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Causes of Pseudotumor Cerebri

Contents
  1. Pseudotumor Cerebri: Introduction
  2. List of Causes
  3. Drugs/substances (4 causes)
  4. Hidden causes
  5. Excerpts from book chapters
  6. Causes of symptoms
  7. Related cause information

List of causes of Pseudotumor Cerebri

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Pseudotumor Cerebri) that could possibly cause Pseudotumor Cerebri includes:

Causes of Pseudotumor Cerebri (Diseases Database):

The follow list shows some of the possible medical causes of Pseudotumor Cerebri that are listed by the Diseases Database:

Source: Diseases Database

Pseudotumor Cerebri Causes: Book Excerpts

Pseudotumor Cerebri as a symptom:

Conditions listing Pseudotumor Cerebri as a symptom may also be potential underlying causes of Pseudotumor Cerebri. Our database lists the following as having Pseudotumor Cerebri as a symptom of that condition:

Medications or substances causing Pseudotumor Cerebri:

The following drugs, medications, substances or toxins are some of the possible causes of Pseudotumor Cerebri as a symptom. This list is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

Read more about medication causes of Pseudotumor Cerebri


Related information on causes of Pseudotumor Cerebri:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Pseudotumor Cerebri may be found in:

Causes of Pseudotumor Cerebri: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Pseudotumor Cerebri.

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

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

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

Optic disc swelling due to increased ICP

  • Pseudotumor cerebri (idiopathic intracranial hypertension)
    –Most common cause of papilledema
    –Young, obese, or pregnant females
    –Associated with vitamin A overdose, OCPs, tetracycline, steroid withdrawal
  • Cerebral tumor (primary or metastatic)
  • Hydrocephalus (e.g., tumor, Arnold-Chiari malformation, aqueductal stenosis, postinfectious)
  • Intracranial hemorrhage (papilledema may not be seen acutely because it takes about 24 hours to develop after the ICP increases)
    –Subdural hematoma
    –Subarachnoid hemorrhage
    –Hemorrhagic stroke
    –Epidural hematoma
  • Intracranial infection
    –Brain abscess
    –Encephalitis (e.g., herpes)
    –Neurosyphilis
    –Toxoplasmosis
  • Meningitis (e.g., bacterial, viral, TB)
  • Malignant hypertension
  • Pre-eclampsia
    Optic disc swelling not due to increased ICP
  • Pseudopapilledema (the vessels traversing the disk margins are obscured, as in true papilledema): Optic disc drusen or congenitally anomalous disc
  • Papillitis: Unilateral, painful, vitreous cells
  • Papillophlebitis: Mild visual loss and disk swelling in young, healthy patient
  • Central retinal vein occlusion: Unilateral, associated with an acute loss of vision
  • Diabetic papillopathy: Disk edema with minimal visual loss, resolves spontaneously
  • Optic-disc vasculitis/ischemic optic neuropathy (giant cell/temporal arteritis)
  • Orbital optic-nerve tumors
  • Graves’ ophthalmopathy: History of thyroid dysfunction; may be associated with lid lag, proptosis, increased intraocular pressure
  • Uveitis: Associated with pain, photophobia, and scleral injection
  • Atypical optic neuritis

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Papilledema (Optic Disc Swelling): Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Pseudotumor cerebri
    –Other symptoms: Headache, nausea, and vomiting all worse in morning, transient visual obscurations, diplopia
    –Diagnosis includes increased ICP, normal imaging, normal CSF
    –More common in obese females
  • Optic neuritis
    –May be associated with postviral syndromes or meningoencephalitis
    –Loss of vision, pain on eye movement
    –Vision usually improves within a few weeks, but not full recovery
  • Optic neuropathy
    –Compressive: Associated with NF1 and optic nerve glioma, presents with progressive visual loss, strabismus, nystagmus, proptosis
    –Infiltrative: From cancers (leukemias, lymphomas), infection, or inflammation (sarcoidosis, TB, toxocariasis, toxoplasmosis, CMV); optic disc swelling, vision loss, and hemorrhages
    –Toxic/nutritional optic neuropathy: Symmetric neuropathy from nutritional deficiency (thiamine, B12), drugs (tobacco/alcohol, chloramphenicol, rifampin), toxins (lead, methanol); visual field and vision loss; may recover with treatment
    –Leber optic neuropathy: Mitochondrial DNA transmission, presents late teens to middle 20s; visual field and vision loss, may spontaneously improve
  • Increased ICP: Idiopathic intracranial hypertension, intracranial hemorrhage, space-occupying lesion
  • Growth hormone supplementation
  • Retinal hemorrhage and loss of vision
  • Retinal vein occlusion
  • Malignant hypertension: Associated with retinal hemorrhage, exudates, and cotton wool spots
  • Optic neuropathy, nonarteritic or arteritic
  • Demyelinating disease
  • Infectious conditions: Toxoplasmosis, Lyme disease, Bartonella; hard exudates may be visible funduscopically

» READ BOOK EXCERPT ONLINE »

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

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

» READ BOOK EXCERPT ONLINE »

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

Blood pressure increase [Hypertension]: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

❑ Anemia. Accompanying elevated systolic pressure in anemia are pulsations in the capillary beds, bounding pulse, tachycardia, systolic ejection murmur, pale mucous membranes and, in patients with sickle cell anemia, ventricular gallop and crackles.

❑ Aortic aneurysm (dissecting). Initially, this life-threatening disorder causes a sudden rise in systolic pressure (which may be the precipitating event), but no change in diastolic pressure. However, this increase is brief. The body's ability to compensate fails, resulting in hypotension.

Other signs and symptoms vary, depending on the type of aortic aneurysm. An abdominal aneurysm may cause persistent abdominal and back pain, weakness, sweating, tachycardia, dyspnea, a pulsating abdominal mass, restlessness, confusion, and cool, clammy skin. A thoracic aneurysm may cause a ripping or tearing sensation in the chest, which may radiate to the neck, shoulders, lower back, or abdomen; pallor; syncope; blindness; loss of consciousness; sweating; dyspnea; tachycardia; cyanosis; leg weakness; murmur; and absent radial and femoral pulses.

❑ Atherosclerosis. With atherosclerosis, systolic pressure rises while diastolic pressure commonly remains normal or slightly elevated. The patient may show no other signs, or he may have a weak pulse, flushed skin, tachycardia, angina, and claudication.

❑ Cushing's syndrome. Twice as common in females as in males, Cushing's syndrome causes elevated blood pressure and widened pulse pressure as well as truncal obesity, moon face, and other cushingoid signs. It's usually caused by corticosteroid use.

❑ Hypertension. Essential hypertension develops insidiously and is characterized by a gradual increase in blood pressure from decade to decade. Except for this high blood pressure, the patient may be asymptomatic or (rarely) may complain of suboccipital headache, light-headedness, tinnitus, and fatigue.

With malignant hypertension, diastolic pressure abruptly rises above 120 mm Hg, and systolic pressure may exceed 200 mm Hg. Typically, the patient has pulmonary edema marked by jugular vein distention, dyspnea, tachypnea, tachycardia, and coughing of pink, frothy sputum. Other characteristic signs and symptoms include severe headache, confusion, blurred vision, tinnitus, epistaxis, muscle twitching, chest pain, nausea, and vomiting.

❑ Increased intracranial pressure (ICP). Increased ICP causes an increased respiratory rate initially, followed by increased systolic pressure and widened pulse pressure. Increased ICP affects the heart rate last, causing bradycardia (Cushing's reflex). Associated signs and symptoms include headache, projectile vomiting, a decreased level of consciousness, and fixed or dilated pupils.

❑ Myocardial infarction (MI). MI is a life-threatening disorder that may cause high or low blood pressure. Common findings include crushing chest pain that may radiate to the jaw, shoulder, arm, or epigastrium. Other findings include dyspnea, anxiety, nausea, vomiting, weakness, diaphoresis, atrial gallop, and murmurs.

❑ Pheochromocytoma. Paroxysmal or sustained elevated blood pressure characterizes pheochromocytoma and may be accompanied by orthostatic hypotension. Associated signs and symptoms include anxiety, diaphoresis, palpitations, tremors, pallor, nausea, weight loss, and headache.

❑ Polycystic kidney disease. Elevated blood pressure is typically preceded by flank pain. Other signs and symptoms include enlarged kidneys; an enlarged, tender liver; and intermittent gross hematuria.

❑ Preeclampsia and eclampsia. Potentially life-threatening to the mother and fetus, preeclampsia and eclampsia characteristically increase blood pressure. They're defined as a reading of 140/90 mm Hg or more in the first trimester, a reading of 130/80 mm Hg or more in the second or third trimester, an increase of 30 mm Hg above the patient's baseline systolic pressure, or an increase of 15 mm Hg above the patient's baseline diastolic pressure. Accompanying elevated blood pressure are generalized edema, sudden weight gain of 3 lb (1.4 kg) or more per week during the second or third trimester, severe frontal headache, blurred or double vision, decreased urine output, proteinuria, midabdominal pain, neuromuscular irritability, nausea, and possibly seizures (eclampsia).

❑ Renovascular stenosis. Renovascular stenosis produces abruptly elevated systolic and diastolic pressures. Other characteristic signs and symptoms include bruits over the upper abdomen or in the costovertebral angles, hematuria, and acute flank pain.

❑ Thyrotoxicosis. Accompanying the elevated systolic pressure associated with thyrotoxicosis, a potentially life-threatening disorder, are widened pulse pressure, tachycardia, bounding pulse, pulsations in the capillary nail beds, palpitations, weight loss, exophthalmos, an enlarged thyroid gland, weakness, diarrhea, a fever over 100° F (37.8° C), and warm, moist skin. The patient may appear nervous and emotionally unstable, displaying occasional outbursts or even psychotic behavior. Heat intolerance, exertional dyspnea and, in females, decreased or absent menses may also occur.

Other causes

❑ Drugs. Central nervous system stimulants (such as amphetamines), sympathomimetics, corticosteroids, nonsteroidal anti-inflammatory drugs, hormonal contraceptives, monoamine oxidase inhibitors, and over-the-counter cold remedies can increase blood pressure, as can cocaine abuse.

HERB ALERT:Ginseng and licorice may cause high blood pressure or an irregular heartbeat. St. John's wort can also raise blood pressure, especially when taken with substances that antagonize hypericin, such as amphetamines, cold and hay fever medications, nasal decongestants, pickled foods, beer, coffee, wine, and chocolate.

❑ Treatments. Kidney dialysis and transplantation cause transient elevated blood pressure.

» READ BOOK EXCERPT ONLINE »

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

Pregnancy-induced hypertension: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

The cause of pregnancy-induced hypertension is unknown, but geographic, ethnic, racial, nutritional, immunologic, and familial factors and pre-existing vascular disease may contribute to its development. Age is also a factor. Primiparas who are older than age 35 are at higher risk for preeclampsia.

Preeclampsia develops in about 7% of pregnancies. Incidence is significantly higher in low socioeconomic groups. About 5% of females with preeclampsia develop eclampsia; of these, about 15% die from PIH itself or its complications. Fetal mortality is high due to the increased incidence of premature delivery and uteroplacental insufficiency.

» READ BOOK EXCERPT ONLINE »

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

Pulmonary hypertension: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Pulmonary hypertension begins as hypertrophy of the small pulmonary arteries. The medial and intimal muscle layers of these vessels thicken, decreasing distensibility and increasing resistance. This disorder then progresses to vascular sclerosis and obliteration of small vessels.

In most cases, pulmonary hypertension occurs secondary to an underlying disease process, including:

❑ alveolar hypoventilation from chronic obstructive pulmonary disease (most common cause in the United States), sarcoidosis, diffuse interstitial disease, pulmonary metastasis, and certain diseases such as scleroderma (In these disorders, pulmonary vascular resistance occurs secondary to hypoxemia and destruction of the alveolocapillary bed. Other disorders that cause alveolar hypoventilation without lung tissue damage include obesity, kyphoscoliosis, and obstructive sleep apnea.)

❑ vascular obstruction from pulmonary embolism, vasculitis, and disorders that cause obstruction of small or large pulmonary veins, such as left atrial myxoma, idiopathic veno-occlusive disease, fibrosing mediastinitis, and mediastinal neoplasm

❑ primary cardiac disease, which may be congenital or acquired. Congenital defects that cause left-to-right shunting of blood — such as patent ductus arteriosus or atrial or ventricular septal defect — increase blood flow into the lungs and, consequently, raise pulmonary vascular pressure. Acquired cardiac diseases, such as rheumatic valvular disease and mitral stenosis, increase pulmonary venous pressure by restricting blood flow returning to the heart.

Primary (or idiopathic) pulmonary hypertension is rare, occurring most commonly — and with no known cause — in women between ages 20 and 40. Secondary pulmonary hypertension results from existing cardiac, pulmonary, thromboembolic, or collagen vascular diseases or from the use of certain drugs.

» READ BOOK EXCERPT ONLINE »

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

Malignant brain tumors: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

The cause of most brain tumors is unknown, but exposure to ionizing radiation is a known environmental risk. Additionally, most malignant tumors of the brain are of metastatic origin; 20% to 40% of patients with cancer develop brain metastasis.

» READ BOOK EXCERPT ONLINE »

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

Renovascular hypertension: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Stenosis or occlusion of the renal artery stimulates the affected kidney to release the enzyme renin, which converts angiotensinogen — a plasma protein — to angiotensin I. As angiotensin I circulates through the lungs and liver, it converts to angiotensin II, which causes peripheral vasoconstriction, increased arterial pressure and aldosterone secretion and, eventually, hypertension.

Atherosclerosis (especially in older males) and fibromuscular diseases of the renal artery wall layers — such as medial fibroplasia and, less commonly, intimal and subadventitial fibroplasia — are the primary causes in 95% of all patients with renovascular hypertension. Other causes include arteritis, anomalies of the renal arteries, embolism, trauma, tumor, and dissecting aneurysm. Less than 5% of patients with high blood pressure display renovascular hypertension; it’s most common in persons younger than age 30 or older than age 50.

PEDIATRIC TIP Fibromuscular dysplasia is the most common cause of renovascular hypertension in children. The surgical cure rate is very high.

» READ BOOK EXCERPT ONLINE »

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

Hydrocephalus: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Hydrocephalus may result from an obstruction in CSF flow (noncommunicating hydrocephalus) or from faulty absorption of CSF (communicating hydrocephalus). (See Normal circulation of CSF.)

In noncommunicating hydrocephalus, the obstruction occurs most frequently between the third and fourth ventricles, at the aqueduct of Sylvius, but it can also occur at the outlets of the fourth ventricle (foramina of Luschka and Magendie) or, rarely, at the foramen of Monro. This obstruction may result from faulty fetal development, infection (syphilis, granulomatous diseases, meningitis), a tumor, cerebral aneurysm, or a blood clot (after intracranial hemorrhage).

In communicating hydrocephalus, faulty absorption of CSF may result from surgery to repair a myelomeningocele, adhesions between meninges at the base of the brain, or meningeal hemorrhage. Rarely, a tumor in the choroid plexus causes overproduction of CSF, producing hydrocephalus.

Hydrocephalus occurs most commonly in neonates but can also occur in adults as a result of injury or disease. It affects 1 of every 1,000 people.

» READ BOOK EXCERPT ONLINE »

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

Hypertension: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Hypertension affects 25% of adults in the United States. If untreated, it carries a high mortality. Risk factors for hypertension include family history, race (most common in blacks), stress, obesity, a diet high in saturated fats or sodium, tobacco use, sedentary lifestyle, and aging.

Secondary hypertension may result from renal vascular disease; pheochromocytoma; primary hyperaldosteronism; Cushing’s syndrome; thyroid, pituitary, or parathyroid dysfunction; coarctation of the aorta; pregnancy; neurologic disorders; and use of hormonal contraceptives or other drugs, such as cocaine, epoetin alfa (erythropoietin), and cyclosporine.

Cardiac output and peripheral vascular resistance determine blood pressure. Increased blood volume, cardiac rate, and stroke volume as well as arteriolar vasoconstriction can raise blood pressure. The link to sustained hypertension, however, is unclear. Hypertension may also result from failure of intrinsic regulatory mechanisms:

❑ Renal hypoperfusion causes release of renin, which is converted by angiotensinogen, a liver enzyme, to angiotensin I. Angiotensin I is converted to angiotensin II, a powerful vasoconstrictor. The resulting vasoconstriction increases afterload. Angiotensin II stimulates adrenal secretion of aldosterone, which increases sodium reabsorption. Hypertonic-stimulated release of antidiuretic hormone from the pituitary gland follows, increasing water reabsorption, plasma volume, cardiac output, and blood pressure.

❑ Autoregulation changes an artery’s diameter to maintain perfusion despite fluctuations in systemic blood pressure. The intrinsic mechanisms responsible include stress relaxation (vessels gradually dilate when blood pressure rises to reduce peripheral resistance) and capillary fluid shift (plasma moves between vessels and extravascular spaces to maintain intravascular volume).

❑ When the blood pressure drops, baroreceptors in the aortic arch and carotid sinuses decrease their inhibition of the medulla’s vasomotor center, which increases sympathetic stimulation of the heart by norepinephrine. This, in turn, increases cardiac output by strengthening the contractile force, increasing the heart rate, and augmenting peripheral resistance by vasoconstriction. Stress can also stimulate the sympathetic nervous system to increase cardiac output and peripheral vascular resistance.

» READ BOOK EXCERPT ONLINE »

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

Blood pressure increase [Hypertension]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Aldosteronism (primary)

In aldosteronism, elevated diastolic pressure may be accompanied by orthostatic hypotension. Other findings include constipation, muscle weakness, polyuria, polydipsia, and personality changes.

Anemia

Accompanying elevated systolic pressure in anemia are pulsations in the capillary beds, bounding pulse, tachycardia, systolic ejection murmur, pale mucous membranes and, in patients with sickle cell anemia, ventricular gallop and crackles.

Aortic aneurysm (dissecting)

Initially, aortic aneurysm—a life-threatening disorder—causes a sudden rise in systolic pressure (which may be the precipitating event), but no change in diastolic pressure. However, this increase is brief. The body’s ability to compensate fails, resulting in hypotension.

Other signs and symptoms vary, depending on the type of aortic aneurysm. An abdominal aneurysm may cause persistent abdominal and back pain, weakness, sweating, tachycardia, dyspnea, a pulsating abdominal mass, restlessness, confusion, and cool, clammy skin. A thoracic aneurysm may cause a ripping or tearing sensation in the chest, which may radiate to the neck, shoulders, lower back, or abdomen; pallor; syncope; blindness; loss of consciousness; sweating; dyspnea; tachycardia; cyanosis; leg weakness; murmur; and absent radial and femoral pulses.

Atherosclerosis

In atherosclerosis, systolic pressure rises while diastolic pressure commonly remains normal or slightly elevated. The patient may show no other signs, or he may have a weak pulse, flushed skin, tachycardia, angina, and claudication.

Cushing’s syndrome

Twice as common in females as in males, Cushing’s syndrome causes elevated blood pressure and widened pulse pressure, as well as truncal obesity, moon face, and other cushingoid signs. It’s usually caused by corticosteroid use.

Hypertension

Essential hypertension develops insidiously and is characterized by a gradual increase in blood pressure from decade to decade. Except for this high blood pressure, the patient may be asymptomatic or (rarely) may complain of suboccipital headache, light-headedness, tinnitus, and fatigue.

In malignant hypertension, diastolic pressure abruptly rises above 120 mm Hg, and systolic pressure may exceed 200 mm Hg. Typically, the patient has pulmonary edema marked by jugular vein distention, dyspnea, tachypnea, tachycardia, and a cough with pink, frothy sputum. Other characteristic signs and symptoms include severe headache, confusion, blurred vision, tinnitus, epistaxis, muscle twitching, chest pain, nausea, and vomiting.

Increased intracranial pressure (ICP)

Increased ICP causes an increased respiratory rate initially, followed by increased systolic pressure and widened pulse pressure. Increased ICP affects heart rate last, causing bradycardia (Cushing’s reflex). Associated signs and symptoms include headache, projectile vomiting, decreased level of consciousness, and fixed or dilated pupils.

Metabolic syndrome

Blood pressure that exceeds 135/85 mm Hg is one of the conditions associated with metabolic syndrome (previously called syndrome X). Other conditions that define this syndrome are obesity, abnormal cholesterol level, and high blood insulin level. Individuals with this combination of risk factors are at a significantly greater risk for developing heart disease, stroke, peripheral vascular disease, and type 2 diabetes. Factors contributing to these conditions include physical inactivity, excessive weight gain, and genetic predisposition. Self-care measures, such as exercising, following a heart-healthy diet, and not smoking, often combined with medical therapy, are essential treatments for this syndrome.

Myocardial infarction (MI)

MI is a life-threatening disorder that may cause high or low blood pressure. The most common symptom is crushing chest pain that may radiate to the jaw, shoulder, arm, or epigastrium. Other findings include dyspnea, anxiety, nausea, vomiting, weakness, diaphoresis, atrial gallop, and murmurs.

Pheochromocytoma

Paroxysmal or sustained elevated blood pressure characterizes pheochromocytoma and may be accompanied by orthostatic hypotension. Associated signs and symptoms include anxiety, diaphoresis, palpitations, tremors, pallor, nausea, weight loss, and headache.

Polycystic kidney disease

Elevated blood pressure is typically preceded by flank pain. Other signs and symptoms include enlarged kidneys, an enlarged and tender liver, and intermittent gross hematuria.

Preeclampsia and eclampsia

Potentially life threatening to the mother and fetus, preeclampsia and eclampsia characteristically increase blood pressure. They’re defined as a reading of 140/90 mm Hg or more in the first trimester, a reading of 130/80 mm Hg or more in the second or third trimester, an increase of 30 mm Hg above the patient’s baseline systolic pressure, or an increase of 15 mm Hg above the patient’s baseline diastolic pressure. Other findings include generalized edema, sudden weight gain of 3 lb (1.4 kg) or more per week during the second or third trimester, severe frontal headache, blurred or double vision, decreased urine output, proteinuria, midabdominal pain, neuromuscular irritability, nausea, and possibly seizures (eclampsia).

Renovascular stenosis

Renovascular stenosis produces abruptly elevated systolic and diastolic pressures. Other characteristic signs and symptoms include bruits over the upper abdomen or in the costovertebral angles, hematuria, and acute flank pain.

Thyrotoxicosis

Accompanying the elevated systolic pressure associated with thyrotoxicosis—a potentially life-threatening disorder—are widened pulse pressure, tachycardia, bounding pulse, pulsations in the capillary nail beds, palpitations, weight loss, exophthalmos, an enlarged thyroid gland, weakness, diarrhea, fever over 100° F (37.8° C), and warm, moist skin. The patient may appear nervous and emotionally unstable, displaying occasional outbursts or even psychotic behavior. Heat intolerance, exertional dyspnea and, in females, decreased or absent menses may also occur.

Other causes

Drugs

Central nervous system stimulants (such as amphetamines), sympathomimetics, corticosteroids, nonsteroidal anti-inflammatory drugs, hormonal contraceptives, monoamine oxidase inhibitors, and over-the-counter cold remedies can increase blood pressure, as can cocaine abuse.

Herb Alert

Ephedra (ma huang), ginseng, and licorice may cause high blood pressure or an irregular heartbeat. (Note: The FDA has banned the sale of dietary supplements containing ephedra on the grounds that they pose an unreasonable risk of injury or illness.) St. John’s wort can also raise blood pressure, especially when taken with substances that antagonize hypericin, such as amphetamines, cold and hay fever medications, nasal decongestants, pickled foods, beer, coffee, wine, and chocolate.

Treatments

Kidney dialysis and transplantation cause transient elevation of blood pressure.

» READ BOOK EXCERPT ONLINE »

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

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

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

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

The cause of PIH is unknown, but it appears to be related to inadequate prenatal care (especially poor nutrition), parity (more prevalent in primigravidas), multiple pregnancies, preexisting diabetes mellitus, and hypertension.

Age is also a factor. Adolescents and primiparas over age 35 are at higher risk for preeclampsia. Other theories postulate a long list of potential toxic sources, such as autolysis of placental infarcts, autointoxication, uremia, maternal sensitization to total proteins, and pyelonephritis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Pulmonary hypertension: Causes
(Handbook of Diseases)

Primary pulmonary hypertension begins as hypertrophy of the small pulmonary arteries. The medial and intimal muscle layers of these vessels thicken, decreasing distensibility and increasing resistance. This disorder then progresses to vascular sclerosis and obliteration of small vessels. Because this form of pulmonary hypertension occurs in association with collagen diseases, it’s thought to result from altered immune mechanisms.

Usually, pulmonary hypertension is secondary to hypoxemia from an underlying disease process, including:

❑ alveolar hypoventilation from chronic obstructive pulmonary disease (most common cause in the United States), sarcoidosis, diffuse interstitial pneumonia, pulmonary metastasis, and certain diseases such as sclero-derma.

These diseases may cause pulmo-nary hypertension through alveolar destruction and increased pulmonary vascular resistance. Other disorders that cause alveolar hypoventilation without lung tissue damage include obesity, kyphoscoliosis, and obstructive sleep apnea.

❑ vascular obstruction from pulmonary embolism, vasculitis, and disorders that cause obstructions of small or large pulmonary veins, such as left atrial myxoma, idiopathic veno-occlusive disease, fibrosing mediastinitis, and mediastinal neoplasm.

❑ primary cardiac disease, which may be congenital or acquired. Congenital defects that cause left-to-right shunting of blood — such as patent ductus arteriosus, or atrial or ventricular septal defect — increase blood flow into the lungs and consequently raise pulmonary vascular pressure.

Acquired cardiac disease, such as rheumatic valvular disease and mitral stenosis, increases pulmonary venous pressure by restricting blood flow returning to the heart.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Brain tumors, malignant: Causes
(Handbook of Diseases)

Some tumors are congenital, whereas others are hereditary. The cause of most brain tumors is unknown.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Hydrocephalus: Causes
(Handbook of Diseases)

Hydrocephalus may result from an obstruction in CSF flow (noncommunicating hydrocephalus) or from faulty absorption of CSF (communicating hydrocephalus).

Noncommunicating hydrocephalus

In noncommunicating hydrocephalus, the obstruction occurs most commonly between the third and fourth ventricles, at the aqueduct of Sylvius, but it can also occur at the outlets of the fourth ventricle (foramina of Luschka and Magendie) or, rarely, at the foramen of Monro.

This obstruction may result from faulty fetal development, infection (syphilis, granulomatous diseases, meningitis), a tumor, a cerebral aneurysm, or a blood clot (after intracranial hemorrhage).

Communicating hydrocephalus

In communicating hydrocephalus, faulty absorption of CSF may result from surgery to repair a myelomeningocele, adhesions between meninges at the base of the brain, or meningeal hemorrhage. Rarely, a tumor in the choroid plexus causes overproduction of CSF, producing hydrocephalus.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Hypertension: Causes
(Handbook of Diseases)

Hypertension affects 15% to 20% of adults in the United States. If untreated, it carries a high mortality. Before age 55, a higher percentage of men than women have high blood pressure. This changes after age 55. (See Incidence of hypertension.)

Risk factors

Family history, race (most common in blacks), stress, obesity, a high intake of saturated fats or sodium, use of tobacco, sedentary lifestyle, and aging are risk factors for essential hypertension. Insulin resistance has also been implicated in some patients.

Clinical tip  Systolic hypertension poses a risk that’s equal to or greater than diastolic elevations. It’s commonly seen in elderly people and presents a risk for stroke or myocardial infarction (MI).

Secondary hypertension may result from renovascular disease; pheochromocytoma; primary hyperaldosteronism; Cushing’s syndrome; thyroid, pituitary, or parathyroid dysfunction; coarctation of the aorta; pregnancy; neurologic disorders; and use of hormonal contraceptives or other drugs, such as cocaine, epoetin alfa, and cyclosporine.

Blood pressure regulators

Cardiac output and peripheral vascular resistance determine blood pressure. Increased blood volume, cardiac rate, and stroke volume as well as arteriolar vasoconstriction can raise blood pressure. The link to sustained hypertension is unclear. Hypertension may also result from the failure of the following intrinsic regulatory mechanisms:

❑ Renal hypoperfusion causes the release of renin, which is converted by angiotensinogen, a liver enzyme, to angiotensin I. Angiotensin I is converted to angiotensin II, a powerful vasoconstrictor. The resulting vasoconstriction increases afterload.

Angiotensin II stimulates adrenal secretion of aldosterone, which increases sodium reabsorption. Hypertonic-stimulated release of antidiuretic hormone from the pituitary gland follows, increasing water reabsorption, plasma volume, cardiac output, and blood pressure.

❑ Autoregulation changes the diameter of an artery to maintain perfusion despite fluctuations in systemic blood pressure. The intrinsic mechanisms responsible include stress relaxation (vessels gradually dilate when blood pressure rises to reduce peripheral resistance) and capillary fluid shift (plasma moves between vessels and extravascular spaces to maintain intravascular volume).

❑ When the blood pressure drops, baroreceptors in the aortic arch and carotid sinuses decrease their inhibition of the medulla’s vasomotor center, which increases sympathetic stimulation of the heart by norepinephrine. This in turn increases cardiac output by strengthening the contractile force, increasing the heart rate, and augmenting peripheral resistance by vasoconstriction.

Stress can also stimulate the sympathetic nervous system to increase cardiac output and peripheral vascular resistance.

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Source: Handbook of Diseases, 2003

Hypertension: Principal Causes of Hypertension
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

  1. Transienthypertension
  2. Sustained hypertension
    1. Birthto one year
      1. Mostcommon
        1. Renalartery thrombosis after umbilical artery catheterization
        2. Coarctation of the aorta
        3. Congenital renal disease
        4. Renal artery stenosis
      2. Less common
        1. Bronchopulmonary dysplasia
        2. Patent ductus arteriosus
        3. Intraventricular hemorrhage
    2. One to ten years
      1. Most common
        1. Renaldisease
        2. Coarctation of the aorta
      2. Less common
        1. Renal artery stenosis
        2. Glucocorticoid excess
        3. Sex hormones
        4. Catecholamine excess
        5. Neuroblastoma
        6. Pheochromocytoma
      3. Mineralocorticoid excess
        1. High aldosteronemineralocorticoid excess
          1. Primary aldosteronism
          2. Glucocorticoid-remediable aldosteronism
          3. Hyperreninemic hyperaldosteronism
        2. Low aldosterone mineralocorticoid excess
          1. 17-Alpha-hydroxylasedeficiency
          2. 11-Beta-hydroxylase deficiency
          3. Apparent mineralocorticoid excess
      4. Hyperthyroidism
      5. Hypercalcemia
      6. Renal tumors
      7. Nervous system disorders
      8. Drugs
      9. Primary or essential hypertension
    3. Eleven years through adolescence
      1. Most common
        1. Renaldisease
        2. Primary or essential hypertension
        3. Less common
          1. All diagnoses listed above

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

Blood pressure, increased [Hypertension]: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Anemia.Accompanying elevated systolic pressure in anemia are pulsations in the capillary beds, bounding pulse, tachycardia, systolic ejection murmur, pale mucous membranes and, in patients with sickle cell anemia, ventricular gallop and crackles.

Aortic aneurysm (dissecting).Initially, this life-threatening disorder causes a sudden rise in systolic pressure (which may be the precipitating event), but no change in diastolic pressure; however, this increase is brief. The body's ability to compensate fails, resulting in hypotension.

Other signs and symptoms vary, depending on the type of aortic aneurysm. An abdominal aneurysm may cause persistent abdominal and back pain, weakness, sweating, tachycardia, dyspnea, a pulsating abdominal mass, restlessness, confusion, and cool, clammy skin. A thoracic aneurysm may cause a ripping or tearing sensation in the chest, which may radiate to the neck, shoulders, lower back, or abdomen; pallor; syncope; blindness; loss of consciousness; sweating; dyspnea; tachycardia; cyanosis; leg weakness; murmur; and absent radial and femoral pulses.

Atherosclerosis.With atherosclerosis, systolic pressure rises while diastolic pressure commonly remains normal or slightly elevated. The patient may show no other signs, or he may have a weak pulse, flushed skin, tachycardia, angina, and claudication.

Cushing's syndrome.Cushing's syndrome causes elevated blood pressure and widened pulse pressure as well as truncal obesity, moon face, and other cushingoid signs. It's usually caused by corticosteroid use.

Hypertension.Essential hypertension develops insidiously and is characterized by a gradual increase in blood pressure from decade to decade. Except for this high blood pressure, the patient may be asymptomatic or (rarely) may complain of suboccipital headache, light-headedness, tinnitus, and fatigue.

With malignant hypertension, diastolic pressure abruptly rises above 120 mm Hg, and systolic pressure may exceed 200 mm Hg. Typically, the patient has pulmonary edema marked by jugular vein distention, dyspnea, tachypnea, tachycardia, and coughing of pink, frothy sputum. Other characteristic signs and symptoms include severe headache, confusion, blurred vision, tinnitus, epistaxis, muscle twitching, chest pain, nausea, and vomiting.

Increased intracranial pressure (ICP).Increased ICP causes an increased respiratory rate initially, followed by increased systolic pressure and widened pulse pressure. Increased ICP affects the heart rate last, causing bradycardia (Cushing's reflex). Associated signs and symptoms include headache, projectile vomiting, a decreased level of consciousness, and fixed or dilated pupils.

Metabolic syndrome.Blood pressure that exceeds 135/85 mm Hg is one of the conditions associated with metabolic syndrome (previously called syndrome X). Other conditions that define this syndrome are obesity, abnormal cholesterol level, and high blood insulin level. Individuals with this combination of risk factors are at a significantly greater risk for developing heart disease, stroke, peripheral vascular disease, and type 2 diabetes. Factors contributing to these conditions include physical inactivity, excessive weight gain, and genetic predisposition.

Myocardial infarction (MI).MI is a life-threatening disorder that may cause high or low blood pressure. Common findings include crushing chest pain that may radiate to the jaw, shoulder, arm, or epigastrium. Other findings include dyspnea, anxiety, nausea, vomiting, weakness, diaphoresis, atrial gallop, and murmurs.

Pheochromocytoma.Paroxysmal or sustained elevated blood pressure characterizes pheochromocytoma and may be accompanied by orthostatic hypotension. Associated signs and symptoms include anxiety, diaphoresis, palpitations, tremors, pallor, nausea, weight loss, and headache.

Polycystic kidney disease.With polycystic kidney disease, elevated blood pressure is typically preceded by flank pain. Other signs and symptoms include enlarged kidneys; an enlarged, tender liver; and intermittent gross hematuria.

Preeclampsia and eclampsia.Potentially life-threatening to the mother and fetus, preeclampsia and eclampsia characteristically increase blood pressure. They're defined as a reading of 140/90 mm Hg or more in the first trimester, a reading of 130/80 mm Hg or more in the second or third trimester, an increase of 30 mm Hg above the patient's baseline systolic pressure, or an increase of 15 mm Hg above the patient's baseline diastolic pressure. Accompanying elevated blood pressure are generalized edema, sudden weight gain of 3 lb (1.4 kg) or more per week during the second or third trimester, severe frontal headache, blurred or double vision, decreased urine output, proteinuria, midabdominal pain, neuromuscular irritability, nausea and, possibly, seizures.

Renovascular stenosis.Renovascular stenosis produces abruptly elevated systolic and diastolic pressures. Other characteristic signs and symptoms include bruits over the upper abdomen or in the costovertebral angles, hematuria, and acute flank pain.

Thyrotoxicosis.Accompanying the elevated systolic pressure associated with thyrotoxicosis, a potentially life-threatening disorder, are widened pulse pressure, tachycardia, bounding pulse, pulsations in the capillary nail beds, palpitations, weight loss, exophthalmos, an enlarged thyroid gland, weakness, diarrhea, a fever over 100° F (37.8° C), and warm, moist skin. The patient may appear nervous and emotionally unstable, displaying occasional outbursts or even psychotic behavior. Heat intolerance, exertional dyspnea and, in females, decreased or absent menses may also occur.

Other causes

Drugs.Central nervous system stimulants (such as amphetamines), sympathomimetics, corticosteroids, nonsteroidal anti-inflammatory drugs, hormonal contraceptives, monoamine oxidase inhibitors, and over-the-counter cold remedies can increase blood pressure, as can cocaine abuse.

Treatments.Kidney dialysis and transplantation cause transient elevated blood pressure.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Hydrocephalus: Hydrocephalus - pathophysiology
(The 5-Minute Pediatric Consult)

  • Normal pathway of CSF: Choroid plexus and interstitial fluid (sources), lateral ventricles, foramina of Monro, 3rd ventricle, aqueduct of Sylvius, 4th ventricle, foramina of Luschka and Magendie, subarachnoid space, arachnoid villi, and venous circulation
  • Hydrocephalus results from obstruction to CSF flow, impaired reabsorption, or overproduction of CSF.
  • Noncommunicating (obstructive) hydrocephalus results from obstruction within the ventricular system.
  • Communicating hydrocephalus usually results from impaired CSF reabsorption or (rarely) overproduction (e.g., due to a choroid plexus papilloma).
  • The noncommunicating/communicating distinction has no prognostic significance, but has implications for etiology and choice of therapeutic intervention.

Hydrocephalus - etiology

  • Intraventricular hemorrhage is most commonly due to prematurity, but may also occur with trauma. It results in impaired CSF absorption due to meningeal adhesions, granular ependymitis, and clots. Posthemorrhagic hydrocephalus (PHH) occurs in 35% of all neonates surviving intraventricular hemorrhage; its incidence increases with increasing severity of hemorrhage.
  • Tumors or cysts near the foramina or the aqueduct, or within the ventricular system
  • Infection (meningitis, intrauterine infection) can lead to leptomeningeal adhesions and granulations which block reabsorption of CSF.
  • Developmental:
    • Chiari malformation, type II (associated with myelomeningocele, brain migrational disorders, small posterior fossa, inferior displacement of medulla and cerebellar vermis, kinking of the brainstem, aqueductal stenosis, beaking of the tectum)
    • Dandy-Walker malformation (absence of cerebellar vermis, small cerebellar hemispheres, enlarged posterior fossa, often with cystic 4th ventricle)
    • X-linked and autosomal dominant hydrocephalus; the former is often associated with aqueductal stenosis and mutations in L1CAM on Xq28.
    • Sporadic primary aqueductal stenosis
    • Dysmorphic syndromes (e.g., Apert syndrome, Cockayne syndrome, Crouzon syndrome, Pfeiffer syndrome, trisomy 13, trisomy 18, trisomy 21, triploidy)
    • Alexander disease
    • Mucopolysaccharidoses (e.g., type II (Hunter), type VI, (Maroteaux-Lamy)
    • Migrational disorders/congenital muscular dystrophies (e.g., Miller-Dieker, muscle-eye-brain disease, Fukuyama congenital muscular dystrophy, Walker-Warburg syndrome)
    • Achondroplasia
    • Neurocutaneous syndromes (e.g., neurofibromatosis type 1, rare)
    • Idiopathic

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008

Hypertension: Hypertension - risk factors
(The 5-Minute Pediatric Consult)

  • Primary hypertension: Obesity, sedentary lifestyle, low birth weight, smoking, alcohol, hyperlipidemia, family history, stress, sodium intake, sleep apnea
  • Secondary hypertension: Umbilical artery catheterization, UTI, genetic disease

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008

Pseudotumor Cerebri Idiopathic Intracranial Hypertension: Pseudotumor Cerebri Idiopathic Intracranial Hypertension - pathophysiology
(The 5-Minute Pediatric Consult)

Pathogenesis may involve decreased CSF absorption owing to arachnoid villi dysfunction or elevated intracranial venous pressure. For example, obesity may lead to increased intra-abdominal, intrathoracic, and cardiac filling pressure, eventually leading to elevated intracranial venous pressure.

Pseudotumor Cerebri Idiopathic Intracranial Hypertension - etiology

  • Numerous precipitants of pseudotumor have been reported. In adolescents, it is clearly associated with obesity and weight gain, but not clearly linked to obesity in children younger than 11 years. Many weaker associations may be due to chance.
  • Pseudotumor is often linked to minocycline, tetracycline, sulfonamides, isotretinoin, and thyroid replacements, and to corticosteroid withdrawal. It is also linked to vitamin A deficiency or intoxication, chronic anemia, and hypothyroidism.

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008


 » Next page: Symptoms of Pseudotumor Cerebri

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