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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty four cases with myocardial rupture among 259 patients with autopsy after death due to myocardial infarction, were compared with patients with acute myocardial infarction and death secondary to other causes. Myocardial rupture occured during the first 72 hours in 58% of the patients and all cases within the first five days. Two thirds of the patients were males and 46% were 70 years of age. There were 24 myocardial ruptures (9.5%). Previous history of arterial hypertension and un-remittent anginal pain were predisposing factors for rupture (p=0.05). Other previously reported bad prognostic factors such as persistent hipertension after acute infarction, severe exercise before infarction and history of Diabetes Mellitus were not statistically significant in this study. Ruptured myocardium was not influenced by a previous history of myocardial infarction, hospitalization delay in the C.C.U., administration of anticoagulants, digitalis or pressor amines. There was no significant difference among the groups compared in enzyme curves or magnitude of leucocytosis. Electromechanic dissociation, sinus bradycardia, nodal rhythm followed by idioventricular rhythm and asystole, were observed following myocardial rupture.
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PMID:[Rupture of the free wall of the heart as cause of death in acute myocardial infarct]. 66 44

In a second-year family medicine course taught using simulated patients the students commented most favourably on the clinical relevance of the topics, the enthusiasm of teachers, and the opportunity to interview simulated patients with their fellow students, in contrast to their basic science courses, which did not give them patient contact. They felt most confident about skills acquired in relation to diseases with a limited number of key symptoms, signs and treatments (meningitis, otitis) and less confident about diseases with many symptoms and treatments (diabetes, trauma, arrhythmias). They made few comments about alternative cases which might have been selected. Their adverse comments were about the workload. During tutor meetings over 4 years, a key concern which emerged was to find cases with a level of complexity suitable to the students. The tutors emphasized these principles of case selection: the cases should be based on real life and include most of the signs and symptoms of the disease; contain one or at most two foci; have nodal decision-making points; emphasize clinical reasoning; reinforce prior knowledge; permit the transfer of knowledge to other cases; and permit the assessment of associated technical skills.
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PMID:Teaching medicine with cases: student and teacher opinion. 161 45

Fifteen cases of chronic heart block were studied. Eight of them could be designated as idiopathic or primary heart block; the others were associated with hypertension, diabetes and ischaemic heart disease, either singly or in various combinations. In six cases, the whole heart was available for histopathological study of the conduction system. In the other 9 cases, only a portion of the heart muscle was available for examination. A V nodal fibrosis extending upto the proximal bundle of His was seen in all the six whole heart autopsy materials. Fibrosis of the adjacent myocardium was seen in five cases. In three cases, conducting system fibrosis was associated with atherosclerotic (1 case) or diabetic changes (3 cases) of the intramural vessels. In the 9 partial autopsy studies, myocardial fibrosis was seen in two cases, diabetic microangiopathy in one and atherosclerotic changes in two including an old thrombus in one. Thus, diabetic microangiopathy was seen in total four cases. These changes may be responsible for the cardiomegaly and cardiac failure associated with conduction defects observed in diabetes. In the idiopathic group also, heart block could be considered as a significant facet of a primary myocardial degenerative process.
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PMID:Cardiac changes implicated in chronic heart block. 181 5

Acute reversible diabetic nerve dysfunction has been associated with a reversible myo-inositol-related (Na+ + K+)-ATPase defect, while poorly reversible chronic nerve dysfunction correlates with progressive axoglial dysjunction of peripheral nerve. The causal relationships between biochemical and neuroanatomical abnormalities and those of nodal membrane function are not known. Nodal clamp examinations were carried out in the sciatic nerve of diabetic BB-rats to elucidate the events underlying diabetic nerve dysfunctions and how these relate to metabolic and structural defects of diabetic nerve. With increasing duration of diabetes, there was a progressive decline in nodal action potentials attributable to decreased Na+ permeability and a decrease in the membranous Na+ gradient. Vigorous insulin therapy in short-term (6-week) diabetic BB-rats normalized the Na+-permeability defect and the membranous Na+ gradient. These defects did not reverse in long-term (24-week) diabetic animals subjected to the same treatment. This poorly reversible nodal dysfunction accounts for the not readily reversible conduction defect in chronic diabetes and is probably directly related to irreversible axoglial dysjunction.
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PMID:Reversible and irreversible nodal dysfunction in diabetic neuropathy. 243 93

The chronic complications of diabetes are thought to be caused by an interaction between hyperglycemia, or other metabolic consequences of insulin deficiency, and independent genetic or environmental factors that are poorly defined. Several potentially relevant biochemical sequelae to hyperglycemia have been identified in tissue susceptible to diabetic complications. Among these, a rise in tissue sorbitol secondary to concentration-dependent activation of polyol pathway activity by glucose, and an accompanying fall in tissue myo-inositol and Na-K-ATPase activity have recently been linked to a self-reinforcing cyclic metabolic defect that accounts for rapidly reversible slowing of conduction in peripheral nerve in diabetes. Impaired Na-K-ATPase activity also appears to be responsible for intracellular Na+ accumulation and resultant localized axonal paranodal swelling that characterizes diabetic neuropathy in both humans and laboratory animals. These swellings are thought to be responsible for the subsequent disruption of the nodal apparatus (axo-glial disjunction) and some component of the loss of large and small myelinated fibers. Recent studies have suggested that microvascular insufficiency may also contribute to diabetic neuropathy, especially in non-insulin-dependent diabetes. Aldose reductase activity is concentrated in endoneurial vessels, and similar biochemical mechanisms (ie, sorbitol accumulation, myo-inositol deficiency, and impaired Na-K-ATPase activity) are thought to be operative in the endoneurial microvessels in diabetes. Administration of an aldose reductase inhibitor to patients with diabetic neuropathy is associated with repair of damaged nerve fibers and the appearance of newly generated fibers, presumably secondary to metabolic correction within the nerve fibers themselves or their supporting microvasculature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pathogenesis and prevention of diabetic neuropathy and nephropathy. 282 23

The effect of pancreatic islet cell allotransplantation on the development of diabetic neuropathy in streptozocin-induced diabetic ACI rats was examined morphometrically with light- and electron-microscopic procedures. Peripheral nerve function was evaluated by nerve conduction velocity and evoked muscle potential amplitude measurements. Diabetes was induced at 4 mo of age, and diabetic animals were transplanted by intracerebral and intraportal grafts 2 wk later. Diabetic animals with accepted grafts returned to euglycemia and showed a normal body-weight gain over the subsequent 14-mo observation period. Transplanted animals with accepted grafts and those in whom graft rejection was induced were compared with age-matched nontransplanted diabetic rats and nondiabetic control rats at 18 mo of age. Successful allotransplantation completely prevented axonal atrophy and the characteristic nodal and paranodal structural abnormalities in diabetic nerve, as well as the typical slowing of nerve conduction velocity. Our data suggest that islet cell allotransplantation is an effective therapeutic approach to the prevention of diabetic neuropathy.
Diabetes 1988 Aug
PMID:Diabetic neuropathy in STZ-induced diabetic rat and effect of allogeneic islet cell transplantation. Morphometric analysis. 313 64

A 65-year-old male with diabetes, hypertension, and mild renal failure developed dizziness and syncope one week after starting clonidine 0.45 mg/day. A continuous ECG recording revealed sinus bradycardia, nodal rhythm, and multiple episodes of sinus arrest lasting up to 4.5 seconds. Upon discontinuation of clonidine, serial continuous ECG recordings revealed gradual decrease in the number and duration of the sinus arrest episodes, until their complete disappearance shortly after the third day off clonidine. This report shows that clonidine may cause a concentration-dependent sinus node dysfunction in addition to the atrioventricular (AV) node abnormalities previously ascribed to it.
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PMID:Sinus arrest associated with clonidine therapy. 334 61

Between 1973 and 1983, 43 patients with histologically proven unresectable pancreatic carcinoma were irradiated in the UCLA Department of Radiation Oncology. Ten patients received irradiation alone and 33 were nonrandomly assigned to receive chemotherapy in addition to irradiation. Of those patients receiving chemotherapy, 30 were given 5-fluorouracil and three were given a combination of agents. Forty-one of the 43 patients have died with a median survival of 7 months. Actuarial survival at 1 and 2 years was 24% and 3%. Local control was achieved in three of 43 patients. Two patients are alive with no evidence of disease at 11 and 30 months. The median survivals with and without chemotherapy were 9.5 and 4 months, respectively (p = 0.06). Survival dependent on nodal status, surgical bypass, primary site, and dose are also reported. No significant differences were found. Acute complications were noted in 23 patients but were a reason for discontinuing therapy in none. Late complications were noted in nine patients. Six patients with an upper gastrointestinal hemorrhage or a small bowel obstruction all had local recurrence. There were two patients with posttreatment diabetes mellitus and one with pancreatitis. The limits of conventional therapy for unresectable pancreatic cancer have been reached. Creative sequencing of induction combination chemotherapy, newer radiation modalities, and maintenance chemotherapy are required if systemic and local progression of this lethal disease is to be eliminated.
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PMID:Results in the management of locally unresectable pancreatic carcinoma. 348 45

Conduction velocity of rat sciatic nerve, estimated both in vivo and in vitro, did not change during 2--21 weeks following induction of diabetes by injection of streptozotocin. During this period blood sugars were in the range 17.6--30.4 mM and symptoms of uncontrolled diabetes were noted. The failure of velocity to decrease contrasts strongly with several previous reports, while the failure to increase with age may be explained with the aid of published morphometric data. Experiments on nerve fibers isolated from streptozotocin-diabetic rats rats confirmed that the nerve function was normal in respect of action and resting potential. Potential clamp analysis of nodal membrane similarly indicated that these fibres had normal permeability properties.
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PMID:Analysis of peripheral nerve function in streptozotocin diabetic rats. 625 6

Verapamil, a potent calcium antagonist, possesses varied systemic effects, including smooth muscle relaxation leading to both peripheral and coronary artery vasodilation, slowed atrioventricular nodal conduction and decreased insulin release from the pancreatic B cells. Reports concerning the effects of acute intoxication with verapamil are scarce. A case is presented of a 22 year old woman who developed profound hyperglycemia and metabolic acidosis after the inadvertent overdose of thirty 80 mg tablets (2,400 mg) of verapamil. This case illustrates the need for physicians to be aware of verapamil's inhibitory effects on insulin release and to exercise special care when prescribing verapamil in patients with preexisting diabetes mellitus.
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PMID:Profound hyperglycemia and metabolic acidosis after verapamil overdose. 635 45


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