Hypertension clinical presentation

Secondary Hypertension Clinical Presentation, Diagnosis, and Treatment, edited by George A. Mansoor, md, 2004 Pediatric Hypertension, edited by Ronald J. Portman, md, Jonathan M. Sorof, md, and Julie R. Ingelfinger, md, 2004... 

RJ is a 47-year-old man with a history of hypertension who presents to your clinic complaining of chest pain that occurred several times over the past few weeks. RJ describes his chest pain as "a heaviness." He states that it first occurred while he was mowing the grass. He later felt the same heavy sensation while raking leaves and again while carrying some boxes. The pain was located in the substernal area and radiated to his neck. The pain resolved after about 5 minutes of rest. 

Clinical Presentation of Cirrhosis and Complications of Portal Hypertension... 

Hypertensive encephalopathy is a classic feature of malignanthypertension. Its clinical presentation consists of severe headache, mental confusion, and apprehension. Blurred vision, nausea and vomiting, and focal neurologic deficits are common. If untreated, the syndrome may progress over a period of 12-48 hours to convulsions, stupor, coma, and even death. 

Cirrhosis and Portal Hypertension CHAPTER 21 I Clinical Presentation of Cirrhosis... 

In a South African study 20 children were identified as suffering from hepatic veno-occlusive disease thought to be caused by the administration of traditional remedies (3). The predominant clinical presentation was ascites and hepatomegaly. Nine children died. The surviving patients progressed to cirrhosis and portal hypertension. In four cases early urine specimens were available, and in all of these the presence of pyrrolizidine alkaloids was confirmed. 

Long after the discovery of renin in the late nineteenth century, the pathophysiology of arterial hypertension has been linked to the activation of vasoactive and salt-retaining hormones the neuroendocrine hypothesis has indeed been the base of a widely used paradigm (vaso-constriction/volume-dependent hypertension) to explain hypertensive pathophysiology and characterize different clinical presentations (Laragh, 1973 Johnson et al, 2005). 

III. Clinical presentation. Manifestations of intoxication result from generalized sympathetic depression and include pupillary constriction, lethargy, coma, apnea, bradycardia, hypotension, and hypothermia. Paradoxic hypertension, caused by stimulation of peripheral alpha-1 receptors, may occur with clonidine, oxymetazoline, and tetrahydrozoline (and possibly guanabenz) and is usually transient. The onset of symptoms is usually within 30-60 minutes, although peak effects may occur more than 6-12 hours after ingestion. Full recovery is usual within 24 hours. In an unusual massive overdose, a 28-year-old man who accidentally ingested 100 mg of clonidine powder had a three-phase intoxication over 4 days initial hypertension, followed by hypotension, and then a withdrawal reaction with hypertension. 

E. Clinical presentation of palytoxin poisoning may initially mimic ciguatera. However, palytoxin produces greater morbidity and mortality, due to severe muscle spasms, rhabdomyolysis, hypertension, and acute respiratory failure. 

III. Clinical presentation. The time course of intoxication by these dmgs is usually brief, with resoiution within 4-6 hours (unless sustained-release preparations are involved). The major toxic effect of these drugs is hypertension, which may lead to headache, confusion, seizures, and intracranial hemorrhage. 

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