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Enlargement of the spleen is not a common sign of non-Hodgkin lymphoma, but it may occur in some cases. It is more likely to be associated with chronic lymphocytic leukemia or Hodgkin lymphoma.

Confusion and agitation are not typical symptoms of non-Hodgkin lymphoma, but they may indicate central nervous system involvement or metabolic disturbances. They are more common in patients with brain tumors or infections.

Painful lesions of the lips and oral mucosa are not characteristic of non-Hodgkin lymphoma, but they may be caused by other conditions such as herpes simplex virus, aphthous ulcers, or oral cancer. They are more common in patients with immunodeficiency or poor oral hygiene.

Glomerulonephritis is an inflammation of the glomeruli, the filtering units of the kidneys. It can cause damage to the renal tissue and lead to intrinsic acute kidney injury, not prerenal acute kidney injury.

Neurogenic bladder is a dysfunction of the bladder caused by a nerve problem. It can affect the ability to store or empty urine. It can cause urinary retention, which increases the pressure in the urinary tract and damages the kidneys. This is a type of postrenal acute kidney injury, which is a result of obstruction to the urine outflow.

Renal calculus is a solid mass formed from crystals in the urine. It can block the ureter, the tube that carries urine from the kidney to the bladder. It can cause hydronephrosis, which is a swelling of the kidney due to accumulation of urine. This is another type of postrenal acute kidney injury.

Macrophages, monocytes, and bradykinin are involved in the inflammatory response, but they do not directly cause the symptoms of asthma. They may activate other cells and mediators that contribute to bronchoconstriction and mucus production.

B lymphocytes, serotonin, and immunoglobulin D are not major players in the pathophysiology of asthma. B lymphocytes produce immunoglobulins, but immunoglobulin E (IgE) is the main antibody involved in allergic asthma. Serotonin is a neurotransmitter that may affect mood and sleep, but it does not cause bronchospasm. Immunoglobulin D is a rare antibody that has no known role in asthma.

Helper T lymphocytes, natural killer cells, and interleukin-1 are involved in the immune response, but they do not directly cause the symptoms of asthma. They may modulate the activation and differentiation of other cells and mediators that contribute to airway hyperresponsiveness and inflammation.

Blood clots in the peripheral blood vessels are not a cause of anemia, but a complication of it. They may occur due to increased blood viscosity, reduced blood flow, or hypercoagulability. They may cause tissue ischemia, pain, and necrosis.

Decrease in bone marrow platelet production is not a cause of anemia, but a result of it. It may occur due to bone marrow suppression, infiltration, or destruction. It may cause bleeding, bruising, and petechiae.

Increase in the number of circulating reticulocytes is not a cause of anemia, but a sign of it. Reticulocytes are immature red blood cells that are released from the bone marrow to compensate for the loss of mature red blood cells. They indicate a regenerative response to anemia.

Bronchial constriction after inhalation of an irritant is a possible trigger for an asthma attack, not emphysema. It causes wheezing, coughing, and dyspnea, but it does not affect the alveolar structure or function.

Damage to the mucociliary lining of the segmental bronchi is a consequence of chronic bronchitis, not emphysema. It impairs the clearance of mucus and pathogens from the airways, leading to recurrent infections and inflammation.

Infiltration of bacteria and inflammatory exudates into the alveoli is a sign of pneumonia, not emphysema. It causes fever, chills, productive cough, and chest pain, but it does not cause permanent damage to the alveoli.

Initiates the fibrinolytic process in the arteries is not a role of inflammation in the development of atherosclerosis, but a protective mechanism against it. Fibrinolysis is the breakdown of blood clots by enzymes such as plasmin. It prevents the formation of thrombi that can occlude the arteries and cause ischemia.

Decreases highly sensitive C-reactive protein (hsCRP) levels is not a role of inflammation in the development of atherosclerosis, but an indicator of it. hsCRP is a marker of systemic inflammation that is produced by the liver in response to cytokines. It is elevated in patients with atherosclerosis and correlates with the risk of cardiovascular events.

Causes diffuse arterial vasoconstriction is not a role of inflammation in the development of atherosclerosis, but a consequence of it. Atherosclerosis narrows the lumen of the arteries and reduces the blood flow to the tissues. This causes ischemia, which stimulates the release of vasoconstrictors such as angiotensin II and endothelin. Vasoconstriction further worsens the ischemia and increases the blood pressure.

Tumor necrosis factor is released by T lymphocytes and lyses the Mycobacterium tuberculosis bacteria in the alveoli is not a correct explanation for the primary immune response to tuberculosis infection. Tumor necrosis factor is a cytokine that activates macrophages and induces inflammation, but it does not directly kill the bacteria. It may also have harmful effects by causing tissue damage and weight loss.

Natural killer cells and neutrophils form a thick purulent debris, which becomes a caseous necrosis is not a correct explanation for the primary immune response to tuberculosis infection. Natural killer cells and neutrophils are part of the innate immune system, which is not very effective against intracellular bacteria like Mycobacterium tuberculosis. Caseous necrosis is a type of tissue death that results from the liquefaction of the granuloma. It is a sign of progressive disease, not primary infection.

The inflammatory response of cytokines activates the complement system and causes permanent lung tissue damage is not a correct explanation for the primary immune response to tuberculosis infection. The inflammatory response of cytokines and the complement system are part of the innate immune system, which is not very effective against intracellular bacteria like Mycobacterium tuberculosis. Permanent lung tissue damage is a complication of chronic or reactivated tuberculosis, not primary infection.

Initiates the fibrinolytic process in the arteries is not a role of inflammation in the development of atherosclerosis, but a protective mechanism against it. Fibrinolysis is the breakdown of blood clots by enzymes such as plasmin. It prevents the formation of thrombi that can occlude the arteries and cause ischemia.

Decreases highly sensitive C-reactive protein (hsCRP) levels is not a role of inflammation in the development of atherosclerosis, but an indicator of it. hsCRP is a marker of systemic inflammation that is produced by the liver in response to cytokines. It is elevated in patients with atherosclerosis and correlates with the risk of cardiovascular events.

Causes diffuse arterial vasoconstriction is not a role of inflammation in the development of atherosclerosis, but a consequence of it. Atherosclerosis narrows the lumen of the arteries and reduces the blood flow to the tissues. This causes ischemia, which stimulates the release of vasoconstrictors such as angiotensin II and endothelin. Vasoconstriction further worsens the ischemia and increases the blood pressure.

The thyroid gland is cancerous is not a correct description of a goiter. A goiter is a non-specific term that refers to any enlargement of the thyroid gland, which may have various causes and may or may not be associated with thyroid cancer.

The client has a low serum calcium level is not a correct description of a goiter. A low serum calcium level is a sign of hypoparathyroidism, which is a condition that affects the parathyroid glands, not the thyroid gland. The parathyroid glands are located behind the thyroid gland and regulate the calcium and phosphorus levels in the blood.

The thyroid gland has been surgically removed is not a correct description of a goiter. A goiter is a condition that involves the presence of an enlarged thyroid gland, not the absence of it. A surgical removal of the thyroid gland is called a thyroidectomy, which may be done for various reasons such as thyroid cancer, hyperthyroidism, or large goiters.

A sacculated aneurysm in the circle of Willis is not the most likely cause of a left-sided embolic stroke. A sacculated aneurysm is a bulging of a weak spot in the wall of an artery, which may occur in the circle of Willis, a network of arteries at the base of the brain. A sacculated aneurysm may cause a hemorrhagic stroke, which is a bleeding into the brain, not an embolic stroke, which is a blockage of a blood vessel by a clot.

Rupture of small cerebral blood vessels is not the most likely cause of a left-sided embolic stroke. Rupture of small cerebral blood vessels may occur due to hypertension, diabetes, or aging, which may damage the integrity of the blood vessel walls. Rupture of small cerebral blood vessels may cause a hemorrhagic stroke, which is a bleeding into the brain, not an embolic stroke, which is a blockage of a blood vessel by a clot.

Diffuse inflammation of the small diameter blood vessels is not the most likely cause of a left-sided embolic stroke. Diffuse inflammation of the small diameter blood vessels may occur due to vasculitis, which is an autoimmune disorder that causes inflammation and narrowing of the blood vessels. Diffuse inflammation of the small diameter blood vessels may cause a thrombotic stroke, which is a formation of a clot within the blood vessel, not an embolic stroke, which is a blockage of a blood vessel by a clot that travels from another site.