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#211
25.07.2006, 16:14
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Усе... пошла в монастырь. Забыла про побочки лития. [Изображения доступны только зарегистрированным пользователям]
Утешает только одно - пациенты теперь от этого не пострадают  
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#212
25.07.2006, 16:38
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A 76-year-old man comes to the clinic because of "urine problems". He tells you that he has "trouble with his urinary stream," that over the past month it has been progressively decreasing in force. He also has the urgency to urinate and he finds himself running to the bathroom, but can only pass a small amount of urine. The trips to the bathroom have increased in frequency over the past couple of days and he has started to leak urine. The leakage is only in small amounts, but can occur at any time. Yesterday, he ruined a new pair of pants and is visibly upset and embarrassed. He has hypertension for which he takes a calcium channel blocker and he underwent a laparoscopic cholecystectomy a few months ago. His abdominal examination reveals a smooth, round suprapubic mass. Percussion of this mass is dull and causes the patient to leak urine per urethra. Penile examination is normal. Rectal examination reveals good sphincter tone with a moderately enlarged, smooth prostate (also unchanged from prior exams). Urine dipstick in the office is negative for glucose, RBC, WBC, and nitrites. You explain to the patient that the most likely primary cause of his incontinence is a/an
A. abnormal bladder sensation B. obstructing prostate C. uninhibited bladder contractions D. vesicocutaneous fistula E. weakened pelvic floor muscles
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#214
25.07.2006, 17:14
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The correct answer is B. The patient has overflow incontinence. The suprapubic mass is actually a distended bladder. The patient is unable to empty his bladder secondary to an enlarged prostate that is obstructing the flow of urine. The incontinence is the result of the failure of the bladder to empty. Male patients who present with outlet obstruction secondary to BPH typically have urinary infrequency, slow weak stream, and small volume voids. The residual urine level is high. In women the cause of overflow incontinence is due to detrusor hypotonicity, with poor emptying, typically from diabetes mellitus, autonomic neuropathy, or anticholinergic medication. The patient with "overflow" usually only urinates the urine that "spills" out. They have a persistently elevated amount of urine in the bladder (post-void residual) and only urinate when their already elevated bladder capacity is surpassed.
Abnormal bladder sensation (choice A) is caused by a number of different possibilities. An interruption in the normal innervation of the bladder may prevent it from storing or emptying. Etiology includes multiple sclerosis, Parkinson's disease, diabetes mellitus, or spinal injury. This patient does not provide a history of any of these nor does he have any physical findings that make any of these causes a high possibility. Urge incontinence is caused by an involuntary rise in intravesical pressure secondary to detrusor contraction, which overcomes outlet resistance. These are called uninhibited bladder contractions (choice C). This can occur from local bladder causes such as infection, bladder stones, bladder tumors, or foreign bodies. It may also occur from a loss of cortical inhibition of the voiding reflex from stroke, dementia or Parkinson's. A vesicocutaneous fistula (choice D) occurs when there is a direct communication between the bladder and the skin. These patients constantly leak urine, frequently from a site other than the urethra. There is frequently a history of radiation, trauma, or manipulation. Weakened pelvic floor muscles (choice E) is also called stress incontinence. It is characterized by the involuntary loss of urine associated with physical activities such as coughing, laughing, sneezing, or exercise. It usually occurs in female patients who have had multiple vaginal deliveries
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#215
25.07.2006, 17:15
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A 45-year-old woman collapses while in her bathroom and is brought to the hospital emergently. On arrival, she is non-responsive with dilated and fixed pupils bilaterally. Her temperature is 37.2 C (99 F), blood pressure is 220/110 mm Hg, pulse is 42/min, and respirations are 18/min. An emergent CT scan of the head reveals blood in all 4 ventricles. An intracranial bolt is placed for intracranial pressure (ICP) monitoring and she is brought to the operating room for decompression craniotomy. After the procedure, she is brought to the intensive care unit where she does well for 48 hours. Her ICP begins to fall and she shows some signs of neurological recovery. On postoperative day number 2 her mental status again deteriorates. There is no new blood present on CT scan. The most appropriate management is to
A. administer nimodipine, intravenously B. administer pressors, intravenously C. administer verapamil, intravenously D. provide no therapy at this time E. return her to the operating room
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#216
25.07.2006, 17:22
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В задаче не сказано про уровень АД на момент ухудшения ментального статуса на 2 день. По-видимому, ответ D (?)
Хотя я слабый специалист по послеоперационному ведению геморрагических инсультов  P.S. В 94 году (на момент обучения неврологии) в память врезалась цифра летальности при геморрагических инсультах - 95%.
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#217
25.07.2006, 17:54
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A....
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#218
25.07.2006, 18:05
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Опять разрываюсь: на этот раз между А и Е.
Хотя VENUS и не показал особых преимуществ нимодипина, дизайн этого исcледования предполагал его (нимодипина) раннее применение у ВСЕХ больных. А тут - по факту ухудшения состояния... С другой стороны, геморрагический инсульт с прорывом в желудочки все-таки не то же самое, что субарахноидальное кровотечение...
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#219
25.07.2006, 18:10
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Цитата:
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#220
25.07.2006, 18:53
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The correct answer is A. This patient has suffered a devastating subarachnoid bleed. The most common non-traumatic cause of SAH is rupture of a preexisting aneurysm. The mortality rate of these bleeds is high, but in managing these patients much has been learned about how to minimize morbidity in the first post-bleed weeks. This patient had a vasospasm. This is a nearly universal event after a SAH since the blood in the CSF is an irritant. The treatment shown to have fairly good benefit is the calcium channel blocker nimodipine. No other blocker, including verapamil (choice C), has been shown to be beneficial.
Starting intravenous pressors (choice B) in these patients is the next management step after nimodipine. This is done to maximize cerebral perfusion pressure (mean arterial pressure minus ICP) in an attempt to maintain cerebral perfusion. Not more than a few years ago, vasospasm was not treated since, many thought that the deterioration after bleeding was the natural history of the disease. Not initiating therapy (choice D) is no longer the standard of care. Since there is no sign of new blood on the CT scan, there is no reason to return to the operating room (choice E).
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#221
25.07.2006, 18:58
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A 68-year-old male is brought to the emergency department because of substernal chest pain. On interview, the patient reports having a past myocardial infarction 5 years ago. He has typical anginal pain, when climbing stairs and when lifting heavy objects, that is relieved by taking nitroglycerin tablets and resting. In the last week, however, his anginal symptoms have become more frequent and occur when walking even short distances. In the hospital, the patient continues having chest pain over his left side accompanied by shooting pain in his left arm. His blood pressure is160/90 mm Hg, pulse is 109/min, and oxygen saturation is 96%. Physical examination is unremarkable. A chest x-ray is clear with normal cardiac size. An electrocardiogram shows Q-waves in leads II, III, and AvF and T-wave inversions in v1-v3. Laboratory studies show a potassium of 3.2 mEq/L, hematocrit of 42%, and initial cardiac markers are negative. The patient receives oxygen, an aspirin, a beta-blocker, intravenous heparin, and is placed on a platelet gp IIb/IIIa inhibitor. In addition, he is made pain-free on intravenous nitroglycerin. A repeat electrocardiogram without pain is unchanged. The most appropriate next step in management is
A. admission to the hospital and observation for 48 hours B. coronary angiography C. emergent coronary artery bypass graft (CABG) D. intra-aortic balloon pump
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#223
25.07.2006, 19:14
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В. Пациент рассматриваетс как относящийся к группе высокого риска, даже несмотря на отрицательные cardiac markers.
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#224
25.07.2006, 19:39
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The correct answer is B. The patient's presentation is highly worrisome for an acute coronary syndrome and therefore requires a coronary angiogram. From his past medical history, the patient has known coronary artery disease. His recent history is a classic description of crescendo angina. On presentation, he complains of chest pain at rest and negative cardiac markers indicating likely unstable angina. His vital signs are stable and there is no evidence of acute congestive heart failure or pulmonary edema by CXR and oxygen saturation. The EKG indicated an old inferior myocardial infarction, but more importantly, the EKG shows T-wave inversions in the anteroseptal precordial leads. This may suggest critical left main coronary artery disease or stenosis (Wallen sign). The patient needs to undergo coronary angiography for several reasons. First, data has shown improved outcomes in patients with unstable angina and primary coronary intervention, so if there is a culprit lesion that can be fixed, (i.e., by stenting), it should be. Secondly, the anterior wall of the left ventricle is at risk. The patient has already had damage to his right ventricle (inferior Q waves), and now his left wall is threatened. Third, the EKG indicates Wallen sign: T-wave inversions in v1-v3 or v4. This correlates to possible left main coronary artery (LMCA) disease. LMCA stenosis risks both the anterior wall and the lateral wall of the left ventricle. Due to the large area at risk, the patient must undergo CABG , and not PTCA. However, without coronary angiography, it is unknown whether the patient has LMCA disease or a proximal LAD lesion.
It is inappropriate to admit him for observation only (choice A). Although the patient has been placed on adequate medications and may potentially improve on medical management, several studies have shown improved outcomes in patients taken to catheterization with acute coronary syndromes. In addition the EKG suggests that the anterior wall may be at risk and this would have serious consequences if allowed to proceed to infarction. The goal is to re-establish perfusion to that area as soon as possible. The patient is stable and it is not known for certain whether or not he requires a CABG (choice C) for LMCA. If he simply has a proximal LAD lesion, he can undergo PCI without a need for cardiac surgery. His vital signs are stable and he is not in cardiogenic shock. In addition, he has no history of valvular disease. Therefore, there is no indication for an intra-aortic balloon pump (choice D). Criteria for thrombolytics (choice E) requires ST segment elevations >1 mm in 2 contiguous leads, ST segment depressions >2mm in the anterior leads (v1-v2), or new left-bundle branch block. The patient does not meet these criteria.
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#225
25.07.2006, 19:40
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A 4-year-old boy is brought to the office because he has refused to walk for the past 24 hours. He was well until yesterday afternoon when he woke from a nap complaining of feeling "wobbly". When his parents got him up to walk he was extremely unsteady and they needed to hold him to keep him from falling over. He has not improved at all over the last day. His unsteadiness persists when he is sitting down. His temperature is 37.0 C (98.6 F), pulse is 100/min, and respirations are 24/min. He has horizontal nystagmus, which is worse at the extremes of gaze. He appears markedly ataxic and his gait is broad based. He has no papilledema. If obtained, the information that would be most pertinent to his current condition is
A. concomitant diarrhea B. a cousin with a brain tumor C. a history of varicella infection 3 weeks ago D. previous history of epilepsy in this patient E. recent streptococcal pharyngitis
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Линейный вид
