Diseases » Cerebral Arteriosclerosis » Diagnosis

Diagnosis of Cerebral Arteriosclerosis

Diagnostic Test list for Cerebral Arteriosclerosis:

The list of medical tests mentioned in various sources as used in the diagnosis of Cerebral Arteriosclerosis includes:

• CT scan
• MRI scan

Cerebral Arteriosclerosis Diagnosis: Book Excerpts

• Ask the Following Questions - HYPERTENSION
• Differential Diagnosis - Hypertension
• Differential Diagnosis - Carotid Bruits
• Differential Diagnosis - Hypertension
• Differential Diagnosis - Umbilicus – Single Umbilical Artery
• Approach to the Diagnosis - HYPERTENSION
• History and physical examination
  - Blood pressure increase [Hypertension]
• Diagnosis - Hypertension
• Diagnosis - Pregnancy-induced hypertension
• Diagnosis - Pulmonary hypertension
• Diagnosis - Renovascular hypertension
• History and physical examination - Blood pressure increase [Hypertension]
• History - Hypertension
• History - Stroke
• Differential Overview - Hypertension
• Differential Overview
  - Stroke Syndromes
• Differential Overview - Arterial Pulse Variants
• Differential Overview - Carotid Bruit
• Diagnosis - Hypertension
• Diagnosis - Stroke
• Diagnosis - Hypertension, pregnancy-induced
• Diagnosis - Pulmonary hypertension
• Clinical Features and Diagnosis - Hypertension
• History and physical examination - Blood pressure, increased [Hypertension]
• Approach to the Diagnosis - HYPERTENSION

Tests and diagnosis discussion for Cerebral Arteriosclerosis:

Computer tomography (CT) and magnetic resonance imaging (MRI) can help reveal the presence of cerebral arteriosclerosis before stroke or hemorrhage occurs. (Source: excerpt from NINDS Cerebral Arteriosclerosis Information Page: NINDS)

Diagnostic Tests for Cerebral Arteriosclerosis: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Cerebral Arteriosclerosis.

HYPERTENSION: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is there systolic hypertension only? The presence of an elevated systolic pressure only would suggest hyperthyroidism, aortic insufficiency, and atherosclerotic aortitis.
2. Is the hypertension paroxysmal? The presence of paroxysmal hypertension should suggest a pheochromocytoma.
3. Is there a normal or low blood pressure in the lower extremities? These findings would suggest a coarctation of the aorta.
4. Is there a flank mass? The presence of a flank mass should suggest hypernephroma, hydronephrosis, and polycystic kidneys.
5. Are there abnormalities of the urinary sediment? These findings suggest glomerulonephritis, collagen disease, Henoch-Schönlein purpura, and chronic nephritis. All primary care physicians should have this capability in their office.

DIAGNOSTIC WORKUP

Routine diagnostic tests include a CBC, sedimentation rate, chemistry panel, total and high-density lipoprotein (HDL) cholesterol, a VDRL test, urinalysis including microscopic, a urine culture with colony count and sensitivity, and an EKG, chest x-ray, and flat plate of the abdomen for kidney size.

If these are normal, a nephrologist should be consulted before undertaking expensive diagnostic tests. It may be wise to observe the results of treatment before further testing also.

Additional tests that may be ordered are an intravenous pyelogram, a 24-hr urine catecholamine, a serum cortisol, a plasma renin level, a 24-hr urine aldosterone determination, a cystoscopy, and retrograde pyelography. A 24-hr free cortisol may be more useful in diagnosing Cushing's syndrome than serum free cortisone. Renal angiography used to be done more frequently, but should be considered in sudden onset of hypertension in the elderly and in hypertension that is resistant to treatment.

Twenty-four-hr blood pressure monitoring can be useful both in diagnosis and in evaluating the results of therapy. Magnetic resonance angiography is a good noninvasive alternative to renal angiography.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Hypertension: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Essential hypertension (95% of cases)
  –Associated with obesity, decreased physical activity, stress, and diets high in sodium or low in potassium, calcium, and/or magnesium
• Medications (e.g., oral contraceptives, pseudoephedrine, steroids, ephedrine, NSAIDs)
• Sleep apnea
• Secondary hypertension
  –Chronic renal disease
  –Renal vascular disease (e.g., renal artery atherosclerosis, fibromuscular dysplasia)
  –Cushing's disease
  –Pheochromocytoma
  –Primary hyperaldosteronism
  –Hyperthyroidism
  –Coarctation of aorta: Arm pulses are stronger than leg pulses and blood pressure is significantly higher in arms than in legs
  • “White coat” hypertension
  • Pain, stress (e.g., surgery, emotional), and postexercise
  • Isolated systolic hypertension
    –More common in elderly
    –Stronger risk factor for heart disease than
    diastolic hypertension in patients >50
  • Excessive alcohol use
  • Cocaine use
  • Malignant hypertension
    –Markedly elevated blood pressure (diastolic BP >120–140 mmHg associated with papilledema)
  • Preeclampsia/eclampsia
  • Pregnancy-induced hypertension
  • Congenital adrenal hyperplasia

  Workup and Diagnosis

  • History and physical examination, including evaluation of risk factors (e.g., history of diabetes, family history of heart disease, smoking, elevated cholesterol, drug use, stress, pain, obesity, body mass index)
  • Evaluate for end organ disease (target organ damage): CAD symptoms, vascular disease, retinal hemorrhage, retinal venous crossing changes, heart exam (murmurs, gallops), lung exam (signs of CHF)
    –Labs may include urinalysis, basic metabolic panel (electrolytes, glucose, BUN/creatinine), calcium, lipids, ECG, echocardiogram, glomerular filtration rate measurement, and urinary albumin (albumin:creatinine ratio)
    • Consider secondary causes of hypertension if sudden onset of hypertension, significant hypertension (>180/110), abnormally young (<30) or old (>50) patient, presence of end-organ symptoms, or poor response to treatment (not controlled with three medications)
      –Elevated creatinine suggests renal parenchymal disease
      –Abdominal bruits and hypokalemia suggest renal vascular disease
      –Cushing's disease is associated with osteoporosis, obesity, muscle weakness, moon facies, hirsutism, elevated lipids and sugar, low potassium
      –Pheochromocytoma is associated with extremely labile blood pressure (episodic or paroxysmal HTN), headaches, palpitations, and diaphoresis
      –Primary hyperaldosteronism is associated with isolated low potassium and non-anion gap metabolic alkalosis
    '>

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Source: In a Page: Signs and Symptoms, 2004

Carotid Bruits: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Internal carotid artery stenosis
• External carotid artery stenosis
• Normal (nonstenotic), yet tortuous, carotid arteries
• Heart murmur with radiation to the neck (e.g., aortic stenosis)
• Excessive compression of the stethoscope over the neck vessels, resulting in deformity of vessel wall and turbulence
• Hyperthyroidism
  –Results in hyperdynamic circulation, tachycardia, and hypertension
• Takayasu's arteritis
  –Decreased pulses and bruits may occur over the abdominal aorta, carotid arteries, brachial arteries, and subclavian arteries
• Fisher's contralateral systolic bruit
  –Heard over the carotid bifurcation, eyeball, and/or skull on the “normal side” due to increased flow, as the “silent” side is completely occluded

Workup and Diagnosis

• Complete history and physical exam, with special attention to cardiac risk factors, TIA symptoms, cardiovascular exam, and neurologic exam
  –Bruit pitch increases as stenosis worsens, but may become silent when full occlusion occurs
  –Amaurosis fugax: Described as a “shade coming down over the eye” contralateral to the stenosis
• Laboratory evaluation includes lipid panel, CBC, glucose, electrolytes, homocysteine level (an independent risk factor for stroke), vitamin B₁₂ and folate levels, TSH, and ESR
• Carotid duplex ultrasound will evaluate the degree of stenosis
• MRA, CTA, or arteriography is indicated to better evaluate symptomatic stenosis that may require surgery

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Source: In a Page: Signs and Symptoms, 2004

Hypertension: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• “White coat” hypertension: Transient, related to anxiety
• Essential hypertension (most common cause in adolescents)
• Obesity
• Drugs: Amphetamines, cocaine, PCP, nicotine, corticosteroids, oral contraceptives, antidepressants, sympathomimetics (including eye and nose drops), decongestants, β-agonists, theophylline, NSAIDs, ephedra, etc.
• Pain/distress
• Trauma: Pain, increased ICP, or spinal cord injury
• Surgery: Transient hypertension secondary to pain or specific procedures such as ductus arteriosus ligation or coarctation repair, renal or urinary tract surgery
• Seizures

• Renal etiologies
  –Chronic renal parenchymal disease: Most common in preadolescents (chronic renal insufficiency, reflux nephropathy, chronic glomerulonephritis, PCKD)
  –Acute renal disease: Poststreptococcal glomerulonephritis, nephritis, renal failure
  –Renal artery stenosis: From fibromuscular dysplasia or by external compression from tumor or hematoma
  –Congenital ureteropelvic junction obstruction
  –Renal ischemic events secondary to umbilical catheters (thrombosis/embolus)

• Endocrine disorders: CAH, Cushing syndrome, hypo-/hyperthyroidism, hyperparathyroidism, primary hyperaldosteronism, pheochromocytoma
• Sleep apnea
• Volume overload
• Hemolytic uremic syndrome
• Pregnancy
• Bronchopulmonary dysplasia
• Hypercalcemia
• Williams syndrome (multiple vascular stenosis, autoimmune vasculitis with large vessel involvement)
• Coarctation of the aorta

Workup and Diagnosis

• History
  –Associated symptoms
  –Birth history, PMH, review of systems
  –Medications (including patient's own, those around the house, and alternative medications/herbs)
  –Social history including substance use, sleep patterns
• Physical exam
  –Complete physical exam with special attention to eyes, abdomen, and neurologic systems
  –Complete cardiac exam: Evaluate cardiovascular stability (four-extremity BP, pulse, perfusion, mental status, tachypnea) as well as heart sounds, murmurs, distal pulses
• Labs
  –CBC, electrolytes, BUN, creatinine, calcium
  –Urinalysis (blood, protein, calcium, creatinine, creatinine clearance)
  –Consider urine toxicology screen
  –ASO titer if poststreptococcal glomerulonephritis is suspected
  –Thyroid function studies if history is consistent with thyroid dysfunction
  • Studies
    –Consider sleep study to rule out sleep apnea
    –Consider echo for coarctation of aorta
    –Consider renal ultrasound, DMSA, renin levels
    –Captopril scan or renal angiography for renal etiology

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Source: In A Page: Pediatric Signs and Symptoms, 2007

Umbilicus – Single Umbilical Artery: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Developmental agenesis or hypoplasia
  –No clear sex ratio
  –Males more likely to have associated malformations
  –Increased incidence in twins, either mono- or dizygotic
  –Increased incidence of placental anomalies
  –More common in low birth weight infants
  –More common in premature infants

• Associated maternal factors
  –Maternal diabetes
  –Maternal epilepsy
  –Toxemia
• Intrauterine thrombosis of other umbilical artery

• Malformations are associated with SUA in 45% of cases
  –Genitourinary (33%): Renal agenesis, dysgenesis, hypoplasia; ambiguous genitalia
  –Musculoskeletal (37%): Clubfoot, vertebral anomalies
  –Cardiovascular (30%): Patent ductus arteriosus, ventricular septal defect, dextrocardia
  –Gastrointestinal (28%): Imperforate anus, tracheoesophageal fistula
  –Respiratory (9%): Pulmonary hypoplasia (malformations due to disruption of blood flow), sirenomelia

• Chromosomal anomalies
  –Trisomy 18

Workup and Diagnosis

• History
  –Prenatal tests such as amniocentesis with karyotype
  –Twinning
• Physical exam
  –Dysmorphic facial features
  –Anomalies with genitourinary, gastrointestinal, cardiac, musculoskeletal organ systems
  –Neurologic signs associated with stroke (e.g., seizures)
• Level II prenatal ultrasound with Doppler examination of umbilical cord
• Examination of placenta and cord at delivery
  –Examine closer to umbilical end of cord since vessels may merge close to placental insertion
• Karyotype
• Genetics consultation
• Thrombophilia evaluation
  –Factor V Leiden or antithrombin III deficiency
  –Anticardiolipin or lupus anticoagulant

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Source: In A Page: Pediatric Signs and Symptoms, 2007

HYPERTENSION: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Take the blood pressure yourself to be sure the hypertension is real; 24-hour blood pressure monitoring is now available. The workup of hypertension includes a family history, serial electrolytes, urinalysis and urine culture, and possibly “hypertensive” IVP and 24-hour urine VMA to rule out treatable causes of hypertension. A complete hypertensive workup is not usually performed today unless there is no family history of hypertension, the hypertension does not respond to treatment, there are other symptoms suggesting a surgical lesion (e.g., paroxysmal headaches), or there is sudden onset of hypertension in a known normotensive individual.

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Source: Differential Diagnosis in Primary Care, 2007

Blood pressure increase [Hypertension]: History and physical examination

(Handbook of Signs & Symptoms (Third Edition))

If you detect sharply elevated blood pressure, quickly rule out possible life-threatening causes. (See Managing elevated blood pressure.)

After ruling out life-threatening causes, complete a more leisurely history and physical examination. Determine if the patient has a history of cardiovascular or cerebrovascular disease, diabetes, or renal disease. Ask about a family history of high blood pressure — a likely finding with essential hypertension, pheochromocytoma, or polycystic kidney disease. Then ask about its onset. Did high blood pressure appear abruptly? Ask the patient's age. The sudden onset of high blood pressure in middle-aged or elderly patients suggests renovascular stenosis. Although essential hypertension may begin in childhood, it typically isn't diagnosed until near age 35. Pheochromocytoma and primary aldosteronism usually occur between ages 40 and 60. If you suspect either, check for orthostatic hypotension. Take the patient's blood pressure with him lying down, sitting, and then standing. Normally, systolic pressure falls and diastolic pressure rises on standing. With orthostatic hypotension, both pressures fall.

Note headache, palpitations, blurred vision, and sweating. Ask about wine-colored urine and decreased urine output; these signs suggest glomerulonephritis, which can cause elevated blood pressure.

Obtain a drug history, including past and present prescriptions, herbal preparations, and over-the-counter drugs (especially decongestants). If the patient is already taking an antihypertensive, determine how well he complies with the regimen. Ask about his perception of elevated blood pressure. How serious does he believe it is? Does he expect drug therapy to help? Explore psychosocial or environmental factors that may impact blood pressure control.

Follow up the history with a thorough physical examination. Using a funduscope, check for intraocular hemorrhage, exudate, and papilledema, which characterize severe hypertension. Perform a thorough cardiovascular assessment. Check for carotid bruits and jugular vein distention. Assess skin color, temperature, and turgor. Palpate peripheral pulses. Auscultate for abnormal heart sounds (gallops, louder second sound, murmurs), rate (bradycardia, tachycardia), or rhythm. Then auscultate for abnormal breath sounds (crackles, wheezing), rate (bradypnea, tachypnea), or rhythm.

Palpate the abdomen for tenderness, masses, or liver enlargement. Auscultate for abdominal bruits. Renal artery stenosis produces bruits over the upper abdomen or in the costovertebral angles. Easily palpable, enlarged kidneys and a large, tender liver suggest polycystic kidney disease. Obtain a urine sample to check for microscopic hematuria.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Hypertension: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Serial blood pressure measurements are obtained and compared to previous readings and trends to reveal an increase in diastolic and systolic pressures. (See Classifying blood pressure readings, page 1094.)

Auscultation may reveal bruits over the abdominal aorta and the carotid, renal, and femoral arteries; ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, papilledema. Patient history and the following additional tests may show predisposing factors and help identify an underlying cause such as renal disease:

❑ Urinalysis: Protein levels and red and white blood cell counts may indicate glomerulonephritis.

❑ Excretory urography: Renal atrophy indicates chronic renal disease; one kidney more than ⅝nbsp;(1.5 cm) shorter than the other suggests unilateral renal disease.

❑ Serum potassium: Levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary hyperaldosteronism).

❑ Blood urea nitrogen (BUN) and serum creatinine: BUN level that’s normal or elevated to more than 20 mg/dl and serum creatinine level that’s normal or elevated to more than 1.5 mg/dl suggest renal disease.

Other tests help detect cardiovascular damage and other complications:

❑ Electrocardiography may show left ventricular hypertrophy or ischemia.

❑ Chest X-ray may show cardiomegaly.

❑ Echocardiography may show left ventricular hypertrophy.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Pregnancy-induced hypertension: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

The following findings suggest preeclampsia:

❑ elevated blood pressure readings: 140 systolic, measured on two occasions, 6 hours apart; 90 diastolic, measured on two occasions, 6 hours apart

❑ proteinuria: at least 300 mg/24 hours.

The following findings suggest severe preeclampsia:

❑ higher blood pressure readings: 160/110 mm Hg or higher on two occasions, 6 hours apart, on bed rest

❑ increased proteinuria: 5 g/24 hours or more

❑ presence of pulmonary edema

❑ ultrasound: may reveal oligohydraminos

❑ oliguria: urine output less than or equal to 400 ml/24 hours.

Seizures strongly suggest eclampsia. Rarely, ophthalmoscopic examination may reveal vascular spasm, papilledema, retinal edema or detachment, and arteriovenous nicking or hemorrhage.

Real-time ultrasonography, stress and nonstress tests, and biophysical profiles evaluate fetal status. In the stress test, oxytocin stimulates contractions; fetal heart tones are then monitored electronically. In the nonstress test, fetal heart tones are monitored electronically during periods of fetal activity, without oxytocin stimulation. Electronic monitoring reveals stable or increased fetal heart tones during periods of fetal activity.

Ultrasonography aids evaluation of fetal health by assessing fetal breathing movements, gross body movements, fetal tone, reactive fetal heart rate, and qualitative amniotic fluid volume.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Pulmonary hypertension: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Characteristic diagnostic findings include:

❑ Auscultation reveals abnormalities associated with the underlying disorder.

❑ Arterial blood gas (ABG) analysis indicates hypoxemia (decreased partial pressure of arterial oxygen).

❑ Electrocardiography shows right axis deviation and tall or peaked P waves in inferior leads in the patient with right ventricular hypertrophy.

❑ Cardiac catheterization reveals pulmonary systolic pressure above 30 mm Hg as well as increased pulmonary artery wedge pressure (PAWP) if the underlying cause is left atrial myxoma, mitral stenosis, or left-sided heart failure (otherwise normal).

❑ Pulmonary angiography detects filling defects in pulmonary vasculature such as those that develop in patients with pulmonary emboli.

❑ Pulmonary function tests may show decreased flow rates and increased residual volume in underlying obstructive disease and decreased total lung capacity in underlying restrictive disease.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Renovascular hypertension: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis is confirmed by the following tests:

CONFIRMING DIAGNOSIS Arterial digital subtraction angiography with assays of venous renin is the definitive diagnostic procedure. When stenosis is significant, transluminal angioplasty can be done during the same procedure.

❑ Gadolinium enhanced magnetic resonance angiography can identify turbulent blood flow indicative of renal stenosis.

❑ Duplex Doppler ultrasonography scans the renal artery and will reveal stenosis but results vary.

❑ Oral captopril renography is the simplest, noninvasive test for detection of renovascular hypertension but has a relatively high false-positive rate.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Blood pressure increase [Hypertension]: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If you detect sharply elevated blood pressure, quickly rule out possible life-threatening causes. (See Managing elevated blood pressure.)

After ruling out life-threatening causes, complete a more leisurely history and physical examination. Determine if the patient has a history of cardiovascular or cerebrovascular disease, diabetes, or renal disease. Ask about a family history of high blood pressure—a likely finding in patients with essential hypertension, pheochromocytoma, or polycystic kidney disease. Then ask about its onset. Did high blood pressure appear abruptly? Ask the patient’s age. Sudden onset of high blood pressure in middle-aged or elderly patients suggests renovascular stenosis. Although essential hypertension may begin in childhood, it typically isn’t diagnosed until near age 35. Pheochromocytoma and primary aldosteronism usually occur between ages 40 and 60. If you suspect either, check for orthostatic hypotension. Take the patient’s blood pressure with him supine, sitting, and then standing. Normally, systolic pressure falls and diastolic pressure rises on standing; in orthostatic hypotension, both pressures fall.

Note headache, palpitations, blurred vision, and sweating. Ask about wine-colored urine and decreased urine output; these signs suggest glomerulonephritis, which can cause elevated blood pressure.

Obtain a drug history, including past and present prescription and over-the-counter drugs (especially decongestants) as well as herbal preparations. If the patient is already taking an antihypertensive, determine how well he complies with the regimen. Ask about his perception of elevated blood pressure. How serious does he believe it is? Does he expect drug therapy to help? Explore psychosocial or environmental factors that may impact blood pressure control.

Follow up the history with a thorough physical examination. Using a funduscope, check for intraocular hemorrhage, exudate, and papilledema, which characterize severe hypertension. Perform a thorough cardiovascular assessment. Check for carotid bruits and jugular vein distention. Assess skin color, temperature, and turgor. Palpate peripheral pulses. Auscultate for abnormal heart sounds (gallops, louder second sound, murmurs), rate (bradycardia, tachycardia), or rhythm. Then auscultate for abnormal breath sounds (crackles, wheezing), rate (bradypnea, tachypnea), or rhythm.

Palpate the abdomen for tenderness, masses, or liver enlargement. Auscultate for abdominal bruits. Renal artery stenosis produces bruits over the upper abdomen or in the costovertebral angles. Easily palpable, enlarged kidneys and a large, tender liver suggest polycystic kidney disease. Obtain a urine specimen to check for microscopic hematuria.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Hypertension: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Assessment for comorbid conditions. The patient’s past medical history should include an assessment for previous blood pressure readings. Any history of secondary disease or comorbid conditions should be documented: age more than 60 years, obesity, ischemic heart disease (IHD), cerebrovascular disease, peripheral vascular disease, retinopathy, nephropathy, dyslipidemia, diabetes mellitus, and menopausal status in women. A family history of these problems should also be documented, with particular emphasis on premature IHD in women aged less than 65 years, and in men aged less than age 55 years.

 B. Medication history. The medication history should document the use of prescription, over-the-counter, and herbal preparations that may have hypertensive side effects.

 C. Social history or habits. In addition, determine the use of tobacco, alcohol, or street drugs. The social history should also address leisure time physical activity and relevant psychosocial factors, which could affect ongoing HTN management.

 D. Dietary history. Explore the ingestion of salt and saturated fats. Note recent weight changes, which can have significant effects on blood pressure.

Physical examination

 A. Blood pressure measurement. Use a standardized technique (2,3) when measuring blood pressure to avoid spuriously high or low values. Patients should be seated in a chair, upright with back support, feet flat on the floor, arms bared, and supported at heart level. The patient should be resting at least 5 minutes before blood pressure measurements are taken. Stimulants such as nicotine and caffeine should be avoided at least 30 minutes prior to measurement. Appropriate cuff size is very important; the bladder within the cuff should circle at least 80% of the arm. Initial blood pressure measurements should include both arms; the arm with the higher reading should be used thereafter. It is recommended that two or more readings, separated by 2 minutes, be averaged. If the first two readings differ by more than 5 mm Hg, then additional readings should be obtained and averaged.

 B. Additional physical examination. Height and weight should be measured. In a focused physical examination, pay particular attention to the fundi (for hemorrhages or vascular changes), the carotid arteries (for bruits), the heart (for murmurs), the abdomen (for bruits), and the extremities (for pulses, bruits, edema).

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Stroke: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Characteristics of the stroke. What is the duration of the deficit? Is the problem acute and lasting several hours? Impaired consciousness can occur in all types of stroke. More specific symptom may help localize the area of stroke:

 1. Carotid circulation: symptoms of hemiplegia, hemianesthesia, aphasia, visual field defects, and loss of spatial function; occasionally, seizures, headache, amnesia, and confusion.

2. Vertebrobasilar circulation: symptoms of diplopia, vertigo, ataxia, facial paresis, Horner’s syndrome, dysphagia, dysarthria, quadraparesis
(a component of bilateral arms or legs), and crossed sensory symptoms (ipsilateral face and contralateral body). Cerebellar lesions often display headache, nausea or vomiting, and ataxia.

B. Past history. A history of trauma, migraine, vasculitis, seizure, and hypoglycemia could produce a condition that can mimic stroke. Fever or infection may suggest abscess. A prior history of stroke or TIA often precedes the presentation of a new stroke. A history of valvular heart disease, atrial fibrillation, or MI is relevant.

 C. Risk factors. Patients need to be assessed for hypertension, cardiac disease (specifically atrial fibrillation), smoking, diabetes mellitus, hypercoagulable states, and hormonal therapy.

 D. Hospitalization. This may be necessary for patients with transient or ongoing ischemic deficits. TIAs can herald a high-grade carotid stenosis or occult left atrial thrombus.

Physical examination (PE)

 A. General examination. This should include vital signs (notably blood pressure), Mini-Mental Status Examination, and an examination of the eyes, including funduscopic. A screening neurologic examination of cranial nerves, coordination, muscle strength, sensation, deep tendon, reflexes, and gait is recommended.

 B. Additional PE. Evaluate the heart (arrhythmia, mitral stenosis) and vascular system (carotid bruits), and palpate the scalp and neck (trauma and migraine) and superficial temporal arteries (arteritis).

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Hypertension: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Essential hypertension

❑ White coat hypertension

❑ Renal artery stenosis

❑ Drug-induced hypertension

❑ Atherosclerotic vascular noncompliance

❑ Pheochromocytoma

❑ Cushing syndrome

❑ Hyperaldosteronism

❑ Aortic coarctation

❑ Acute renal artery obstruction

❑ Toxemia

Diagnostic Approach

The level of blood pressure associated with 50% increase in cardiovascular mortality: men younger than 45 years old, 130/90; men older than 45 years, 140/95; women, 160/95. An ankle-brachial systolic blood pressure ratio of less than 0.9 predicts a fourfold increase in cardiovascular mortality.

Clues to secondary hypertension include onset at a young age (,35), abrupt onset of hypertension, blood pressure difficult to control requiring high dosages of two or more drugs, and very high or labile blood pressure. Hypertension with relative tachycardia may be a clue to sympathetic effect or diastolic dysfunction. Headaches with severe hypertension are occipital and worse in the morning.

Hypertensive end organ damage must be searched for when the diastolic BP is greater than 130 mm Hg and the patient exhibits confusion, dyspnea, restlessness, or blurred vision. Perform fundoscopy looking for papilledema or retinal hemorrhages, and cardiopulmonary exam for third heart sound or bibasilar rales. Clues to hypertension-associated left ventricular hypertrophy include a fourth heart sound, an apical impulse greater than two intercostal spaces, a holosystolic sustained apical impulse diameter, and a hypertensive response to exercise ( .210 systolic). Cotton wool spots, which are caused by anoxic edema with axon degeneration, are seen in advanced hypertension (also in diabetes, dysproteinemia, and fat emboli).

Grading hypertensive retinopathy provides a marker of end-organ damage, which is tied to prognosis:

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Source: Field Guide to Bedside Diagnosis, 2007

Stroke Syndromes: Differential Overview

(Field Guide to Bedside Diagnosis)

TIA/Stroke

❑ Middle cerebral artery stroke

❑ Anterior cerebral artery stroke

❑ Posterior cerebral artery stroke

❑ Watershed stroke

❑ Thalamic lacune

❑ Vertebrobasilar ischemia

❑ Pontine lacune

❑ Pontine stroke

❑ Midbrain stroke

❑ Pure motor hemiplegia

❑ Ataxic hemiparesis

❑ Lateral medullary stroke

❑ Temporal lobe stroke

Hemorrhage

❑ Subarachnoid hemorrhage

❑ Cerebellar hemorrhage

❑ Thalamic hemorrhage

❑ Pontine hemorrhage

❑ Putaminal hemorrhage

Diagnostic Approach

Brain ischemia leading to stroke may be due to embolism from carotid or cardiac sources, systemic hypoperfusion, or in situ thrombosis. Embolic strokes occur suddenly with maximal focal deficits at the onset. Rapid improvement favors an embolic TIA. Thrombosis symptoms fluctuate in a stepwise pattern. Intracerebral hemorrhage progresses gradually over minutes to hours. Aneurysmal subarachnoid hemorrhage occurs in an instant, and focal brain dysfunction is usually absent. Strokelike symptoms due to migraine are recognized by a headache, epiphenomena such as anorexia/nausea and photophobia, and occurrence in younger patients.

A TIA proceeds to stroke in 10% to 40%. Risk is especially high in “crescendo TIA,” which is usually caused by an ulcerated carotid plaque. Amaurosis fugax (“a shade coming down” or transient monocular loss of vision) is a classic presentation. Amaurosis fugax, an anterior circulation event, should be distinguished from transient hemianopsia, a posterior circulation event. An asymptomatic carotid bruit is an imperfect indicator of carotid stenosis and subsequent stroke risk, with an annual risk of an ipsilateral stroke not preceded by a TIA of 1% to 3% per year.

Examination of the optic fundus may reveal a cholesterol crystal, white platelet-fibrin or red clot emboli. Subhyaloid hemorrhage often accompanies a subarachnoid or intracerebral hemorrhage. A red patch with a white center (Roth spot) may be seen in bacterial endocarditis. With occlusion of the carotid artery, the iris may appear speckled and the ipsilateral pupil dilated and poorly-reactive.

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Source: Field Guide to Bedside Diagnosis, 2007

Arterial Pulse Variants: Differential Overview
(Field Guide to Bedside Diagnosis)

Phenomena

❑ Irregularly irregular pulse

❑ Asymmetric pulses

❑ Bounding pulse

❑ Bisferiens pulse

❑ Bigeminal pulse

❑ Pulsus alternans

❑ Pulsus paradoxus

❑ Thready pulse

❑ Pulsus parvus et tardus

❑ Narrow pulse pressure

Diagnostic Approach

Examine the pulse using the method of trisection: apply pressure until the pulse is maximal, and then vary pressure while concentrating on phases of the pulse.

Early Chinese medicine based diagnosis primarily on careful examination of the pulse. There were six sets of pulses, each connected with a specific part of the body and each believed to register even the subtlest physiological changes within it. The principal pulses were Fu, a light-flowing pulse like a piece of wood floating on water; Ch’en, a deeply impressed pulse like a stone thrown into water; Ch’ih, a pulse with three beats to one cycle of respiration; and Shu, a pulse with six beats to one cycle of respiration.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Carotid Bruit: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Carotid artery stenosis

❑ Carotid artery ruptured plaque

❑ Transmitted valvular murmur

❑ Carotid tortuosity

❑ Carotid compression

❑ Jugular venous hum

❑ Thyrotoxicosis

Diagnostic Approach

Carotid bruits are imperfect markers of increased stroke risk because stroke is usually not due to progressive carotid stenosis, but rather to ruptured plaque, cardiac emboli from atrial fibrillation, emboli from aortic sources, or watershed ischemia due to decreased flow. A bruit is, however, an important marker of generalized atherosclerosis. The annual incidence of stroke in the territory of a carotid bruit is 1.7%/year and increases to 5.5%/year as stenosis exceeds 75%. The risk of death (usually cardiac) in a patient with a carotid bruit is 4%/yr. Bruits are clinically significant when associated with transient ipsilateral anterior circulation symptoms such as amaurosis fugax (transient monocular blindness), contralateral homonymous hemianopsia, hemiparesis, and hemisensory defect. Left hemispheric lesions are associated with aphasia, and right with visuospatial neglect and constructional apraxia.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Hypertension: Diagnosis
(Handbook of Diseases)

Serial blood pressure measurements that are greater than 120/80 mm Hg but less than 140/90 mm Hg indicate prehypertension; measurements that are greater than 140/90 mm Hg confirm hypertension. Moderate (stage 1) and severe (stage 2) stages are based on systolic and diastolic levels. Auscultation may reveal bruits over the abdominal aorta and the carotid, renal, and femoral arteries; ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, papilledema.

The patient history and the following additional tests may show predisposing factors and help identify an underlying cause such as kidney disease:

❑ Urinalysis — The presence of protein, red blood cells, and white blood cells may indicate glomerulonephritis.

❑ Excretory urography — Renal atrophy indicates chronic kidney disease; one kidney that is more than ⅝"(1.5 cm) shorter than the other suggests unilateral kidney disease.

❑ Serum potassium — Levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary hyperaldosteronism).

❑ Blood urea nitrogen (BUN) and serum creatinine levels — A BUN level that’s normal or elevated to more than 20 mg/dl and a serum creatinine level that’s normal or elevated to more than 1.5 mg/dl suggest kidney disease.

Other tests help detect cardiovascular damage and other complications:

❑ Electrocardiography may show left ventricular hypertrophy or ischemia.

❑ Chest X-ray may show cardiomegaly.

❑ Echocardiography may show left ventricular hypertrophy.

❑ Oral captopril challenge tests for renovascular hypertension. This functional diagnostic test depends on the abrupt inhibition of circulating angiotensin II by angiotensin-converting enzyme (ACE) inhibitors, removing the major support for perfusion through a stenotic kidney. The acutely ischemic kidney immediately releases more renin and undergoes a marked decrease in glomerular filtration rate and renal blood flow.

❑ Renal arteriography may show renal artery stenosis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Stroke: Diagnosis
(Handbook of Diseases)

Confirmation of stroke is based on symptoms, a history of risk factors, and the results of diagnostic tests.

❑ Computed tomography scan shows evidence of hemorrhagic stroke immediately but may not show evidence of thrombotic infarction for 48 to 72 hours.

❑ Magnetic resonance imaging may help identify ischemic or infarcted areas and cerebral swelling.

UNDER STUDY: Positron emission tomography can quantify cerebral blood flow. Single-photon emission tomography, computed tomography perfusion, and magnetic resonance perfusion techniques report relative blood flow and are research tools.

❑ Ophthalmoscopy may show signs of hypertension and atherosclerotic changes in retinal arteries.

❑ Angiography outlines blood vessels and pinpoints atherosclerotic plaques, vessel occlusion, or the rupture site.

❑ EEG helps to localize the damaged area.

Other baseline laboratory studies include urinalysis, coagulation studies, complete blood cell count, serum osmolality, and electrolyte, glucose, triglyceride, creatinine, and blood urea nitrogen levels.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Hypertension, pregnancy-induced: Diagnosis
(Handbook of Diseases)

The following findings suggest mild preeclampsia:

❑ elevated blood pressure readings — 140 mm Hg systolic or a rise of 30 mm Hg or more above the patient’s normal systolic pressure measured on two occasions, 6 hours apart; 90 mm Hg diastolic or a rise of 15 mm Hg or more above the patient’s normal diastolic pressure measured on two occasions, 6 hours apart

❑ proteinuria — greater than 500 mg/24 hours.

The following findings suggest severe preeclampsia:

❑ much higher blood pressure readings — 160/110 mm Hg or higher on two occasions, 6 hours apart, while on bed rest

❑ increased proteinuria — 5 g or more/24 hours

❑ oliguria — urine output less than or equal to 400 ml/24 hours

❑ deep tendon reflexes — possibly hyperactive as central nervous system (CNS) irritability increases.

Typical clinical features — especially seizures — with typical findings for severe preeclampsia strongly suggest eclampsia. An ophthalmoscopic examination may reveal vascular spasm, papilledema, retinal edema or detachment, and arteriovenous nicking or hemorrhage.

Real-time ultrasonography and stress and nonstress tests evaluate fetal well-being. In the stress test, oxytocin stimulates contractions; fetal heart tones are then monitored electronically.

In the nonstress test, fetal heart tones are monitored electronically during periods of fetal activity without oxytocin stimulation. Electronic monitoring reveals stable or increased fetal heart tones during periods of fetal activity.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Pulmonary hypertension: Diagnosis
(Handbook of Diseases)

Characteristic diagnostic findings in patients with pulmonary hypertension include the following:

❑ auscultation: abnormalities associated with the underlying disorder

❑ arterial blood gas (ABG) analysis: hypoxemia (decreased partial pressure of oxygen)

❑ electrocardiography: in right ventricular hypertrophy, shows right-axis deviation and tall or peaked P waves in inferior leads

❑ cardiac catheterization: increased PAP — pulmonary systolic pressure above 30 mm Hg; pulmonary artery wedge pressure (PAWP) increased if the underlying cause is left-sided myxoma, mitral stenosis, or left-side failure — otherwise normal

❑ pulmonary angiography: detects filling defects in pulmonary vasculature, such as those that develop in patients with pulmonary emboli

❑ pulmonary function tests: in underlying obstructive disease, may show decreased flow rates and increased residual volume; in underlying restrictive disease, total lung capacity may decrease.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Hypertension: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Transient Hypertension

Frequentcauses are stress related (e.g., anxiety, pain, and burns). BP becomesnormal with relief of stress.

Another cause is increase in intravascularvolume with excessive use of saline, blood, or plasma. When intravascularvolume normalizes, BP returns to normal.

Finally, immobilization with placementin traction may cause increased BP, which resolves when immobilizationis no longer necessary.

Sustained Hypertension

Birth–1 Yr

Renal Artery Thrombosis after Umbilical Artery Catheterization

BP shouldbe monitored in infants with umbilical artery catheter; they shouldcontinue to be monitored after catheter has been removed.

Unilateral or bilateral enlarged kidneysand hematuria are clues to this diagnosis, which is usually confirmedby abdominal U/S with Doppler methods.

If thrombosis involves aorta, femoralpulses may not be palpable and blood flow to lower extremities maybe compromised.

Coarctation of Aorta

Usuallyinvolves thoracic aorta, although it can involve abdominal aorta.

Increased BP occurs at least in rightupper arm with decreased BP and diminished or absent pulses in lowerextremities.

2-D echocardiography, MRI, or aorticangiography can confirm diagnosis.

After surgical repair, transient increasein BP may occur within 1–2 days. Sustained increase inBP may be observed during week after repair, and often a few weeksto a few months thereafter.

Mechanism for persistent hypertensionin some patients after successful repair of coarctation may be relatedto overactivity of renin-angiotensin-aldosterone system.

Congenital Renal Disease

Hypertension may occur with renal dysplasia,hydronephrosis, nephrotic syndrome, and polycystic kidney disease.See Chap. 1, Abdominal Masses; Chap. 28, Hematuria; and Chap. 50, Proteinuria.

Renal Artery Stenosis

Stenosisof main or segmental renal artery caused by intrinsic or extrinsicrenal disease may result in severe hypertension.

Causes of intrinsic disease includemedial fibromuscular dysplasia (neurofibromatosis, idiopathic),intimal fibroplasia (neurofibromatosis), arteritis (Kawasaki disease,Takayasu disease, moyamoya, radiation), trauma (blunt, surgical),atherosclerosis (familial dyslipoproteinemia), posttransplantation(surgical, immune), aneurysm, embolism, and specific syndromes (Williams,Turner).

Causes of extrinsic disease includetumor (Wilms, pheochromocytoma, neuroblastoma, lymphoma), fibrousbands (congenital, postsurgical), and perirenal hematoma (trauma).

Renal arteriography remains gold standardfor visualization of lesions. Other useful tests include abdominalU/S with Doppler methods, captopril renography, and CTfor detection of mass lesions.

Bronchopulmonary Dysplasia

Infants with bronchopulmonary dysplasia maydevelop hypertension, even after discharge from nursery. See Chap. 10, Cough; Chap. 56, Respiratory Distress and Apnea;and Chap. 75, Wheezing.

Patent Ductus Arteriosus

Common in neonates, especially in preterminfants. Diastolic pressure is typically low or normal, and pulsepressure is increased. Increase in systolic BP is presumably dueto larger LV stroke volume. See Chap.7, Cardiac Failure, and Chap. 27, Heart Murmurs (Asymptomatic).

Intraventricular Hemorrhage

Common occurrence in preterm infants, especiallythose <32 wks' gestation. The more severe the hemorrhage(grades III and IV), the more likely that increased intracranialpressure will occur with an associated increase in BP.

1–10 Yrs

Renal Disease

Hypertension may occur with glomerulonephritis,pyelonephritis, hydronephrosis, hemolytic-uremic syndrome, and refluxnephropathy. See Chap. 1, AbdominalMasses; Chap.15, Dysuria; Chap.28, Hematuria; and Chap.50, Proteinuria.

Coarctation of Aorta

See previous section Coarctation of Aorta.

Renal Artery Stenosis

See previous section Renal Artery Stenosis.

Glucocorticoid Excess

Most commoncause is use of corticosteroids or adrenocorticotropic hormone (ACTH)for underlying medical disorder.

Less common cause is Cushing syndrome,which is usually due to adrenal hyperplasia or adrenal tumor thatresults in excess production of glucocorticoids and androgens. Usualcause of Cushing disease is pituitary adenoma producing excessiveamount of ACTH.

Produces increased weight gain, hypertension,and slow linear growth. See Chap.44, Obesity.

Sex Hormones

Oral contraceptives may produce hypertension.So may anabolic steroids that contain testosterone.

Catecholamine Excess

Major catecholaminesare dopamine, norepinephrine, and epinephrine.

Tumors that secrete excess catecholaminesinclude neuroblastoma and pheochromocytoma.

Neuroblastoma

Malignanttumor that may arise from adrenal medulla or other sympathetic nervous tissue.

Abdominal mass is common finding. Thereis usually increase in 24-hr urinary excretion of catecholamines.

Abdominal U/S and CT can usuallylocate the tumor. See Chap. 1,Abdominal Masses.

Pheochromocytoma

Peak incidenceof pheochromocytoma is in older children and adolescents. It maybe associated with neurofibromatosis and multiple endocrine neoplasiasyndromes.

Clinical manifestations include paroxysmalhypertension, palpitations, headache, nausea, vomiting, and emotionallability.

Increased concentration of catecholaminesand their metabolites (vanillymandelic acid is major metaboliteof epinephrine and norepinephrine) may be found in blood or 24-hrurine collection

If suspected by biochemical tests,abdominal U/S, CT, or MRI can usually locate tumor in adrenalgland or along sympathetic chain. Another useful test is scintigraphywith metaiodobenzyl guanidine (MIBG) labeled with ¹²³I.This compound concentrates in tissues that actively synthesize catecholaminesand can locate small tumors that may be otherwise difficult to detect.

Mineralocorticoid Excess

Rare inchildhood.

Plasma aldosterone concentration isincreased in true aldosterone excess, whereas in apparent mineralocorticoidexcess, features of aldosterone excess occur without increase inplasma aldosterone concentration.

Causes of mineralocorticoid excessproducing hypertension are listed in Table32.3.

'>

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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Blood pressure, increased [Hypertension]: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If you detect sharply elevated blood pressure, quickly rule out possible life-threatening causes. (See Managing elevated blood pressure, page 84.)

After ruling out life-threatening causes, complete a history and physical examination. Determine if the patient has a history of cardiovascular or cerebrovascular disease, diabetes, or renal disease. Ask about a family history of high blood pressure—a likely finding with essential hypertension, pheochromocytoma, or polycystic kidney disease. Then ask about its onset. Did high blood pressure appear abruptly? Ask the patient's age. The sudden onset of high blood pressure in middle-aged or elderly patients suggests renovascular stenosis. Although essential hypertension may begin in childhood, it typically isn't diagnosed until near age 35. Pheochromocytoma and primary aldosteronism usually occur between ages 40 and 60. If you suspect either, check for orthostatic hypotension. Take the patient's blood pressure with him lying down, sitting, and then standing. Normally, systolic pressure falls and diastolic pressure rises on standing. With orthostatic hypotension, both pressures fall.

Note headache, palpitations, blurred vision, and sweating. Ask about wine-colored urine and decreased urine output; these signs suggest glomerulonephritis, which can cause elevated blood pressure.

Obtain a drug history, including past and present prescriptions, herbal medicines, and over-the-counter drugs (especially decongestants). If the patient is already taking an antihypertensive, determine how well he complies with the regimen. Ask about his perception of elevated blood pressure. How serious does he believe it is? Does he expect drug therapy to help? Explore psychosocial or environmental factors that may impact blood pressure control.

Follow up the history with a thorough physical examination. Using a funduscope, check for intraocular hemorrhage, exudate, and papilledema, which characterize severe hypertension. Perform a thorough cardiovascular assessment. Check for carotid bruits and jugular vein distention. Assess skin color, temperature, and turgor. Palpate peripheral pulses. Auscultate for abnormal heart sounds (such as gallops, louder second sound, or murmurs), rate (for example, bradycardia or tachycardia), or rhythm. Then auscultate for abnormal breath sounds (such as crackles or wheezing), rate (for example, bradypnea or tachypnea), or rhythm.

Palpate the abdomen for tenderness, masses, or liver enlargement. Auscultate for abdominal bruits. Renal artery stenosis produces bruits over the upper abdomen or in the costovertebral angles. Easily palpable, enlarged kidneys and a large, tender liver suggest polycystic kidney disease. Obtain a urine sample to check for microscopic hematuria.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

HYPERTENSION: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Take the blood pressure yourself to be sure the hypertension is real; 24-hour blood pressure monitoring is now available. The workup of hypertension includes a family history, serial electrolytes, urinalysis and urine culture, and possibly “hypertensive” IVP and 24-hour urine VMA to rule out treatable causes of hypertension. A complete hypertensive workup is not usually performed today unless there is no family history of hypertension, the hypertension does not respond to treatment, there are other symptoms suggesting a surgical lesion (e.g., paroxysmal headaches), or there is sudden onset of hypertension in a known normotensive individual.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

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