Renal 3 Flashcards
- Short Answer
Q: What is the genetic mutation responsible for autosomal dominant polycystic kidney disease (ADPKD)?
A:
Mutation in the polycystin-1 gene (PKD1) or polycystin-2 gene (PKD2).
These proteins are critical for tubular epithelial cell adhesion in the nephron.
Loss of function leads to cyst formation and kidney enlargement.
- Multiple Choice
Q: Which of the following is NOT a complication associated with polycystic kidney disease?
A) Hypertension
B) Berry aneurysms
C) Diabetes mellitus
D) Liver cysts
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Answer:
C) Diabetes mellitus
(Diabetes is not a direct complication; liver cysts, aneurysms, and hypertension are.)
Q: Describe the pathological mechanism by which diabetes mellitus causes diabetic nephropathy.
Model Answer:
Chronic hyperglycemia leads to non-enzymatic glycosylation of proteins, producing AGEs (Advanced Glycation End products).
AGEs cause thickening of the glomerular basement membrane (GBM), impairing selective filtration.
Intracellular sorbitol accumulation from high glucose damages renal cells (osmotic injury).
Microangiopathy develops with hyaline thickening of afferent and efferent arterioles, leading to glomerulosclerosis.
Results in proteinuria, progressive renal fibrosis, and eventual chronic renal failure.
Q: How does polycystic kidney disease lead to hypertension?
A:
Loss of normal renal architecture causes reduced nephron filtration.
Fluid accumulation stimulates renin release, activating the RAAS system (Renin-Angiotensin-Aldosterone System).
Leads to vasoconstriction and sodium retention, causing hypertension.
Q: Name two microscopic findings seen in diabetic nephropathy.
A:
Thickened glomerular basement membranes (GBM).
Expansion of the mesangial matrix (sometimes Kimmelstiel-Wilson nodules).
Podocyte foot process effacement.
Q: What is acute pyelonephritis, and what are its histological features?
Q: What is acute pyelonephritis, and what are its histological features?
A:
Acute pyelonephritis is infection and inflammation of the renal pelvis and renal parenchyma, often due to ascending uropathogenic bacteria like E. coli.
Histological features include:
Heavy neutrophil infiltration.
Tubular necrosis and pus formation (proteinaceous debris).
Small abscesses in cortex and medulla.
Q: Explain how urinary tract obstruction can predispose a patient to acute pyelonephritis.
Model Answer:
Obstruction (e.g., kidney stones, prostate enlargement, strictures) impedes urine flow.
Urinary stasis promotes bacterial growth ascending from bladder to kidneys.
Infections (commonly E. coli) colonize stagnant urine, leading to infection of renal tissue.
This results in inflammatory destruction, abscess formation, and potential scarring if chronic.
Q: A 45-year-old patient has roughened renal surfaces, small renal abscesses, and reports flank pain with fever.
What is the most likely diagnosis?
A:
Acute pyelonephritis.
Q: Which structural anomaly is often asymptomatic but can increase risk for hydronephrosis?
A) Hypoplasia
B) Horseshoe kidney
C) Ectopic kidney
D) Renal agenesis
Answer:
B) Horseshoe kidney
(Fusion of lower poles may cause ureteral entrapment and urine flow obstruction.)
Q: In diabetic nephropathy, strict __________ control can significantly delay progression to end-stage renal disease.
Answer:
Glycemic control.
Horseshoe Kidney
Fusion of the kidneys at their lower poles, forming a U-shape; associated with increased risk of obstruction. (~1/1000 births)
Ectopic Kidney
Kidney located outside its normal position, usually in the iliac fossa.
Renal Hypoplasia
A small but otherwise structurally normal kidney, often unilateral (affects one side).
Renal Dysplasia
Presence of abnormal tissue, like cartilage, within the kidney, along with immature collecting ducts; usually associated with cysts and poor filtration.
Polycystic Kidney Disease
Mutation in polycystin-1 or polycystin-2 → poor tubular epithelial adhesion → cyst formation → kidney enlargement → hypertension & renal failure.
Diabetic Nephropathy
Chronic hyperglycemia → AGE (advanced glycation end products) formation → thickened GBM → proteinuria → sclerosis of glomeruli → chronic renal failure.
Acute Pyelonephritis
Bacterial infection (often E. coli) ascending from the lower urinary tract, often due to urinary obstruction → neutrophil infiltration, abscess formation, renal tissue necrosis.
Which protein is mutated in autosomal dominant polycystic kidney disease?
A) Albumin
B) Polycystin-1
C) Collagen IV
D) Fibrillin
b
Which structure is primarily involved in diabetic glomerular damage?
A) Renal pelvis
B) Podocytes
C) Proximal tubule
D) Loop of Henle
b
What is the most common pathogen causing acute pyelonephritis?
A) Staphylococcus aureus
B) E. coli
C) Klebsiella pneumoniae
D) Pseudomonas aeruginosa
b
What feature distinguishes diabetic nephropathy on light microscopy?
A) Collagen breakdown
B) Glomerular basement membrane thickening
C) Podocyte proliferation
D) Loss of Bowman’s capsule
b
Horseshoe kidney is associated with:
A) Increased risk of obstruction
B) Rapid renal failure
C) Always fatal outcome
D) No clinical significance
a
Polycystic kidney disease is most often recessive in adults. T/F
F
Hypertension occurs in about 75% of polycystic kidney disease patients. T/F
T
