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Systemic lupus erythematosus (SLE) is an autoimmune disease where the immune system produces autoantibodies, such as anti-nuclear antibodies, that attack healthy tissues like joints, skin, kidneys, and other organs. This leads to chronic inflammation and tissue damage. B-cell hyperactivity and T-cell dysfunction drive this process, causing systemic effects. This statement is accurate, as autoimmunity defines SLE’s pathology, distinguishing it from non-autoimmune disorders.

Most individuals with SLE survive due to improved treatments like immunosuppressive drugs, with over 90% surviving beyond 10 years. However, it can be fatal due to complications such as kidney failure, cardiovascular disease, or infections during severe flares. This statement is accurate, reflecting the disease’s manageable yet potentially lethal nature, especially with organ involvement.

SLE is a chronic, progressive connective tissue disorder characterized by periods of flares and remission. It affects connective tissues like joints and skin, with progressive organ damage possible in severe cases. This statement is accurate, as SLE’s chronic nature and connective tissue involvement are central to its pathophysiology, often requiring long-term management.

Staphylococcus aureus is a gram-positive coccus that can cause UTIs, particularly in catheterized or hospitalized patients, but it accounts for less than 5% of cases. It is more commonly associated with skin or bloodstream infections. Its lower prevalence in UTIs compared to E. coli makes it a less likely cause.

Pseudomonas aeruginosa, a gram-negative bacillus, is an opportunistic pathogen causing UTIs primarily in immunocompromised or catheterized patients. It accounts for less than 10% of UTIs. Its resistance to antibiotics and preference for nosocomial settings make it less common than E. coli in community-acquired infections.

Klebsiella pneumoniae, another gram-negative bacillus, causes about 5-10% of UTIs, often in hospitalized or immunocompromised patients. While it can adhere to urinary epithelium, its prevalence is significantly lower than E. coli, which dominates due to its ubiquitous presence in the gut and urogenital proximity.

Spironolactone, a potassium-sparing diuretic, inhibits aldosterone in the distal tubule, reducing sodium reabsorption and increasing urine output. However, its diuretic effect is weaker than furosemide, as it affects only 2-3% of filtered sodium. It is primarily used for managing hyperaldosteronism or potassium retention, not rapid urine flow increase.

Hydrochlorothiazide, a thiazide diuretic, inhibits sodium-chloride reabsorption in the distal convoluted tubule, increasing urine output. Its effect is milder than furosemide, impacting about 5-10% of filtered sodium. It is commonly used for hypertension but is less potent for rapid diuresis in conditions requiring significant urine flow.

Mannitol, an osmotic diuretic, increases urine flow by preventing water reabsorption in the proximal tubule and loop of Henle. It is effective in acute settings like cerebral edema but less commonly used for routine diuresis compared to furosemide, which has a broader and more rapid effect on urine output.

Stress is a well-documented trigger for IBS symptoms. The brain-gut axis, involving the hypothalamic-pituitary-adrenal axis, modulates gut motility and sensitivity. Psychological stress can exacerbate visceral pain, diarrhea, or constipation by altering neurotransmitter release and gut microbiome interactions, making this statement accurate for IBS pathophysiology.

IBS treatment focuses on symptom relief, as there is no cure. Strategies include dietary modifications (e.g., low FODMAP diet), antispasmodics, laxatives, or antidiarrheals to manage pain, bloating, and bowel irregularities. This statement is accurate, reflecting the symptomatic approach to improving quality of life in IBS patients.

IBS symptoms commonly include constipation, diarrhea, or alternating patterns, along with abdominal pain and bloating. These result from dysregulated gut motility and visceral hypersensitivity, affecting the enteric nervous system. This statement is accurate, as variable bowel habits are a hallmark of IBS diagnostic criteria.

Acetaminophen reduces fever by acting on the hypothalamic thermoregulatory center but is ineffective for heat stroke, a hyperthermic emergency caused by environmental heat overload. It does not address core temperature elevation or systemic effects like dehydration and organ dysfunction, making it inappropriate for immediate heat stroke management.

Placing a client with heat stroke in a hot bath would exacerbate hyperthermia, worsening organ damage and cardiovascular strain. Heat stroke requires rapid cooling via cold water immersion or evaporative methods, not additional heat exposure, making this intervention dangerous and contraindicated in this life-threatening condition.

Encouraging oral fluids like cold water is inappropriate for a lethargic heat stroke patient, who may have impaired swallowing or consciousness, risking aspiration. Intravenous fluids are preferred to correct dehydration and electrolyte imbalances safely, as oral intake does not address the urgent need for rapid cooling and systemic stabilization.

Hypothyroidism is less directly linked to obesity than type 2 diabetes. While it can cause weight gain due to slowed metabolism, obesity is not a primary risk factor for hypothyroidism. Thyroid dysfunction arises more from autoimmune or iodine-related causes, making it a less likely complication compared to diabetes.

Osteoporosis risk is not strongly associated with obesity. Excess body weight may increase bone density due to mechanical loading, but it does not directly cause bone loss. Obesity-related inflammation may have minor effects, but type 2 diabetes poses a far greater risk due to metabolic changes.

Migraine headaches are not a primary complication of obesity. While obesity may exacerbate migraines through inflammatory pathways or comorbidities like sleep apnea, the association is weaker than with type 2 diabetes. Metabolic and insulin-related effects of obesity make diabetes the most significant and direct risk.

Low aldosterone levels do not cause ascites; instead, high aldosterone in liver disease (e.g., cirrhosis) promotes sodium and water retention, exacerbating fluid accumulation. This statement is inaccurate, as secondary hyperaldosteronism due to reduced liver metabolism of aldosterone is a key factor in ascites development.

The liver’s failure to produce clotting factors can lead to bleeding tendencies, like variceal hemorrhage, but this does not directly cause ascites. Ascites is driven by fluid leakage from capillaries, not bleeding. This statement is inaccurate, as clotting factor deficiency is unrelated to peritoneal fluid accumulation.

While fluid imbalance contributes to ascites, the primary mechanism involves portal hypertension and capillary permeability, not just osmotic pressure changes. This statement is overly vague and less accurate than the specific role of inflammatory molecules increasing capillary leakage in the peritoneal cavity.

Ecchymosis, or bruising, may occur with a fracture due to soft tissue injury and bleeding but is not specific to fractures. It results from ruptured blood vessels in the skin, not bone disruption, and can occur in many trauma scenarios, making it less definitive than crepitus for fracture assessment.

Shock can occur with severe fractures due to blood loss or pain but is not a direct manifestation of the fracture itself. It reflects systemic response to trauma, not the localized bone injury, making it less specific than crepitus for identifying a fracture during assessment.

Deformity is a common fracture sign due to bone misalignment but is not always present, especially in hairline or non-displaced fractures. Crepitus is more consistently detectable in physical exams, as it directly results from bone fragment movement, making it a more reliable clinical manifestation.

Undisplaced fractures, where bone segments remain aligned, heal faster, typically in 6-8 weeks. Minimal disruption to blood supply and periosteum allows efficient callus formation and remodeling. These fractures require less intervention, as the stable bone structure supports osteoblast activity and collagen deposition, leading to quicker recovery.

Greenstick fractures, common in children, involve partial bone breaks due to flexible bones. They heal relatively quickly, in 4-8 weeks, as the intact periosteum supports rapid callus formation. The partial break preserves some blood supply, facilitating osteoblast activity and bone remodeling, making healing faster than compound fractures.

Oblique fractures, with angled breaks, heal in 6-12 weeks, depending on stability. While more complex than undisplaced fractures, they have less soft tissue damage than compound fractures. Blood supply disruption is moderate, and surgical fixation may be needed, but healing is faster than in open fractures due to lower infection risk.

Calcium levels in plasma are primarily regulated by parathyroid hormone and vitamin D, not insulin. Insulin has minimal direct effect on calcium transport into cells. Calcium is critical for bone health and muscle function, but its movement is not significantly influenced by insulin’s action on cellular membranes.

Magnesium is regulated by renal and gastrointestinal mechanisms, not directly by insulin. While insulin may indirectly influence magnesium via metabolic effects, it does not actively drive magnesium into cells like potassium. Magnesium is essential for enzymatic reactions, but its plasma levels are not significantly altered by insulin.

Sodium is primarily regulated by aldosterone and the renin-angiotensin system, not insulin. Insulin does not directly force sodium into cells but may influence sodium-potassium ATPase indirectly. Sodium’s extracellular role in fluid balance is distinct from insulin’s intracellular potassium transport, making it an incorrect choice.