Describe the key pathophysiological changes in chronic kidney disease (CKD) progression.
Loss of nephrons leads remaining nephrons to hyperfilter (↑GFR per nephron) and experience intraglomerular hypertension. Over time this causes glomerulosclerosis, tubular atrophy, interstitial fibrosis, progressive decline in overall GFR, and accumulation of uremic toxins.
Explain the mechanism by which diabetic nephropathy develops.
Chronic hyperglycemia causes nonenzymatic glycation of proteins, leading to thickening of the glomerular basement membrane, mesangial expansion, and nodular glomerulosclerosis. Increased intraglomerular pressure and podocyte injury cause albuminuria and progressive loss of nephron function.
How does polycystic kidney disease (PKD) impair renal function?
Multiple expanding fluid-filled cysts arise from nephron tubules and compress surrounding parenchyma. This distorts normal architecture, obstructs tubular flow, reduces blood supply, and progressively destroys functional nephrons, leading to reduced GFR and eventual kidney failure.
What is the pathophysiology of acute tubular necrosis (ATN)?
ATN results from ischemic or nephrotoxic injury to tubular epithelial cells, especially in the proximal tubule and thick ascending limb. Injured cells slough into the lumen, forming casts, causing tubular obstruction and back-leak of filtrate, which lowers effective GFR and leads to acute kidney injury.
Describe the formation of calcium oxalate kidney stones.
Stones form when urine becomes supersaturated with calcium and oxalate ions, promoting crystal nucleation and growth. Low urine volume, altered pH, and deficiency of stone inhibitors favor precipitation of calcium oxalate crystals that aggregate into stones.
Explain the role of the renin–angiotensin–aldosterone system (RAAS) in renal hypertension.
Reduced renal perfusion (e.g., renal artery stenosis) stimulates renin release, increasing angiotensin II and aldosterone. Angiotensin II causes vasoconstriction and efferent arteriolar constriction, while aldosterone promotes sodium and water retention, together raising systemic blood pressure and glomerular pressure.
How does benign prostatic hyperplasia (BPH) affect urinary flow?
Enlargement of the periurethral prostate compresses the prostatic urethra, increasing outflow resistance. This leads to weak stream, hesitancy, incomplete bladder emptying, and compensatory bladder hypertrophy and irritative symptoms.
What is the pathophysiology of stress urinary incontinence?
It results from urethral hypermobility and/or intrinsic sphincter deficiency due to weakened pelvic floor or connective tissue. When intra-abdominal pressure suddenly rises (coughing, sneezing, lifting), the urethra cannot stay closed and urine leaks.
Describe the mechanism of action of loop diuretics on renal function.
Loop diuretics inhibit the Na⁺–K⁺–2Cl⁻ cotransporter in the thick ascending limb of the loop of Henle. This reduces reabsorption of sodium and chloride, diminishes the medullary concentration gradient, and increases excretion of water, Na⁺, K⁺, Ca²⁺, and Mg²⁺.
Explain how nephrotic syndrome leads to edema and hyperlipidemia.
Increased glomerular permeability causes heavy proteinuria and hypoalbuminemia, lowering plasma oncotic pressure and promoting fluid movement into interstitial spaces (edema). The liver compensates by increasing protein synthesis, including lipoproteins, leading to hyperlipidemia and lipiduria.
What is the impact of uncontrolled hypertension on the glomerulus?
Chronic high pressure causes hyaline arteriolosclerosis and glomerular capillary damage, leading to glomerulosclerosis. This reduces filtration surface area, decreases GFR, and contributes to proteinuria and progression of CKD.
Describe the pathophysiology of urge incontinence.
Urge incontinence is caused by detrusor overactivity, often due to neurologic dysfunction or bladder irritation. Involuntary bladder contractions occur at low volumes, causing sudden urgency and involuntary urine loss.
How does vesicoureteral reflux (VUR) increase the risk of pyelonephritis?
In VUR, urine flows retrograde from the bladder into the ureters and kidneys. This allows bacteria from the lower urinary tract to reach the renal pelvis and parenchyma, promoting recurrent pyelonephritis and renal scarring.
Explain the concept of intrinsic kidney injury.
Intrinsic kidney injury refers to damage within the kidney parenchyma itself—glomeruli, tubules, interstitium, or renal vasculature. Examples include ATN, acute interstitial nephritis, and glomerulonephritis, where the primary pathology is not perfusion-related or purely obstructive.
What are the key pathophysiological differences between pre-renal, intra-renal, and post-renal acute kidney injury (AKI)?
Pre-renal AKI: Due to decreased renal perfusion (e.g., hypovolemia, heart failure); kidney structure initially intact. Intra-renal AKI: Due to direct parenchymal damage (e.g., ATN, GN). Post-renal AKI: Due to obstruction of urine outflow (e.g., stones, BPH), causing backpressure and decreased GFR.
Describe the role of inflammation in the development of glomerulonephritis.
Immune complexes or antibodies deposit in or target the glomerular capillary wall, activating complement and recruiting leukocytes. This inflammatory response damages the filtration barrier, causing hematuria, proteinuria, reduced GFR, and sometimes crescent formation.
How does chronic kidney disease affect erythropoiesis?
CKD reduces production of erythropoietin by peritubular interstitial cells in the kidney. Lower EPO levels impair bone marrow’s ability to produce RBCs, leading to a normocytic, normochromic anemia.
Explain the pathophysiology of renal osteodystrophy.
CKD causes phosphate retention and decreased activation of vitamin D, leading to hypocalcemia. This stimulates secondary hyperparathyroidism and high bone turnover, along with defective mineralization, resulting in bone pain, fractures, and skeletal deformities.
What is the impact of urinary tract obstruction on bladder function?
Chronic obstruction increases intravesical pressure, causing detrusor muscle hypertrophy and trabeculation. Over time, the bladder becomes less compliant, develops instability or eventually decompensation with poor contractility and urinary retention.
Describe the mechanism by which recurrent urinary tract infections can lead to kidney damage.
Recurrent UTIs can ascend to involve the kidneys, causing repeated episodes of pyelonephritis. The resulting chronic inflammation and scarring of the renal parenchyma reduce nephron number and contribute to hypertension and CKD.
What is the functional unit of the kidney?
The nephron.
What are the vascular components of the nephron?
Glomerulus and peritubular capillaries.
What are the tubular components of the nephron?
PCT → Loop of Henle → DCT → Collecting duct.
What is the function of the nephron?
Filter fluid/solutes, reabsorb needed substances, secrete unneeded substances → form urine.
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Basis of genetics81
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Stress, Cellular Adaptation, Cell Injury,Necrosis & Apoptosis34
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Teratogens & Congenital Disorders64
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Neoplasims, Cancer and Cell Cycle20
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Fluids/Electrolytes/ABGs70
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Female and Male Reproductive disorders71
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GI D/O61
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Resp D/O50
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GI D/O pt 250
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GI D/O50
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Cardiac58
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Immunity0
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Endocrine103
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Diabetes38
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Blood Disorders137
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Neuro68
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Renal84
