A nurse is cleansing a patient’s infected pressure ulcer. Wh…
Questions
A nurse is cleаnsing а pаtient’s infected pressure ulcer. What type оf equipment wоuld be apprоpriate to use?
Addisоn Diseаse (Primаry Adrenаl Insufficiency) (Study Outline) Fоr study оnly—this is not medical advice or a substitute for professional care. 1. Background Definition:Primary adrenal insufficiency due to destruction or dysfunction of the adrenal cortex, leading to deficient production of glucocorticoids (cortisol), mineralocorticoids (aldosterone), and androgens. Pathophysiology: Loss of cortisol → ↓ gluconeogenesis, ↓ stress response. Loss of aldosterone → ↑ sodium loss, ↓ potassium and hydrogen excretion → hyponatremia, hyperkalemia, metabolic acidosis. Loss of androgens (in women) → ↓ axillary/pubic hair and libido. ↑ ACTH and melanocyte-stimulating hormone (MSH) → hyperpigmentation. Common Causes: Autoimmune destruction (most common in U.S.) — part of autoimmune polyglandular syndrome type II. Infectious: tuberculosis (worldwide), fungal, CMV, HIV. Hemorrhage/infarction: Waterhouse–Friderichsen syndrome (meningococcemia), anticoagulant use. Metastatic cancer (lung, breast). Adrenoleukodystrophy (X-linked). Epidemiology: Most frequent in women aged 30–50 years. Autoimmune cases often coexist with other autoimmune disorders (thyroid disease, type 1 diabetes). 2. History Symptoms (Gradual Onset): Fatigue, weakness, weight loss. Anorexia, nausea, vomiting, abdominal pain. Salt craving (due to hyponatremia). Dizziness or lightheadedness (from hypotension). Muscle/joint pain. Skin Changes: Hyperpigmentation (palmar creases, gums, scars, sun-exposed areas) due to ↑ ACTH/MSH. Acute Presentation (Adrenal Crisis): Hypotension, shock, hypoglycemia, confusion, vomiting, often precipitated by stress (infection, surgery, trauma). Historical Clues: History of autoimmune disease or chronic steroid use (risk of secondary insufficiency after withdrawal). 3. Exam Findings General: Weight loss, dehydration, fatigue. Vital Signs: Hypotension (especially orthostatic). Skin: Diffuse hyperpigmentation, especially in creases and buccal mucosa. Cardiovascular: Postural tachycardia. Abdomen: Nonspecific tenderness or mild pain. Neurologic: Lethargy, confusion (severe cases). In Women: Loss of body hair (due to low adrenal androgens). 4. Making the Diagnosis Step 1 – Initial Evaluation: Morning (8 AM) serum cortisol: Low cortisol (
Hyperоsmоlаr Hyperglycemic Stаte (HHS) (Study Outline) Fоr study only—this is not medicаl advice or a substitute for professional care. 1. Background Definition:A severe complication of diabetes mellitus, characterized by marked hyperglycemia, hyperosmolarity, and dehydration, without significant ketoacidosis. Pathophysiology: Relative insulin deficiency prevents adequate glucose utilization but is sufficient to suppress ketogenesis. Excess counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone) exacerbate hyperglycemia. Osmotic diuresis from extreme hyperglycemia causes massive water and electrolyte losses, leading to profound dehydration and hyperosmolarity. Epidemiology: Occurs mainly in Type 2 diabetes (older adults most commonly). Mortality rate higher than DKA (up to 20%). Precipitating Factors: Infection (most common, e.g., pneumonia, UTI). Inadequate insulin or missed doses. Stress events: stroke, MI, trauma, surgery. Medications: glucocorticoids, thiazides, β-blockers, atypical antipsychotics. 2. History Gradual onset (days to weeks). Symptoms of hyperglycemia and dehydration: Polyuria, polydipsia, weight loss, weakness. Confusion, lethargy, or altered mental status (often profound). Often no history of ketosis or abdominal pain (contrast with DKA). Historical clues: Elderly patient with poor access to fluids or underlying infection. Type 2 diabetic with poor glycemic control or noncompliance. 3. Exam Findings General: Marked dehydration: dry mucous membranes, poor skin turgor, sunken eyes. Tachycardia, hypotension (signs of volume depletion). Neurologic: Altered sensorium: confusion, obtundation, focal deficits, or seizures due to high osmolality (>320 mOsm/kg). Respiratory: No Kussmaul respirations (unlike DKA, since acidosis minimal). Temperature: May be elevated if infection is precipitating factor. Abdomen: Typically benign; absence of abdominal pain distinguishes from DKA. 4. Making the Diagnosis Key Diagnostic Criteria: Parameter HHS DKA (for comparison) Plasma glucose >600 mg/dL >250 mg/dL Arterial pH >7.30 18 mEq/L 320 mOsm/kg Variable Anion gap Normal or mildly elevated Elevated Laboratory Findings: Severe hyperglycemia and elevated serum osmolality. Prerenal azotemia (↑ BUN/creatinine ratio). Mild hyponatremia (from osmotic dilution). Potassium: May be normal or elevated at presentation, but total body stores are depleted. Gold Standard: Laboratory evidence of marked hyperosmolarity with minimal ketosis or acidosis. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment regimens.) Primary Goals: Aggressive fluid resuscitation — correct dehydration first. Gradual correction of hyperglycemia — insulin therapy after rehydration initiated. Monitor and replace electrolytes (especially potassium, phosphate). Identify and treat precipitating cause (infection, MI, etc.). Monitoring: Hourly glucose checks. Frequent electrolytes and serum osmolality. Avoid rapid osmolar shifts → prevent cerebral edema. Complications: Cerebral edema (especially with rapid osmolar correction). Seizures due to hyperosmolarity. Thromboembolic events from severe dehydration and hyperviscosity. Disposition: Usually requires ICU-level monitoring due to high mortality and risk of recurrence. QUESTION An 80-year-old woman with type 2 diabetes presents with confusion and lethargy. Her daughter reports several days of poor oral intake and missed medication doses. On exam, she is tachycardic and hypotensive with dry mucous membranes. Laboratory results show: Glucose: 980 mg/dL Serum osmolality: 345 mOsm/kg Bicarbonate: 22 mEq/L Negative serum ketones Which of the following mechanisms best explains her altered mental status? A. Accumulation of ketoacids due to insulin deficiencyB. Cerebral hypoperfusion from hypotension and dehydrationC. Increased serum osmolarity causing neuronal dehydrationD. Respiratory acidosis from hypoventilation
Hypоthyrоidism (Study Outline) Fоr study only—this is not medicаl аdvice or а substitute for professional care. 1. Background Definition:A clinical syndrome resulting from deficient production of thyroid hormones (T₄ and T₃) or impaired action at the tissue level. Pathophysiology: Primary hypothyroidism (most common): failure of the thyroid gland → ↑ TSH, ↓ free T₄. Secondary (central): pituitary dysfunction → ↓ TSH and ↓ T₄. Tertiary: hypothalamic failure (↓ TRH). Common Causes (Primary): Autoimmune (Hashimoto thyroiditis) – most common in the U.S. Iatrogenic: post-thyroidectomy, radioactive iodine, or antithyroid medications. Iodine deficiency or excess. Congenital hypothyroidism (thyroid dysgenesis, enzyme defects). Drugs: lithium, amiodarone, interferon-α, tyrosine kinase inhibitors. Epidemiology: More common in women and older adults. Hashimoto’s thyroiditis often associated with other autoimmune disorders (e.g., type 1 DM, pernicious anemia). 2. History Symptoms (Gradual Onset): Fatigue, weakness, cold intolerance. Weight gain despite decreased appetite. Constipation. Dry skin, hair loss, brittle nails. Depression, memory impairment, slowed thinking. Menstrual irregularities, infertility. Severe Forms: Myxedema: severe, long-standing hypothyroidism → nonpitting edema, facial puffiness, hoarseness, periorbital swelling. Myxedema coma: life-threatening decompensation with hypothermia, bradycardia, hypotension, and hypoventilation (precipitated by illness or sedatives). Historical Clues: Prior thyroid surgery or radioactive iodine therapy. Family history of autoimmune disease. Recent medication changes (e.g., lithium, amiodarone). 3. Exam Findings General: Fatigued appearance, weight gain, coarse dry hair, pallor. Skin: Cool, dry, thickened skin; nonpitting edema (myxedema). Cardiovascular: Bradycardia, diastolic hypertension, pericardial effusion (severe). Neurologic: Delayed relaxation of deep tendon reflexes (especially Achilles). HEENT: Puffy face, periorbital edema, enlarged or atrophic thyroid. Other: Macroglossia, hoarseness, carpal tunnel syndrome. Pediatric Findings: Growth retardation, delayed bone age, developmental delay if congenital. 4. Making the Diagnosis Initial Test (Gold Standard): Serum TSH — most sensitive screening test. Interpretation: Primary hypothyroidism: ↑ TSH, ↓ free T₄. Secondary (pituitary): ↓ or inappropriately normal TSH, ↓ free T₄. Subclinical hypothyroidism: mildly ↑ TSH with normal free T₄. Autoimmune Confirmation: Positive anti-thyroid peroxidase (anti-TPO) or anti-thyroglobulin antibodies → Hashimoto thyroiditis. Other Findings: Lipid abnormalities: hypercholesterolemia, ↑ LDL. Hyponatremia: due to decreased free water clearance. Anemia: normocytic or macrocytic. Imaging: Thyroid ultrasound: heterogenous or atrophic gland (Hashimoto). MRI of pituitary: indicated if secondary hypothyroidism suspected. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment directives.) General Principles: Thyroid hormone replacement (e.g., levothyroxine) is standard. Primary hypothyroidism: lifelong replacement and regular TSH monitoring. Secondary hypothyroidism: monitor free T₄, not TSH, for adjustment. Special Situations (Conceptual): Myxedema coma: medical emergency—requires ICU care and supportive management. Pregnancy: increased thyroid hormone requirement; check TSH each trimester. Exam Tip: Drug-induced hypothyroidism → lithium, amiodarone. Most sensitive test: serum TSH. Hashimoto thyroiditis: firm, irregular, painless goiter + positive anti-TPO antibodies. Monitoring: Reassess TSH every 6–8 weeks after dose adjustment. Evaluate for improvement in symptoms, energy, and metabolic parameters. QUESTION A 45-year-old woman presents with fatigue, weight gain, and constipation. Physical exam shows dry skin, bradycardia, and delayed relaxation of deep tendon reflexes. Laboratory results reveal TSH 9.8 mIU/L (elevated) and free T₄ below normal. Which of the following additional findings is most likely? A. Elevated anti-thyroid peroxidase (anti-TPO) antibodiesB. Elevated free T₃ and suppressed TSHC. Elevated serum calcium and decreased phosphateD. Decreased LDL cholesterol