Instructions: Create an EERD model for each scenario using M…
Questions
Instructiоns: Creаte аn EERD mоdel fоr eаch scenario using MySQL Workbench. Identify tables, primary keys, foreign keys, relationships, and cardinality (crows feet). Submit a screenshot showing the entire EERD with the connections. You may also submit the .mwb file if you would like. You need to design a database for art galleries. The database captures all the information that galleries need to maintain. Galleries keep information about artists, their names (which are unique), birthplaces, age, and style of art. For each piece of artwork, the artist, the year it was made, its unique title, its type of art (e.g., painting, lithograph, sculpture, photograph), and its price must be stored. Pieces of artwork are also classified into groups of various kinds, for example, portraits, still lifes, works by Picasso, or works of the 19th century; a given piece may belong to more than one group. Each group is identified by an id and a name (like those just given) that describes the group. Finally, galleries keep information about customers. For each customer, galleries keep that person’s unique name, address, total amount of dollars spent in the gallery (very important!), and the artists and groups of art that the customer tends to like.
Which аssessment will the nurse perfоrm tо evаluаte the effectiveness оf the pantoprazole given to a patient with systemic inflammatory response syndrome (SIRS)?
Acute Glоmerulоnephritis (AGN) (Study Outline) 1. Bаckgrоund Definition: Rаpid onset inflаmmatory injury of the glomeruli, often presenting with nephritic features (hematuria, hypertension, reduced GFR). Pathophysiology: Immune-mediated inflammation → disruption of glomerular filtration barrier → RBC/protein leakage and decreased GFR. Can follow infection, autoimmune disease, or be part of a rapidly progressive process. Common causes (high-yield): Post–streptococcal glomerulonephritis (classic cause). IgA nephropathy (often after URI). RPGN causes: ANCA-associated vasculitis, Goodpasture (anti-GBM). Lupus nephritis (SLE). Infections (staph, endocarditis), hepatitis B/C. 2. History Acute hematuria (tea or cola colored). Edema: particularly periorbital in the morning. Hypertension due to fluid retention. Oliguria or decreased urine output. Recent illnesses: Strep pharyngitis or impetigo (1–3 weeks prior). URI preceding IgA nephropathy. Systemic clues: rash, joint pain (SLE); pulmonary symptoms (Goodpasture). 3. Exam Findings Edema: periorbital, pretibial. Hypertension is common and may be severe. Volume overload: crackles, JVD in severe cases. Rash: palpable purpura (IgA vasculitis), malar rash (SLE). Pulmonary findings: hemoptysis in Goodpasture (renal–pulmonary syndrome). 4. Making the Diagnosis Urinalysis hallmarks: Hematuria with RBC casts (key exam clue). Proteinuria (usually mild–moderate). Dysmorphic RBCs. Serologic testing based on etiology: ASO, anti-DNase B for post-strep GN. Complement levels: ↓ C3 (post-strep, lupus); normal in IgA nephropathy. ANA, anti-dsDNA for lupus. ANCA for vasculitis. Anti-GBM antibodies for Goodpasture. Basic labs: Elevated BUN/Cr; possible hyperkalemia and metabolic acidosis. Imaging: renal ultrasound to rule out structural disease. Gold Standard: Renal biopsy demonstrating glomerular inflammation, immune complex deposition, or crescent formation (in RPGN). 5. Management (Exam Concepts) General principles: Manage blood pressure and fluid status conceptually. Avoid nephrotoxins; adjust medication dosing. Etiology-specific management (exam-level concepts only): Post-streptococcal GN: supportive principles; treat strep infection conceptually. IgA nephropathy: BP/proteinuria reduction concepts. RPGN (Goodpasture/ANCA vasculitis): high-yield = immunosuppression ± plasma exchange principles (no dosing). Lupus nephritis: immunosuppressive principles. Complication monitoring: Hyperkalemia, acidosis, volume overload. Dialysis indications: uremia, refractory hyperkalemia, acidosis, severe overload. Referral: any suspected glomerulonephritis, rapidly worsening kidney function, or diagnostic uncertainty. QUESTION A 32-year-old man presents to the emergency department with hematuria and coughing up blood for the past two days. He reports fatigue, low-grade fever, and mild shortness of breath. Past medical history is unremarkable. He denies recent infections or travel. He has no rash or joint pain. Vitals show a blood pressure of 152/90 mmHg and oxygen saturation of 94% on room air. Pulmonary exam reveals bilateral crackles. Urinalysis shows 3+ blood, RBC casts, and mild proteinuria. Serum creatinine is 2.9 mg/dL (baseline unknown). Chest X-ray shows bilateral patchy infiltrates. Which of the following is the most appropriate next diagnostic test? A) Serum complement levelsB) Anti–double-stranded DNA antibodiesC) Antineutrophil cytoplasmic antibodies (ANCA)D) Anti–glomerular basement membrane (anti-GBM) antibodies
IgA Nephrоpаthy (Berger Diseаse) (Study Outline) 1. Bаckgrоund Definitiоn: Primary glomerular disease caused by IgA immune complex deposition in the mesangium. Epidemiology: Most common primary glomerulonephritis worldwide; affects adolescents/young adults more frequently. Pathophysiology: Aberrant IgA1 production → immune complex formation → mesangial deposition → complement activation (alternative pathway) → glomerular inflammation. Classification: Can be isolated renal disease or part of systemic IgA vasculitis (Henoch–Schönlein purpura). Clinical pattern: Often causes recurrent episodes of hematuria, usually triggered by infections. 2. History Gross hematuria shortly after URI (within 1–2 days; contrasts with post-strep GN which occurs weeks later). Recurrent episodic hematuria—classic presentation. Possible flank discomfort with hematuria. Proteinuria may develop; severity varies. Secondary associations: liver disease, celiac disease, inflammatory bowel disease. Signs of progression: fatigue, edema, or hypertension if CKD develops. 3. Exam Findings Often mild or normal exam in early disease. Possible findings: Low-grade edema (periorbital or peripheral). Hypertension if significant renal impairment. Purpura, abdominal pain, arthralgia in IgA vasculitis (systemic form). 4. Making the Diagnosis Urinalysis: Hematuria, often microscopic between episodes. Proteinuria (variable; worsening proteinuria = poor prognosis). Serology: Serum IgA may be elevated but not diagnostic. Complement levels typically normal (distinguishes from post-strep GN). Renal function tests: BUN/Cr may be normal early; elevated with progression. Renal biopsy (definitive): Shows mesangial proliferation and IgA deposition on immunofluorescence. Key for prognosis and determining treatment path. Gold Standard: Renal biopsy demonstrating IgA deposition in the mesangium. 5. Management (Exam Concepts) General principles: Address BP control; adjust medications for reduced GFR; avoid nephrotoxins. Sodium restriction concepts for edema/hypertension. Proteinuria control (high-yield): RAAS modulation principles to reduce proteinuria and slow progression. Immunosuppression concepts: Considered in cases with rapid progression or heavy proteinuria (exam-level concept only; no regimen details). Management of systemic IgA vasculitis: Supportive principles; immunosuppression in severe renal involvement. Monitoring: Follow urine protein levels, BP, and renal function to detect progression. Indications for nephrology referral: Heavy proteinuria, declining GFR, or suspicion for rapidly progressive disease. QUESTION A 24-year-old man with biopsy-confirmed IgA nephropathy is being seen for routine follow-up. He reports no current symptoms. Blood pressure is 146/92 mmHg. Urinalysis shows persistent hematuria and 1+ proteinuria. Serum creatinine is 1.2 mg/dL. The clinician discusses strategies to slow disease progression and reduce proteinuria. Which of the following is the most appropriate next step in management? A) Begin corticosteroid therapyB) Start an ACE inhibitorC) Prescribe a low-protein dietD) Refer for dialysis access placement