救过来,每天都要吃diuretic+ACE inhibitor+beta blocker+digoxin
药量这些都是要医生根据你外婆的情况来做出决定的。这些药都不是什么新药,国内都
会有的。
每天都要吃,可以缓解symptom, slow disease progress,但是根治是不可能的。
s*********i
发帖数: 916
8
谢谢你 麻烦你这么费心了 ^-^

【在 f****o 的大作中提到】
: heart failure的药美国有的国内基本上也都有,其实没有必要从美国弄的。
: 现在已经住院了就让医院处理吧。maintenance med和emergency treatment都是不一样
: 的。
: 现在这个阶段你可以看看你外婆有什么未完成的愿望,可以让她生前实现,如果突然去
: 了不会有遗憾。heart failure prognosis是很难断定的,很多临终的病人都会死的很
: 突然。
: 如果这次能救过来,每天都要吃diuretic+ACE inhibitor+beta blocker+digoxin
: 药量这些都是要医生根据你外婆的情况来做出决定的。这些药都不是什么新药,国内都
: 会有的。
: 每天都要吃,可以缓解symptom, slow disease progress,但是根治是不可能的。

r****e
发帖数: 148
9
呵, 看来说话难听的人未必不是好人. :) 但说话好听点不是会更好吗?
多谢指教!
u**********l
发帖数: 2036
10
2楼板斧说的挺好,很有经验
利尿降低心脏负荷+地高辛增强心力
需密切监控用药,
国内省级大医院心内科处理心力衰竭应该都相当专业
这方面没有什么其他特效药,但考验医生的水平
我估计感冒发烧好了就可以过关
bless
相关主题
包子求推荐:入门级的cancer therapy相关书籍 (转载)恳请大家帮忙几个翻译
问个也是关于可达龙和心脏求关于治疗MRSA的药
血压控制的目标是什么???问问,NAPLEX的PK部分
进入Pharmacy版参与讨论
s*********i
发帖数: 916
11
谢谢大家这么帮忙 我相信我外婆一定会挺过这一关的!
再次谢谢大家 捐100伪币到版面上 支持所有像这样热心费心解答大家问题的好人!
c*******n
发帖数: 1214
12
Thanks a lot for the donation!
s*********i
发帖数: 916
13
不好意思麻烦大家
我外婆86岁 现在高烧在医院 说是得了感冒 但实际上一直都有心率衰竭的病
现在日渐严重 有时候全身浮肿 全身乏力 说话都没有劲
我是菜鸟一个 不知道什么药理病理 到专业药版来求求大家
谁好心告诉我 在美国这边 有没有心率衰竭的特效药 或者是急救药什么的
我也知道老人年岁大了 到时候了 但是外婆对我的疼爱 使我不能就这么轻易说放弃
总要尽最大努力和最大孝心
麻烦大伙告知药名 什么途径才能买到 我知道在美国这类处方药不是轻易能到手的
回帖的都发包子 谢谢大伙费心帮忙了!
c*******n
发帖数: 1214
14
At the moment, use furosemide to reduce the edema and work load of heart may
be OK. For a 86 year old heart failure patient, use digoxin may help the
quality of life.
f****o
发帖数: 2770
15
这个病没得治的,能活到86岁不错了。
如果她平时没有吃什么beta-blocker和其他一些maintenance的药的话,现在都住院了
,那很有可能就不行了。
不是什么病都有特效药的,特别是到了现在这个地步。
而且就算能买到药,你知道吃什么strength,dose,frequency么?这种事情不是你写在
网上我们就能做出therapeutic regimen recommendation的。
你还是告诉医院让他们治疗吧。如果不行了也没办法。而且会死的很突然。
你要是想尽最大努力和最大孝心,如果真要死,还是开始准备后事吧。
r****e
发帖数: 148
16
楼上朋友的话听得让人难受,更何况是对一位想尽力尽点小心的人.
楼主不要伤心, 目前这种情况医院肯定是会紧急处理的,而且现代医学都有成熟的常规
处理方案, 国内外差别应该不会很大.我想如果是在国内几个大城市,特别是省会城市,
医疗设施和条件都不会太差, 要相信此时正在为你外婆尽力抢救的医生和护士.
而且就象普通看病, 必须要医生看到病人,亲自检查诊断才能做出合适的处理. 任何医
生都不能仅凭几页纸的检查报告为病人提供诊疗的建议.这是对保护患者应尽的职业规
范.
而药师本来就不具处方权,更不能随便给您提出治疗药用药建议.这也是为了对您外婆负
责.请见谅!
愿您外婆能顺利脱离险境,转危为安.
f****o
发帖数: 2770
17
我讲话难听由于家庭遗传,真不好意思。
我吧书本上的东西全部贴出来,你能看懂多少算多少吧。
Heart Failure
DEFINITION
Heart failure (HF) is a clinical syndrome caused by the inability of the
heart to pump sufficient blood to meet the metabolic needs of the body.
Heart failure can result from any disorder that reduces ventricular filling
(diastolic dysfunction) and/or myocardial contractility (systolic
dysfunction).
PATHOPHYSIOLOGY
Causes of systolic dysfunction (decreased contractility) are reduction in
muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies,
and ventricular hypertrophy. Ventricular hypertrophy can be caused by
pressure overload (e.g., systemic or pulmonary hypertension, aortic or
pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation,
shunts, high-output states).
Causes of diastolic dysfunction (restriction in ventricular filling) are
increased ventricular stiffness, ventricular hypertrophy, infiltrative
myocardial diseases, myocardial ischemia and infarction, mitral or tricuspid
valve stenosis, and pericardial disease (e.g., pericarditis, pericardial
tamponade).
The most common underlying etiologies are ischemic heart disease,
hypertension, or both.
As cardiac function decreases, the heart relies on the following
compensatory mechanisms: (1) tachycardia and increased contractility through
sympathetic nervous system activation; (2) the Frank-Starling mechanism,
whereby increased preload increases stroke volume; (3) vasoconstriction; and
(4) ventricular hypertrophy and remodeling. Although these compensatory
mechanisms initially maintain cardiac function, they are responsible for the
symptoms of heart failure and contribute to disease progression.
The neurohormonal model of HF recognizes that an initiating event (e.g.,
acute MI) leads to decreased cardiac output but that the HF state then
becomes a systemic disease whose progression is mediated largely by
neurohormones and autocrine/paracrine factors. These substances include
angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine
vasopressin, and proinflammatory cytokines (e.g., tumor necrosis factor &#
206;±, interleuleins-6 and interleukins-1Î2), endothelin-1.
Common precipitating factors that may cause a previously compensated patient
to decompensate include noncompliance with diet or drug therapy, coronary
ischemia, inappropriate medication use, cardiac events (e.g., MI, atrial
fibrillation), and pulmonary infections.
Drugs may precipitate or exacerbate HF because of their negative inotropic,
cardiotoxic, or sodium-retaining properties.
CLINICAL PRESENTATION
The patient presentation may range from asymptomatic to cardiogenic shock.
The primary symptoms are dyspnea (particularly on exertion) and fatigue,
which lead to exercise intolerance. Other pulmonary symptoms include
orthopnea, paroxysmal nocturnal dyspnea, tachypnea, and cough.
Fluid overload results in pulmonary congestion and peripheral edema.
Nonspecific symptoms may include nocturia, hemoptysis, abdominal pain,
anorexia, nausea, bloating, ascites, and mental status changes.
P.72
Physical examination findings may include pulmonary crackles, an S3 gallop,
pleural effusions, Cheyne-Stokes respiration, tachycardia, cardiomegaly,
peripheral edema, jugular venous distention, hepatojugular reflux, and
hepatomegaly.
DIAGNOSIS
A diagnosis of HF should be considered in patients exhibiting characteristic
signs and symptoms. A complete history and physical examination with
appropriate laboratory testing are essential in the initial evaluation of
patients suspected of having HF.
Ventricular hypertrophy can be demonstrated on chest x-ray or
electrocardiogram (ECG).
The New York Heart Association (NYHA) Functional Classification System is
intended primarily to classify symptomatic HF patients according to the
physician's subjective evaluation. Functional class (FC)-I patients have no
limitation of physical activity, FC-II patients have slight limitation, FC-
III patients have marked limitation, and FC-IV patients are unable to carry
on physical activity without discomfort.
The recent American College of Cardiology/American Heart Association (ACC/
AHA) staging system provides a more comprehensive framework for evaluating,
preventing, and treating HF (Figure 8-1).
DESIRED OUTCOME
The therapeutic goals for chronic HF are to improve symptoms and quality of
life, reduce symptoms, reduce hospitalizations, slow disease progression,
and prolong survival.
f****o
发帖数: 2770
18
GENERAL PRINCIPLES
The first step in managing chronic HF is to determine the etiology or
precipitating factors. Treatment of underlying disorders (e.g., anemia,
hyperthyroidism) may obviate the need for treatment of HF.
Nonpharmacologic interventions include cardiac rehabilitation and
restriction of fluid intake (maximum 2 L/day from all sources) and dietary
sodium (approximately 1.5 to 2 g of sodium per day).
Stage A: The emphasis is on identifying and modifying risk factors to
prevent development of structural heart disease and subsequent HF.
Strategies include smoking cessation and control of hypertension, diabetes
mellitus, and dyslipidemia according to current treatment guidelines. ACE
inhibitors should be strongly considered for antihypertensive therapy in
patients with multiple atherosclerotic vascular risk factors.
Stage B: In these patients with structural heart disease but no symptoms,
treatment is targeted at minimizing additional injury and preventing or
slowing the remodeling process. In addition to treatment measures outlined
for stage A, patients with a previous MI should receive both ACE inhibitors
and Î2 blockers regardless of the ejection fraction (EF). Patients with
reduced EFs (less than 40%) should also receive both agents, regardless of
whether they have had an MI.
Stage C: Patients with structural heart disease and previous or current HF
symptoms may also have their symptoms classified according to the NYHA
P.73
system. Most patients should be treated routinely with four medications: an
ACE inhibitor, a diuretic, a beta2 blocker, and digoxin (see Figure 8-2).
Aldosterone receptor antagonists, angiotensin-receptor blockers (ARBs), and
hydralazine/isosorbide dinitrate are useful in selected patients. Other
general measures include moderate sodium restriction, daily weight
measurement, immunization against influenza and pneumococcus, modest
physical activity, and avoidance of medications that can exacerbate HF.
Standard First-Line Therapies
Angiotensin-Converting Enzyme Inhibitors
ACE inhibitors (see Table 8-1) decrease angiotensin II and aldosterone,
attenuating many of their deleterious effects, including reducing
ventricular remodeling, myocardial fibrosis, myocyte apoptosis, cardiac
hypertrophy,
P.74
P.75
norepinephrine release, vasoconstriction, and sodium and water retention.
Hemodynamic effects observed with long-term therapy include significant
increases in cardiac index, stroke work index, and stroke volume index, as
well as significant reductions in left ventricular filling pressure,
systemic vascular resistance (SVR), mean arterial pressure (MAP), and heart
rate. Significant improvements in clinical status, functional class,
exercise tolerance, left ventricular size, and mortality are also well
documented.
Blockers
Beneficial effects Î2 blockers may result from slowing or reversing the
detrimental ventricular remodeling caused by sympathetic simulation,
decreased myocyte death from catecholamine-induced necrosis or apoptosis,
antiarrhythmic effects, and prevention of other effects of sympathetic
nervous system activation. These drugs consistently increase left
ventricular ejection fraction, decrease ventricular mass, and reduce
systolic and diastolic volumes.
There is overwhelming evidence that stable patients initiated on low doses
of a Î2 blocker with slow upward dose titration over several weeks
derive significant benefits, including slowed disease progression and
reduced hospitalizations and mortality. Many studies (but not all) have also
shown improvement in NYHA functional class, patient symptom scores or
quality-of-life assessments, and exercise performance.
The ACC/AHA guidelines recommend use of Î2 blockers in all patients
with stable systolic HF unless they have a contraindication or have been
shown clearly to be unable to tolerate Î2 blockers. Patients should
receive a Î2 blocker even if symptoms are well controlled with an ACE
inhibitor and diuretic because they remain at risk for disease progression.
Because greater benefit is seen at higher doses, patients should be titrated
to target doses when possible. However, even lower doses have benefits over
P.76
placebo, so inability to titrate to the target dose is not justification to
discontinue therapy.
On the basis of clinical trial data, therapy should be limited to carvedilol
, metoprolol CR/XL, or bisoprolol. It cannot be assumed that immediate-
release metoprolol will provide benefits equivalent to metoprolol CR/XL.
Because bisoprolol is not available in the necessary starting dose of 1.25
mg, the choice is typically limited to either carvedilol or metoprolol CR/XL
. On the basis of regimens proven in large clinical trials to reduce
mortality, initial and target oral doses are as follows:
Bisoprolol, 1.25 mg daily initially; target dose, 10 mg daily.
Carvedilol, 3.125 mg twice daily initially; target dose, 25 mg twice daily (
the target dose for patients weighing more than 85 kg is 50 mg twice daily).
Metoprolol succinate CR/XL, 12.5 to 25 mg daily initially; target dose, 200
mg daily.
Doses should be doubled approximately every 2 weeks or as tolerated until
the target dose or the highest tolerated dose is reached.
Diuretics
Compensatory mechanisms in HF stimulate excessive sodium and water retention
, often leading to systemic and pulmonary congestion. Consequently, diuretic
therapy is indicated for all patients with evidence of fluid retention.
However, because they do not alter disease progression or prolong survival,
they are not considered mandatory therapy for patients without fluid
retention.
Thiazide diuretics (e.g., hydrochlorothiazide) are relatively weak diuretics
and are used alone infrequently in HF. However, thiazides or the thiazide-
like diuretic metolazone can be used in combination with a loop diuretic if
needed to promote effective diuresis.
Loop diuretics (furosemide, bumetanide, torsemide) are the most widely used
diuretics for HF. In addition to acting in the thick ascending limb of the
loop of Henle, they induce a prostaglandin-mediated increase in renal blood
flow that contributes to their natriuretic effect. Unlike thiazides, loop
diuretics maintain their effectiveness in the presence of impaired renal
function, although higher doses are necessary.
Doses of loop diuretics above the recommended ceiling doses produce no
additional diuresis in HF. Thus, once those doses are reached, more frequent
dosing should be used for additional effect, rather than giving
progressively higher doses.
Ranges of doses and ceiling doses for loop diuretics in patients with
varying degrees of renal function are listed in Table 8-2.
Digoxin
In patients with HF and supraventricular tachyarrhythmias such as atrial
fibrillation, digoxin should be considered early in therapy to help control
ventricular response rate.
For patients in normal sinus rhythm, digoxin does not improve survival, but
its positive inotropic effects, symptom reduction, and its effect on symptom
reduction and quality-of-life improvement are evident in patients with mild
to severe HF. Therefore, it should be used together with other standard HF
therapies (ACE inhibitors, Î2 blockers, and diuretics) in patients with
symptomatic HF. Consideration should be given to adding it after
instituting Î2-blocker therapy so that digoxin-associated bradycardia
does not preclude Î2-blocker use.
Most of the benefit from digoxin is achieved at low plasma concentrations.
For most patients, the target plasma digoxin concentration should be 0.5 to
1 ng/mL. Most patients with normal renal function can achieve this level
with a dose of 0.125 mg/day. Patients with decreased renal function, the
elderly, or those receiving interacting drugs (e.g., amiodarone) should
receive 0.125 mg every other day. In the absence of supraventricular
tachyarrhythmias, a loading dose is not indicated because digoxin is a mild
inotropic agent that produces gradual effects over several hours, even after
loading.
f****o
发帖数: 2770
19
heart failure的药美国有的国内基本上也都有,其实没有必要从美国弄的。
现在已经住院了就让医院处理吧。maintenance med和emergency treatment都是不一样
的。
现在这个阶段你可以看看你外婆有什么未完成的愿望,可以让她生前实现,如果突然去
了不会有遗憾。heart failure prognosis是很难断定的,很多临终的病人都会死的很
突然。
如果这次能救过来,每天都要吃diuretic+ACE inhibitor+beta blocker+digoxin
药量这些都是要医生根据你外婆的情况来做出决定的。这些药都不是什么新药,国内都
会有的。
每天都要吃,可以缓解symptom, slow disease progress,但是根治是不可能的。
s*********i
发帖数: 916
20
谢谢你 麻烦你这么费心了 ^-^

【在 f****o 的大作中提到】
: heart failure的药美国有的国内基本上也都有,其实没有必要从美国弄的。
: 现在已经住院了就让医院处理吧。maintenance med和emergency treatment都是不一样
: 的。
: 现在这个阶段你可以看看你外婆有什么未完成的愿望,可以让她生前实现,如果突然去
: 了不会有遗憾。heart failure prognosis是很难断定的,很多临终的病人都会死的很
: 突然。
: 如果这次能救过来,每天都要吃diuretic+ACE inhibitor+beta blocker+digoxin
: 药量这些都是要医生根据你外婆的情况来做出决定的。这些药都不是什么新药,国内都
: 会有的。
: 每天都要吃,可以缓解symptom, slow disease progress,但是根治是不可能的。

相关主题
请问: 抗生素那一章要掌握到什么程度大家帮我看要选哪个Specialty track?
OMG,上了贼船了。。。strep throat 用amoxicillin的dosage regimen应该是怎样的?
dose and dose strengthLong-term healthcare pharmacy
进入Pharmacy版参与讨论
r****e
发帖数: 148
21
呵, 看来说话难听的人未必不是好人. :) 但说话好听点不是会更好吗?
多谢指教!
u**********l
发帖数: 2036
22
2楼板斧说的挺好,很有经验
利尿降低心脏负荷+地高辛增强心力
需密切监控用药,
国内省级大医院心内科处理心力衰竭应该都相当专业
这方面没有什么其他特效药,但考验医生的水平
我估计感冒发烧好了就可以过关
bless
s*********i
发帖数: 916
23
谢谢大家这么帮忙 我相信我外婆一定会挺过这一关的!
再次谢谢大家 捐100伪币到版面上 支持所有像这样热心费心解答大家问题的好人!
c*******n
发帖数: 1214
24
Thanks a lot for the donation!
M***e
发帖数: 40
25
Bless!
美国这边有的治心衰的药国内都有,都是非常成熟的药物,我想你外婆的医生现在应该
focus on 控制症状。像digoxin (地高辛)如果你外婆这样的情况要用药,应该要做
血药浓度监控的,所以我们能帮忙的也有限,相信医生,他们会尽力的。
LZ也不要太着急,我的一位亲人也是心衰,10年内数次报病危,但每次都平安挺过来,
祝你外婆平安。

【在 s*********i 的大作中提到】
: 不好意思麻烦大家
: 我外婆86岁 现在高烧在医院 说是得了感冒 但实际上一直都有心率衰竭的病
: 现在日渐严重 有时候全身浮肿 全身乏力 说话都没有劲
: 我是菜鸟一个 不知道什么药理病理 到专业药版来求求大家
: 谁好心告诉我 在美国这边 有没有心率衰竭的特效药 或者是急救药什么的
: 我也知道老人年岁大了 到时候了 但是外婆对我的疼爱 使我不能就这么轻易说放弃
: 总要尽最大努力和最大孝心
: 麻烦大伙告知药名 什么途径才能买到 我知道在美国这类处方药不是轻易能到手的
: 回帖的都发包子 谢谢大伙费心帮忙了!

f******k
发帖数: 5329
26
治心衰的药都很传统。
b**o
发帖数: 5769
27
很多学医学药的人刚开始的时候都会有这些缺点的吧。一腔热情有时候反而会被人误解
的。
我们上Practice课的时候还有特别讲过。
一个例子就是一个intern在pharmacy实习,关门的时候看见一个妇人在很着急地找温度
计。
然后他们就帮她,她说自己的小孩发烧而且有抽搐。intern说自己当时下巴都要掉下来
了,
就想说不得了,你还在这里做什么,赶紧回家送小孩去急诊。可是preceptor却很
镇静,告诉她抽搐已经是很严重的状况了,建议她立刻离开回家送小朋友去急诊。
还有一个例子是有病人来问intern,说自己尿多,口渴,没有精力,求推荐复合维他命
。Intern
差点就说你可能有糖尿病,需要看医生。可是他慎重考虑了,告诉她,她的症状不是复
合维他命能缓解的,需要去看医生,请她尽快约PCP。没有提糖尿病。
所以说做为health care provider,说话还是要很小心的,既要解释清楚,又要考虑到
病人/家属的心情。我们都需要好好学习!

【在 r****e 的大作中提到】
: 呵, 看来说话难听的人未必不是好人. :) 但说话好听点不是会更好吗?
: 多谢指教!

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