Review Kaplan Pathophysiology NGN (2024)

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.

Frequent respiratory infections are a possible manifestation of non-Hodgkin lymphoma, as the disease affects the immune system and makes the client more susceptible to infections. The respiratory tract is one of the most common sites of infection in patients with non-Hodgkin lymphoma.

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.

Fluid volume deficit is a condition in which the body loses more fluid than it takes in. It can cause hypovolemia, which reduces the blood flow to the kidneys and impairs their function. This is the most common cause of prerenal acute kidney injury, which is a result of decreased perfusion to the kidneys.

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.

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.

Histamine, leukotrienes, and prostaglandins are the main inflammatory mediators that cause the clinical manifestations of asthma. They are released by mast cells and other cells in response to allergens or irritants. They cause bronchial smooth muscle contraction, increased vascular permeability, edema, mucus secretion, and airway inflammation.

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.

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.

Redistribution of blood to the heart and brain is a compensatory mechanism for anemia. It occurs to maintain adequate oxygen delivery to the vital organs. It causes vasoconstriction and shunting of blood away from the skin and mucous membranes, resulting in pallor.

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.

Enlargement of the alveoli with destruction of the alveolar walls is the hallmark of emphysema. It reduces the surface area for gas exchange, increases the dead space, and decreases the elastic recoil of the lungs. It causes tachypnea, use of accessory muscles, and hypoxia, which can lead to decreased mental alertness.

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.

Damages the endothelium of the arteries is the main role of inflammation in the development of atherosclerosis. Endothelial injury exposes the subendothelial layer to the blood, which triggers the adhesion of monocytes and platelets. Monocytes differentiate into macrophages and engulf oxidized low-density lipoproteins (LDL), forming foam cells. Foam cells accumulate in the intima and form fatty streaks, which are the earliest lesions of atherosclerosis.

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.

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.

Damages the endothelium of the arteries is the main role of inflammation in the development of atherosclerosis. Endothelial injury exposes the subendothelial layer to the blood, which triggers the adhesion of monocytes and platelets. Monocytes differentiate into macrophages and engulf oxidized low-density lipoproteins (LDL), forming foam cells. Foam cells accumulate in the intima and form fatty streaks, which are the earliest lesions of atherosclerosis.

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 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.

The thyroid gland is enlarged is the best description of a goiter. A goiter is a condition that involves the enlargement of the thyroid gland, which may be due to iodine deficiency, autoimmune disease, inflammation, infection, benign nodules, or thyroid hormone imbalance. A goiter may cause symptoms such as difficulty swallowing, breathing, or speaking, hoarseness, cough, or neck discomfort.

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.

Migration of a clot from the left atrium of the heart is the best explanation for the most likely cause of a left-sided embolic stroke. An embolic stroke is a type of ischemic stroke, which is a lack of blood flow to the brain due to a blockage of a blood vessel by a clot. A clot may form in the left atrium of the heart due to conditions such as atrial fibrillation, which is an irregular heartbeat that causes blood to pool and clot in the heart. A clot may then break off and travel through the bloodstream until it reaches a smaller blood vessel in the brain, where it causes an embolic stroke.