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Labile hypertension

Elevated blood pressure is usually caused by a combination of several abnormalities (multifactorial). Epidemiologic evidence points to genetic inheritance, psychological stress, and environmental and dietary factors (increased salt and decreased potassium or calcium intake) as perhaps contributing to the development of hypertension. Increase in blood pressure with aging does not occur in populations with low daily sodium intake. Patients with labile hypertension appear more likely than normal controls to have blood pressure elevations after salt loading. [Pg.226]

A 30-year-old man who had taken olanzapine 20 mg/ day for 10 days developed typical neuroleptic malignant syndrome with raised body temperature (39.7°C), obtundation, tremor, rigidity, sweating, fluctuating pupillary diameter, tachycardia, labile hypertension, raised serum creatine kinase activity, and severe hypernatremia (190 mmol/1) (108). [Pg.309]

Some individuals, however, have a condition called labile hypertension, in which blood pressure stays up longer than it should. Those men and women are likely to experience increases in blood pressure more frequently than others, responding more dramatically to the stress and anxiety that everyone has to one degree or another. [Pg.29]

It has central depressant and sedative actions and a primarily peripheral antihypertensive effect accompanied by bradycardia. It is also used for the management and treatment of hypertensive specifically in patients with mild labile hypertension associated with tachycardia. [Pg.837]

A fatality has been reported in a 49-year-old man taking ritonavir 200 mg twice daily and indinavir 800 mg twice daily in addition to stavu-dine and lamivudine. After taking three tablets of Cafergot (ergotamine tartrate 1 mg and caffeine 100 mg) his headache worsened, he developed progressive lower extremity weakness, severe peripheral vasoconstriction, labile hypertension and livedo reticularis (skin discolouration due to underlying capillary changes). He lapsed into coma and on day 5 was declared brain dead . ... [Pg.601]

With regard to the clinical manifestations. Sack and Koll distinguish asymptomatic forms, paroxysmal hypertension, permanent hypertension, extremely labile hypertension, and the malignant phaeochromocytoma (phaeochromoblastoma) with metastases. The latter are rare and show hormonal activity only in some cases. By far the most frequently... [Pg.92]

A 45-year-old man presented to hospital with a 1-month history of a pruritic, papular, violaceous rash that started on thighs and progressively spread to back, upper limbs and lower legs. Four months prior the pahent suffered a type A aortic dissection that was treated surgically. He was positive for labile hypertension and was... [Pg.268]

The syntheses, structures and properties of wide varieties of metal nitrosyl complexes have been well documented [4, 5, 20-23]. However, the bulk of the complexes reviewed previously are of academic interest and only a few of these metal nitrosyl complexes have been considered as biologically effective NO donors. It was observed that the metal nitrosyls with significant NO+ character are subject to attack from a variety of nucleophiles and have hypertensive properties. This could be due to the strong trans- labilizing effect of NO. In contrast, the metal nitrosyl compounds with the general formula [M(CN)5NO]n, where the NO ligand was either neutral (for M = Co) or anionic (for M = Cr) showed no vasodilatory effect [24]. [Pg.109]

Less labile metal ions can be used to control the levels of biologically active ligands in the body. Thus Fe(III) in sodium nitroprusside delivers NO to tissues and is used for the treatment of hypertension and control of blood pressure. The possibility arises of utilizing Ru(III) to scavenge NO in the treatment of septic shock. [Pg.186]

Steroids have mineralocorticoid and glucocorticoid effects. Betamethasone has little, if any, mineralocorticoid effect. However, it should be used with caution in patients predisposed to hypertension since mineralocorticoid effects may lead to sodium and water retention and an increase in blood pressure. When used systemically, especially at high doses, steroid therapy is associated with a risk of psychiatric reactions such as euphoria, irritability, mood lability and sleep disorders. Glucocorticoid side-effects include diabetes and osteoporosis. [Pg.332]

Symptoms Hyperarousal anxiety, irritability, insomnia, restlessness Autonomic lability sweating, tachycardia, hypertension, tremor, dizziness... [Pg.475]

At higher doses, cocaine can produce undesirable effects, including tremor, emotional lability, restlessness, irritability, paranoia, panic, and repetitive stereotyped behavior. At even higher doses, it can induce intense anxiety, paranoia, and hallucinations, along with hypertension, tachycardia, ventricular irritability, hyperthermia, and respiratory depression. In overdose, cocaine can cause acute heart failure, stroke, and seizures. Acute intoxication with cocaine produces these various clinical effects, depending on the dose these effects are mediated by inhibition of the dopamine transporter and in turn by the effects of excessive dopamine activity in dopamine synapses, as well as by norepinephrine and serotonin in their respective synapses. [Pg.505]

In summarizing evidence for the participation of deranged sympatho-adrenal ( neurogenic ) factors in human hypertension, it must be concluded that such factors have been conclusively demonstrated only in cases of pheochromocytoma, central nervous system trauma, and increased intracranial pressure. There is presumptive evidence that neurogenic factors may be important during the early, labile phases of essential hypertension and that the effects of this early sympatho-adrenal activity may lead to a persistent hypertension on a renal basis later in life. However, the development of hypertension through this or any other mechanism occurs only in individuals predisposed by some completely unknown, but probably hereditary, influence. [Pg.30]

Phenacylthiazolium derivatives, relatively readily prepared from phenacyl bromide and an appropriate thiazole, react with dicarbonyls and make the C-C bond between them labile.602 This is thought to take place as depicted in Scheme 14.3. Phenacylthiazolium compounds have shown promise in preclinical studies of vascular stiffness and have reached Phase II clinical trials for systolic hypertension.603... [Pg.166]

A 67-year-old man with bipolar disorder became confused, delirious, and manic (99). His only medications were olanzapine 10 mg/day and divalproex sodium 500 mg bd. On day 6, typical neuroleptic malignant syndrome developed. He had a fever (39.9°C), obtundation, rigidity, tremor, sweating, fluctuating pupillary diameter, labile tachycardia and hypertension, hypernatremia, and raised serum creatine kinase. Olanzapine was withdrawn and the syndrome resolved by day 12. [Pg.309]

Hypertension, whether labile or fixed, borderline or definite, casual or basal, systolic or diastolic, at any age regardless of gender is the most common and a powerful contributor to atherosclerotic coronary vascular disease. Morbidity and mortality increase progressively with the degree of elevation of either systolic or diastolic pressure and pulse pressure, and no discernible critical value exists (see Chap. 13). Numerous trials have documented the reduction in risk associated with blood pressure lowering however, most of these studies show that mortality and morbidity reduction is a result of fewer strokes and... [Pg.271]

Fig. 5.9 Prediction of infarct growth. A 65-year-old man, improving clinically at 5 h postictus, was monitored in the Neurology ICU based on his labile blood pressure, a fixed left M2 occlusion on CTA, and a significant core/penumbra mismatch on CTP/MRP. His 24-h follow-up DWI showed a small infarction. However, 24 h after cessation of hypertensive therapy there was infarct growth into the region of penumbra. Admission CTA (top) CTP (CBV/CBF/ MTT) at 4.5 h second row) MR-perfusion weighted imaging (MR-PWI) (CBV/CBF/MTT) at 5.25 h (third row) DWI at 24 h (fourth row) and follow-up DWI at 48 h (bottom). The CTP and MR-PWI demonstrate a mismatch between the CBV (no abnormality) and the CBF/MTT penumbra (arrows). After cessation of hypertensive therapy, the DWI abnormahty grows into the region predicted by the CBF/MTT maps... Fig. 5.9 Prediction of infarct growth. A 65-year-old man, improving clinically at 5 h postictus, was monitored in the Neurology ICU based on his labile blood pressure, a fixed left M2 occlusion on CTA, and a significant core/penumbra mismatch on CTP/MRP. His 24-h follow-up DWI showed a small infarction. However, 24 h after cessation of hypertensive therapy there was infarct growth into the region of penumbra. Admission CTA (top) CTP (CBV/CBF/ MTT) at 4.5 h second row) MR-perfusion weighted imaging (MR-PWI) (CBV/CBF/MTT) at 5.25 h (third row) DWI at 24 h (fourth row) and follow-up DWI at 48 h (bottom). The CTP and MR-PWI demonstrate a mismatch between the CBV (no abnormality) and the CBF/MTT penumbra (arrows). After cessation of hypertensive therapy, the DWI abnormahty grows into the region predicted by the CBF/MTT maps...
P.A induces synthesis of polyclonal antibodies in B lymphocytes of human and mouse origin, and it is probably a T-cell-regulated polyclonal activator of human B cells. It is chemotactic, blocks heat-labile and heat-stable opsonins, activates or inhibits complement fixation (depending on the dose) and has hypertensive activity when injected in some animals and humans. [Pg.558]

The clinical symptoms of phaeochromocytoma and of paraganglioma, whether occurring in the form of paroxysmal attacks or simulating a labile or a permanent hypertension, are largely explained by the abnormal output of catecholamines by the tumour tissues. Symptoms and development are modified by the magnitude, the duration, and by the composition of the augmented excretion. [Pg.95]


See other pages where Labile hypertension is mentioned: [Pg.222]    [Pg.194]    [Pg.29]    [Pg.307]    [Pg.109]    [Pg.963]    [Pg.222]    [Pg.194]    [Pg.29]    [Pg.307]    [Pg.109]    [Pg.963]    [Pg.30]    [Pg.80]    [Pg.27]    [Pg.79]    [Pg.338]    [Pg.655]    [Pg.1230]    [Pg.1269]    [Pg.511]    [Pg.98]    [Pg.53]    [Pg.17]   
See also in sourсe #XX -- [ Pg.29 ]




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