Chapter 22_2 flashcards
(27 cards)
Acute Glomerulonephritis (AGN): Pathophysiology
Inflammation of the glomerulus. Most commonly poststreptococcal (PSGN), where an immunological reaction damages glomerular membranes, making them hyperpermeable.
AGN: Clinical Presentation
Sudden edema (often periorbital), hematuria (cola-colored urine), proteinuria (foamy urine), and hypertension. Onset is often 7-21 days after a streptococcal infection.
AGN: Diagnosis
Gold standard is kidney biopsy. Often diagnosed clinically. Urinalysis shows proteinuria and hematuria. Serum creatinine and BUN are elevated. ASO titer (streptozyme test) confirms prior streptococcal infection.
AGN: Treatment
Antibiotics (if strep infection is active), antipyretics, analgesics. Antihypertensives and diuretics may be needed. Dietary restrictions on sodium and protein.
Nephrotic Syndrome: Core Pathophysiology & Features
Caused by glomerular damage leading to hyperpermeability. Key Features: Massive Albuminuria/Proteinuria (>3g/day), Hypoalbuminemia (<3.5 g/dL), and generalized Edema.
Nephrotic Syndrome: Common Causes & Complications
Common Causes: Diabetes mellitus, amyloidosis, and SLE. Complications: Hyperlipidemia (liver tries to compensate for low albumin) and increased risk of thromboembolism (loss of anticoagulant proteins in urine).
Nephrotic Syndrome: Treatment
Dietary: Adequate protein and calories, low sodium diet (<1500 mg/day). Medications: ACE inhibitors or ARBs to lower BP and slow kidney disease progression. May require statins for hyperlipidemia or anticoagulants.
Nephrolithiasis (Kidney Stones): Definition & Pain Pattern
Formation of stones (calculi) in the kidney. Classic pain is renal colic (comes in waves), which is excruciating flank pain that radiates to the abdomen and groin.
Nephrolithiasis: Types of Stones
Most common (75%) are calcium stones (usually calcium oxalate). Others include struvite (associated with UTI), uric acid (associated with gout), and cystine stones.
Nephrolithiasis: Diagnosis & Treatment
Diagnosis: Urinalysis (hematuria, crystalluria), CT scan (gold standard). Treatment: Pain relief, high fluid intake (>3 L/day), straining urine to catch stone for analysis. If stone doesn’t pass: lithotripsy (ESWL) or surgery.
Pyelonephritis: Definition & Classic Signs
Infection of the renal pelvis and interstitium, usually from an ascending lower UTI. Classic Signs: Costovertebral angle (CVA) tenderness, fever, and chills.
Pyelonephritis: Causes & Risk Factors
Cause: Ascending bacteria (most often E. coli). Risk Factors: Obstructive uropathy (e.g., kidney stones, enlarged prostate), vesicoureteral reflux (VUR), neurogenic bladder, urinary catheters, female anatomy, pregnancy.
Pyelonephritis: Diagnosis & Treatment
Diagnosis: Urinalysis (shows pyuria - WBCs), positive leukocyte esterase and nitrite tests. Urine culture confirms bacteria. Treatment: Antibiotics, antipyretics, analgesics, hydration.
Polycystic Kidney Disease (PKD): Pathophysiology
Genetic disorder (usually autosomal dominant - ADPKD) causing fluid-filled cysts to form in kidneys. Cysts compress and destroy normal renal tissue, leading to kidney enlargement and eventual failure.
PKD: Clinical Presentation & Extrarenal Manifestations
Pain (from cyst pressure/hemorrhage), kidney stones, hypertension, hematuria. Extrarenal Manifestations: Cysts in liver/pancreas/spleen, colonic diverticula, mitral valve prolapse, and cerebral aneurysms.
PKD: Diagnosis & Treatment
Diagnosis: Ultrasound, CT, or MRI can visualize cysts. Genetic testing can identify gene mutation (PKD1 or PKD2). Treatment: Control HTN (ACEi/ARBs), prevent UTIs, manage pain. Tolvaptan can decrease cyst formation. Hemodialysis or kidney transplant for ESRD.
Goodpasture’s Syndrome (Anti-GBM Disease): Pathophysiology
Autoimmune disease where antibodies attack the collagen in the glomerular basement membrane (GBM) and pulmonary alveolar membranes, causing glomerulonephritis and pulmonary hemorrhage.
Goodpasture’s Syndrome: Presentation, Diagnosis & Treatment
Presentation: Renal (hematuria, edema, HTN) and Pulmonary (cough, dyspnea, hemoptysis). Diagnosis: Presence of anti-GBM antibodies in blood. Treatment: Plasmapheresis (to remove antibodies), immunosuppressants (corticosteroids, cyclophosphamide).
Acute Kidney Injury (AKI): Definition & Key Feature
An abrupt insult to the kidney causing a rapid decrease in renal filtration function, leading to accumulation of nitrogenous wastes. A key feature is it is often reversible with timely treatment.
AKI: Stages (Based on Creatinine & Urine Output)
AKI is staged from 1 to 3 based on the magnitude of serum creatinine increase and the duration/severity of oliguria (low urine output).
AKI: Pathophysiological Phases
- Initial: From precipitating insult to initial manifestations. 2. Oliguria: Significant decrease in GFR, retention of waste, fluid overload. 3. Diuresis: Kidneys begin to recover, high volume of urine that is not concentrated. 4. Recovery: Final repair, GFR returns to normal.
Chronic Kidney Disease (CKD): Definition
Irreversible, progressive loss of kidney function over months to years. Defined as GFR < 60 mL/min for > 3 months and/or signs of kidney damage.
CKD: Most Common Causes
Diabetes Mellitus and Hypertension are the two most common causes.
CKD: Five Stages
Stage 1: Kidney damage, GFR >90. Stage 2: Mild GFR reduction (60-89). Stage 3: Moderate GFR reduction (30-59). Stage 4: Severe GFR reduction (15-29). Stage 5: Kidney failure / ESRD (GFR <15).
