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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.

"My feet swell up during the evening." is not a specific statement for systolic heart failure, but a general sign of fluid retention. Fluid retention may occur in both systolic and diastolic heart failure, as well as other conditions such as kidney disease, liver disease, or venous insufficiency.

"It's harder to breathe during hot and humid weather." is not a specific statement for systolic heart failure, but a common complaint of many people with respiratory problems. Hot and humid weather may increase the workload of the lungs and the heart, but it does not indicate a reduced ejection fraction, which is the hallmark of systolic heart failure.

"I have stomach pain that is worse after meals." is not a specific statement for systolic heart failure, but a possible symptom of gastrointestinal disorders. Stomach pain may be caused by gastritis, ulcers, gallstones, or pancreatitis, among other conditions. It does not reflect the cardiac function or output, which are impaired in systolic heart failure.

Serum glucose 158 mg/dL (8.77 mmol/L) is not the most significant observation for an acute adrenal crisis, but a mild elevation of blood sugar. A mild elevation of blood sugar may occur due to stress, infection, medication, or diet, among other factors. It does not indicate a severe deficiency of adrenal hormones, which is the cause of an acute adrenal crisis.

Weight gain 3 pounds (1.36 kg) in 24 hours is not the most significant observation for an acute adrenal crisis, but a possible sign of fluid retention. Fluid retention may occur due to heart failure, kidney disease, liver disease, or medication, among other causes. It does not indicate a severe deficiency of adrenal hormones, which is the cause of an acute adrenal crisis.

Insomnia and restlessness are not the most significant observations for an acute adrenal crisis, but possible symptoms of anxiety, stress, or hyperthyroidism. Anxiety, stress, and hyperthyroidism may cause difficulty sleeping, nervousness, or agitation, among other effects. They do not indicate a severe deficiency of adrenal hormones, which is the cause of an acute adrenal crisis.

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.

Prostaglandins are inflammatory mediators that are derived from arachidonic acid. They are involved in both the early and late phases of type 1 hypersensitivity response, but they do not cause immediate bronchoconstriction and vasodilation. They mainly cause pain, fever, and inflammation.

Leukotrienes are inflammatory mediators that are derived from arachidonic acid. They are involved in the late phase of type 1 hypersensitivity response, which occurs several hours after exposure to an allergen. They cause sustained bronchoconstriction and inflammation, as well as increased mucus production and airway edema.

Bradykinin is an inflammatory mediator that is formed from plasma proteins. It is not directly involved in type 1 hypersensitivity response, but it may be activated by the complement system, which is part of the innate immune system. It causes vasodilation, increased vascular permeability, and pain.

Ischemia of the motor and sensory neurons in the brain is not the cause of multiple sclerosis, but a possible consequence of it. Ischemia is a lack of blood supply to the tissues, which may result from inflammation, thrombosis, or embolism. It may cause neuronal death, stroke, or dementia.

Infection of the parietal and temporal lobes of the brain is not the cause of multiple sclerosis, but a rare complication of it. Infection of the brain, also called encephalitis, may occur due to viral, bacterial, or fungal agents. It may cause fever, headache, confusion, seizures, or coma.

Increased amounts of epinephrine and acetylcholine in the brain are not the cause of multiple sclerosis, but a possible effect of it. Epinephrine and acetylcholine are neurotransmitters that regulate the sympathetic and parasympathetic nervous systems, respectively. They may be affected by the demyelination of the nerve fibers, which may alter the autonomic functions such as heart rate, blood pressure, digestion, or bladder control.

Herpes simplex 2 virus is not the microorganism that causes infectious mononucleosis, but a different type of herpes virus that causes genital herpes. Genital herpes is a sexually transmitted infection that causes painful blisters and ulcers in the genital area.

Hepatitis C virus is not the microorganism that causes infectious mononucleosis, but a different type of virus that causes hepatitis C. Hepatitis C is a blood-borne infection that affects the liver. It causes inflammation, scarring, and cirrhosis of the liver, which may lead to liver failure or cancer.

Rubella virus is not the microorganism that causes infectious mononucleosis, but a different type of virus that causes rubella. Rubella, also known as German measles, is a mild infection that causes a rash, fever, and swollen glands. It is preventable by vaccination and can be dangerous for pregnant women, as it may cause birth defects or miscarriage.

Increased acetylcholine levels and cholinergic activity in the brain are not the primary factors causing the manifestations of Parkinson's disease. In fact, Parkinson's disease is characterized by a decrease in dopamine levels, not an increase in acetylcholine.

Cell-mediated immune response and muscle fiber damage are not the main mechanisms underlying the clinical manifestations of Parkinson's disease. While inflammation and immune responses may play a role in the progression of the disease, they are not the primary cause of the symptoms observed.

Increased production of dopamine in the motor cortex is not the cause of the symptoms in Parkinson's disease. In fact, patients with Parkinson's disease experience a decrease in dopamine production due to the degeneration of dopamine-producing neurons in the substantia nigra.

Overall, the most plausible explanation for the patient's clinical manifestations is thrombosis of the small blood vessels in the substantia nigra, leading to a decrease in dopamine production.

Increased serum hydrostatic pressure is not the best explanation for the edema because it is caused by fluid overload, not malnutrition. Fluid overload can result from heart failure, kidney failure, or excessive fluid intake.

Increased kidney filtration pressure is not the best explanation for the edema because it is caused by increased blood flow to the kidneys, not malnutrition. Increased blood flow to the kidneys can result from hypertension, diabetes, or renal artery stenosis.

Intracellular dehydration is not the best explanation for the edema because it is caused by loss of water from the cells, not malnutrition. Loss of water from the cells can result from hypernatremia, hyperglycemia, or osmotic diuresis.

A client with a 10-year history of chronic lung disease is not the most at risk to develop metabolic acidosis because chronic lung disease causes respiratory acidosis, not metabolic acidosis. Respiratory acidosis is a condition where the lungs cannot eliminate enough carbon dioxide, resulting in a low pH and a high bicarbonate level in the blood.

A client receiving parenteral nutrition for 2 weeks is not the most at risk to develop metabolic acidosis because parenteral nutrition does not affect the acid-base balance of the body, unless there is an infection or a complication. Parenteral nutrition is a method of providing nutrients through a vein, bypassing the digestive system.

A client with a temperature of 102°F (38.9°C) for 48 hours is not the most at risk to develop metabolic acidosis because fever does not directly cause metabolic acidosis, unless there is dehydration or sepsis. Fever is a symptom of an infection or inflammation, which can increase the metabolic rate and the production of carbon dioxide, but the lungs can usually compensate by increasing the ventilation.

Weight gain is not a common complication of Crohn's disease because Crohn's disease causes inflammation and ulceration of the digestive tract, which can lead to malabsorption, diarrhea, and weight loss.

Vomiting after meals is not a common complication of Crohn's disease because Crohn's disease mainly affects the small intestine and the colon, not the stomach. Vomiting after meals can be a sign of gastric ulcers, gastritis, or gastroparesis.

Urinary tract infections are not a common complication of Crohn's disease because Crohn's disease does not directly affect the urinary system. However, some people with Crohn's disease may develop enterovesical fistulas, which are abnormal connections between the bowel and the bladder. Enterovesical fistulas can cause urinary tract infections, hematuria, and pneumaturia.

"I was short of breath when I walked around the block yesterday." is not the most significant statement because it is a common symptom of chronic bronchitis, but it does not indicate the severity or the progression of the condition. Shortness of breath is caused by the inflammation and narrowing of the airways, which reduce the airflow and oxygen delivery to the lungs.

"My respiratory secretions are greenish-yellow colored today." is not the most significant statement because it is a sign of a possible infection, but it does not necessarily indicate chronic bronchitis. Greenish-yellow colored sputum can be caused by various respiratory conditions, such as pneumonia, tuberculosis, or cystic fibrosis.

"My feet are swollen and painful at the end of the afternoon." is not the most significant statement because it is a sign of a possible complication of chronic bronchitis, but it does not directly relate to the condition. Swollen and painful feet can be caused by right-sided heart failure, which can result from chronic bronchitis. Chronic bronchitis can increase the pressure in the pulmonary arteries, which can strain the right ventricle and cause it to fail. This can lead to fluid retention and edema in the lower extremities.

There is still too much swelling in the area of the surgery and fluid is accumulating is not the correct explanation because it does not address the underlying cause of the edema. Swelling is a normal response to surgery, but it usually subsides within a few days or weeks. The edema caused by lymph node removal is chronic and persistent, and it does not improve with time.

The veins were removed from the axilla during surgery and there is poor circulation now is not the correct explanation because it is not true. The veins are not removed during a radical mastectomy, only the lymph nodes are. The veins are part of the circulatory system, which carries blood throughout the body. The blood flow to the arm and hand is not affected by the surgery, unless there is a complication such as a blood clot or an infection.

You will need to wear a compression bandage to help fluids move from the area is not the correct explanation because it is a treatment, not a cause. A compression bandage is a type of elastic bandage that applies pressure to the arm and hand, which helps to reduce the swelling and prevent further fluid accumulation. However, it does not address the root cause of the edema, which is the removal of the lymph nodes.

Hemothorax is not the correct explanation because it is a condition where blood accumulates in the pleural space, which is the area between the lungs and the chest wall. Hemothorax can cause low blood pressure, rapid breathing, and reduced breath sounds, but it does not cause tracheal deviation, which is a sign of increased pressure in the chest.

Absorption atelectasis is not the correct explanation because it is a condition where the alveoli, which are the tiny air sacs in the lungs, collapse due to lack of oxygen. Absorption atelectasis can cause reduced breath sounds, but it does not cause low blood pressure, rapid breathing, or tracheal deviation, which are signs of a life-threatening emergency.

Hypovolemic shock is not the correct explanation because it is a condition where the body loses a large amount of blood or fluid, which reduces the blood volume and the blood pressure. Hypovolemic shock can cause low blood pressure and rapid breathing, but it does not cause absent breath sounds or tracheal deviation, which are signs of a chest injury.

Formation of a clot in the middle cerebral artery is not the most likely cause of death because it is a condition that affects the brain, not the heart. A clot in the middle cerebral artery can cause a stroke, which is a sudden interruption of blood flow to the brain, resulting in brain damage and neurological deficits. A stroke can be fatal, but it does not usually cause cardiopulmonary arrest, which is a sudden cessation of heart and lung function.

Fluid volume overload and decreased serum potassium levels are not the most likely cause of death because they are conditions that affect the fluid and electrolyte balance of the body, not the heart. Fluid volume overload is a condition where the body retains too much fluid, which can cause edema, hypertension, and heart failure. Decreased serum potassium levels are a condition where the blood has too little potassium, which is an electrolyte that helps regulate the nerve and muscle function, including the heart. Both conditions can affect the heart function, but they are not usually the direct cause of cardiopulmonary arrest.

Diffuse atherosclerosis in the left main coronary artery circulation is not the most likely cause of death because it is a condition that affects the blood vessels, not the heart. Atherosclerosis is a disease that causes the buildup of plaque, which is a fatty substance, in the walls of the arteries, which are the blood vessels that carry oxygen-rich blood to the organs. Diffuse atherosclerosis in the left main coronary artery circulation means that the plaque affects the entire length of the artery that supplies blood to the left side of the heart, which is the side that pumps blood to the rest of the body. Atherosclerosis can cause coronary artery disease, which is a condition where the heart does not receive enough blood and oxygen, leading to chest pain, angina, or heart attack. A heart attack can cause cardiopulmonary arrest, but it is not as common as sudden cardiac death in young adults.

Shallow respirations and a smooth, beefy red tongue are not the expected findings because they are signs of pernicious anemia, not acute blood loss. Pernicious anemia is a condition where the body cannot produce enough red blood cells due to a lack of vitamin B12, which is needed for DNA synthesis and cell division. Pernicious anemia can cause shallow respirations due to hypoxia, which is a low level of oxygen in the tissues, and a smooth, beefy red tongue due to atrophy of the tongue papillae, which are the small projections that give the tongue its rough texture.

Facial flushing with distended neck veins are not the expected findings because they are signs of polycythemia, not acute blood loss. Polycythemia is a condition where the body produces too many red blood cells, which increases the blood volume and the blood viscosity, making the blood thicker and harder to flow. Polycythemia can cause facial flushing due to increased blood flow to the skin, and distended neck veins due to increased pressure in the venous system.

Bilateral numbness and tingling of the extremities are not the expected findings because they are signs of peripheral neuropathy, not acute blood loss. Peripheral neuropathy is a condition where the nerves that carry signals from the brain and spinal cord to the rest of the body are damaged or impaired, causing sensory and motor disturbances. Peripheral neuropathy can cause bilateral numbness and tingling of the extremities due to reduced nerve conduction and sensation.