Renal 2 Flashcards
Define analgesic nephropathy. What is the mechanism of kidney injury in this condition?
✅ Model Answer:
* Definition:
Analgesic nephropathy is chronic kidney injury caused by long-term overuse of compound analgesic medications (paracetamol, aspirin, ibuprofen), usually over 3–5 years and >4g/day consumption.
* Mechanisms:
o Direct tubular toxicity:
Metabolites of phenacetin and paracetamol damage renal tubular epithelial cells via oxidative stress.
o Vascular dysfunction:
Aspirin inhibits prostaglandin synthesis, reducing vasodilation and causing ischemia, particularly affecting the renal medulla.
o Result:
Papillary necrosis, cortical thinning, interstitial fibrosis, possible calcification of necrotic papillae.
* Clinical Associations:
o Chronic kidney disease.
o Hypertension.
o Increased risk of transitional cell carcinoma of the renal pelvis.
What are the main pathological findings in kidneys affected by analgesic nephropathy?
✅ Model Answer:
* Necrosis of renal papillae:
o Leads to obstruction of tubules, interstitial inflammation, fibrosis.
* Sloughing of necrotic papillae:
o May obstruct ureters, causing ureteric colic or hydronephrosis.
* Calcification of necrotic tissue:
o Stiffens renal tissue.
* Loss of counter-current concentration mechanism:
o Results in impaired urine concentration, dehydration, electrolyte imbalances.
* Secondary hypertension:
o Due to renal ischemia and scarring.
✏️ Question 3:
Describe the types of urinary calculi and the main factors that promote their formation.
✅ Model Answer:
* Types of Stones:
o Calcium oxalate/phosphate: Most common; linked to dehydration, hypercalciuria.
o Magnesium ammonium phosphate (struvite): Associated with recurrent UTIs and alkaline urine.
o Uric acid stones: Formed in acidic urine; associated with gout.
o Cystine stones: Result from genetic disorders of amino acid transport.
* Factors Promoting Stone Formation:
o Low urine volume (dehydration).
o Changes in urine pH.
o Hypercalciuria or hyperphosphaturia.
o Urinary stasis (obstruction).
o Foreign bodies acting as crystallization nidus.
o Loss of stone inhibitors (e.g., mucoproteins, pyrophosphate).
✏️ Question 4:
What is hydronephrosis? List causes and describe its pathological consequences.
✅ Model Answer:
* Definition:
Dilation of renal pelvis and calyces due to urinary outflow obstruction, leading to renal parenchymal atrophy.
* Causes:
o Congenital:
Abnormal ureters/urethra (atresia, valves).
o Acquired:
Calculi, tumors (e.g., prostate cancer, cervical cancer), strictures, pregnancy, neurogenic bladder.
* Pathological Consequences:
o Tubular damage.
o Decreased concentrating ability.
o Progressive parenchymal thinning and fibrosis.
o Irreversible kidney damage if obstruction persists (after 3 weeks for complete, 3 months for partial obstruction).
✏️ Question 5:
Describe the pathogenesis, key clinical features, and prognosis of renal cell carcinoma (RCC).
✅ Model Answer:
* Pathogenesis:
o Arises from epithelial cells of proximal renal tubules.
o Often associated with lipid-rich clear cytoplasm (hence “clear cell carcinoma”).
* Clinical Features:
o Hematuria (10–15%).
o Flank pain.
o Palpable mass.
o Systemic symptoms: weight loss, fever, hypertension, hypercalcemia.
* Prognosis:
o 5-year survival:
No metastasis: ~70%.
With metastasis: ~10%.
o Common metastasis sites: lungs and bones via hematogenous spread or renal vein invasion.
✏️ Question 6:
How does RCC spread, and what are the current management strategies?
✅ Model Answer:
* Spread:
o Local invasion into renal vein → inferior vena cava → potential spread to heart or lungs.
o Lymphatic spread to lungs and bones (common metastasis sites).
* Management:
o Surgical removal: Partial or radical nephrectomy (depending on tumor size and location).
o Radiation therapy: In selected cases.
o Immunotherapy: Used for metastatic RCC.
o Systemic chemotherapy is less effective and used rarely.
Question 1:
What is analgesic nephropathy, and how does analgesic abuse cause kidney damage?
✅ Model Answer:
* Definition:
Analgesic nephropathy is kidney injury caused by prolonged, excessive use of compound analgesics (paracetamol, aspirin, ibuprofen), typically over 3–5 years at doses >4g/day.
* Mechanism:
o Direct tubular toxicity:
Metabolites of phenacetin/paracetamol enhance oxidative stress, damaging tubular epithelial cells.
o Vascular dysfunction:
Aspirin inhibits prostaglandin-mediated vasodilation → chronic ischemia, especially in the medulla.
o Resulting Pathology:
Papillary necrosis.
Interstitial fibrosis.
Cortical scarring and atrophy.
Risk of secondary transitional cell carcinoma in the renal pelvis.
How do lower urinary tract infections (UTIs) occur, and how can they lead to bladder and kidney colonization?
✅ Model Answer:
* Mechanism of Infection:
o Ascending bacterial colonization from the urethra to bladder (cystitis).
o If untreated, bacteria can ascend via ureters to infect kidneys (pyelonephritis).
* Risk Factors:
o Urinary stasis (e.g., due to obstruction).
o Foreign bodies (e.g., catheters, stones).
o Anatomical abnormalities.
* Common Organisms:
o Escherichia coli (most common).
o Other Gram-negative rods (Proteus, Klebsiella).
* Pathological Impact:
o Inflammation damages urothelium.
o Dead bacterial remnants act as nidus for stone formation (especially struvite stones in alkaline urine).
List and explain the main factors that contribute to kidney stone (calculi) formation.
✅ Model Answer:
* Key Factors:
o Low urine volume: Dehydration concentrates salts → precipitation.
o Urine pH alterations:
Acidic urine → favors urate and calcium oxalate stones.
Alkaline urine → favors phosphate (struvite) stones.
o Excess solute excretion:
Hypercalciuria/phosphaturia (e.g., hyperparathyroidism, diet, immobilization).
Excess uric acid retention (gout).
o Presence of crystallization nuclei:
Bacterial fragments.
Foreign bodies.
o Loss of inhibitors:
Deficiency in mucoproteins, pyrophosphate.
* Types of Stones:
o Calcium oxalate/phosphate (most common).
o Magnesium ammonium phosphate (struvite).
o Uric acid stones.
o Cystine stones (genetic).
What is hydronephrosis? Explain its causes, progression, and consequences.
✅ Model Answer:
* Definition:
Dilation of renal pelvis and calyces due to obstruction of urinary flow, leading to renal parenchymal atrophy.
* Causes:
o Stones obstructing ureter.
o Tumors (e.g., prostate, cervical cancer).
o Ureteral strictures.
o Pregnancy-induced ureteral compression.
o Congenital abnormalities (e.g., ureteral atresia).
* Pathological Progression:
o Initial tubular damage.
o Impaired concentrating ability.
o Progressive cortical thinning.
o Parenchymal atrophy.
* Consequences:
o Irreversible kidney damage after prolonged obstruction (3 weeks for complete, 3 months for partial).
o Hydroureter often coexists.
Describe the cell of origin, histological features, and mechanism of development in renal cell carcinoma (RCC).
✅ Model Answer:
* Cell of Origin:
o Proximal tubule epithelial cells of the kidney.
* Histological Features:
o Clear cell type due to fat and glycogen accumulation.
o Acinar/glandular patterns with pseudo-capsules.
o Necrosis and hemorrhage common.
* Mechanism of Development:
o Mutations affecting pathways regulating cellular growth and metabolism.
o Lipid accumulation via upregulation of LDL receptors.
o Neoangiogenesis (VEGF-driven) due to hypoxia.
o Ability to invade renal vein → inferior vena cava → metastasize to lungs/bones.
* Clinical Presentation:
o Hematuria.
o Flank pain.
o Palpable abdominal mass.
o Paraneoplastic syndromes (e.g., hypercalcemia, hypertension).
