renal 6 Flashcards
(30 cards)
MCQ Example
Q1: Which region of the kidney is most often affected during a renal infarction?
A. Renal pelvis
B. Renal cortex
C. Renal medulla
D. Renal capsule
Correct Answer: B. Renal cortex
Q2 (2 marks): Explain the two primary causes of renal infarction.
Model Answer:
Thromboemboli: Commonly originate in the heart (e.g., from atrial fibrillation) or the aorta, traveling to the renal artery.
In-situ thrombosis: Rare, involves clot formation within the renal artery itself.
MCQ Example
Q3: What histological feature characterizes the zone surrounding a focal infarct in the kidney?
A. Fibrotic capsule
B. Apoptotic core
C. Neutrophil-rich inflammatory border
D. Necrotic glomeruli
Correct Answer: C. Neutrophil-rich inflammatory border
Q4 (3 marks): Describe the cascade of cellular events following acute renal ischaemia.
Model Answer:
Acute obstruction leads to necrosis in the core area due to oxygen deprivation.
Surrounding tissue undergoes apoptosis from secondary damage.
Neutrophils migrate into the border zone, releasing MMPs which promote macrophage infiltration and fibrosis.
Q5: Which of the following is most characteristic of nephrotic syndrome?
A. Hematuria
B. Proteinuria > 3.5 g/day
C. Oliguria
D. White cell casts
Correct Answer: B. Proteinuria > 3.5 g/day
Q6 (3 marks): Compare nephrotic and nephritic syndromes in terms of pathophysiology and symptoms.
Model Answer:
Nephrotic: Chronic immune-mediated damage to glomerular basement membrane → proteinuria, hypoalbuminemia, hyperlipidemia.
Nephritic: Acute inflammation of glomeruli → hematuria, hypertension, moderate proteinuria.
Nephritic shows hypercellular glomeruli; nephrotic shows podocyte and GBM changes.
Q7: What is the most common organism responsible for UTIs?
A. Staphylococcus aureus
B. Proteus mirabilis
C. Escherichia coli
D. Klebsiella pneumoniae
Correct Answer: C. Escherichia coli
Q8 (2 marks): Explain how urinary obstruction contributes to pyelonephritis.
Model Answer:
Obstruction leads to urinary stasis, allowing ascending bacteria to proliferate.
Retrograde infection reaches renal pelvis and parenchyma, causing abscesses and inflammation.
Normal Anatomy and Physiology of the Prostate
A healthy adult prostate weighs about 20 grams. It typically increases in size with age, especially under the influence of androgens.
Encircles neck of bladder & prostatic urethra
The prostate is a compound tubuloalveolar gland, meaning it has branching ducts ending in secretory sacs.
It is embedded in a fibromuscular stroma, a supportive tissue composed of fibrous and smooth muscle elements.
5 lobes (embryology)
=> Embryologically, the prostate is divided into 5 lobes:
- Anterior
- Posterior
- Median
- Right lateral
- Left lateral
The prostate depends on androgens (male sex hormones), especially dihydrotestosterone (DHT).
Castration or androgen deprivation therapy (ADT)—also known as androgen ablation—results in prostatic atrophy, especially of glandular components.
Q10 (3 marks): List and explain three factors that contribute to renal stone formation.
Model Answer:
Low urine volume: Leads to salt supersaturation.
Urinary pH: Acidic pH promotes urate and calcium oxalate stones; alkaline favors phosphate stones.
Hypercalciuria: From diet, bone loss, or genetics, increases calcium excretion.
Zonal Anatomy
4 zones
Peripheral Zone (PZ)
- Largest zone, located posteriorly.
- Most prostate cancers arise here (malignancy).
- Palpable during a digital rectal exam (DRE).
Transitional Zone (TZ)
- Surrounds the urethra.
- Site of benign prostatic hyperplasia (BPH).
- This zone grows with age, potentially compressing the urethra.
Periurethral Zone
- Tiny glands adjacent to the urethra.
- Can also undergo hyperplasia, contributing to urinary symptoms.
Central Zone (CZ)
- Surrounds the ejaculatory ducts.
- Can show hyperplasia, but is less commonly involved in cancer compared to the peripheral zone.
Benign Prostatic Hyperplasia (BPH) Key Features
Thickened Bladder Wall:
- Due to increased effort required to void urine against obstruction.
- Muscle hypertrophy occurs in the bladder wall as a compensatory mechanism.
Trabeculation of Mucosal Surface:
- Irregular ridges and outpouchings appear due to chronic high pressure during urination.
- Indicates bladder decompensation over time.
Posterior Lobe Growth into Bladder Lumen:
- Prostatic tissue can protrude into the bladder, further obstructing urine outflow.
Enlarged Prostate:
- Increase in size, especially in the transitional zone, compresses the urethra.
- Normal weight is ~20g; significantly more in BPH.
Obstructed Urethra:
- The urethra is pinched, leading to lower urinary tract symptoms (LUTS) such as:
=> Hesitancy
=> Weak stream
=> Incomplete emptying
=> Increased frequency and urgency
Benign Prostatic Hyperplasia (BPH) Pathophysiology
Androgen-dependent: Dihydrotestosterone (DHT), a metabolite of testosterone, stimulates prostate cell growth.
Hormonal Imbalance with Aging: Increased estrogen-to-androgen ratio may contribute to BPH development.
Adenocarcinoma of the Prostate
adenocarcinoma of the prostate is a malignant (cancerous) tumor. It is the most common type of prostate cancer, originating from the glandular epithelium of the prostate, particularly in the peripheral zone.
Nodular Tumor Invading the Lumen of the Bladder:
- Shows multiple yellowish-white nodules infiltrating into the bladder from the prostate.
- clonal expansion of malignant epithelial cells
begin to divide uncontrollably, invade into the bladder
- Bladder involvement often leads to hematuria and urinary obstruction.
Tumor Invading Recto-Vesical Space (space is between the rectum and the bladder)
=> Tumor extension here signifies posterior invasion
Ureter Embedded in Cancer:
local spread to the ureter, which can lead to hydronephrosis and renal dysfunction due to impaired urine flow.
Suggests an aggressive and extensive tumor.
Nephrotic Syndrome
🧪 Key Features:
Massive Proteinuria: > 3.5 g/day
Generalized Edema: Due to loss of plasma oncotic pressure (from low albumin).
Hypoalbuminemia: Low serum albumin due to urinary loss.
Hyperlipidemia & Lipiduria: Liver compensates for protein loss by overproducing lipoproteins; lipids may spill into urine.
🧠 Pathophysiology:
Immune complex-mediated damage to podocytes or basement membrane.
- Often due to:
=Minimal change disease (children)
=Focal segmental glomerulosclerosis
=Membranous nephropathy
No inflammation initially; damage is non-inflammatory and progressive.
Nephritic Syndrome (Acute and Inflammatory)
🧪 Key Features:
Hematuria: Visible or microscopic blood in urine.
Variable Proteinuria: Less than nephrotic range.
Azotemia: Elevated BUN and creatinine due to impaired renal filtration.
Hypertension: Due to fluid retention and reduced renal function.
🧠 Pathophysiology:
Acute inflammation of glomeruli with:
- Glomerular endothelial and mesangial proliferation
- Leukocyte infiltration
- Capillary wall injury
Common causes:
- Post-streptococcal GN
- IgA nephropathy
- Lupus nephritis
Pathogenesis of UTI:
Entry of Bacteria:
The primary route of infection is ascending, where bacteria from outside the body enter through the urethra and move against the flow of urine into the bladder.
This leads to cystitis (inflammation of the bladder).
Anatomical Predisposition:
Females are more prone to UTIs due to:
A short, straight urethra, allowing easier bacterial access.
Closer proximity of the urethra to the anal and vaginal areas (sources of bacteria).
Males have a longer, curved urethra and antimicrobial properties of prostatic fluid, offering more resistance.
UTI 🦠 Causative Organisms:
Most Common Pathogen:
➤ Escherichia coli (E. coli), a normal inhabitant of the gastrointestinal (GI) tract.
Other potential organisms include:
Klebsiella, Proteus, Enterococcus, Staphylococcus saprophyticus (especially in young women).
UTI Risk Factors and Causes:
Poor Hygiene:
Facilitates transfer of GI bacteria to the urethral opening.
Improper wiping techniques or infrequent changing of sanitary products.
Obstructive Causes:
- Anything that restricts urine flow increases infection risk:
= Benign prostatic hyperplasia (BPH) in men.
= Kidney stones.
= Congenital anomalies or tumors.
Stagnant urine allows bacteria to multiply.
Factors Leading to Calculi Formation (Nephrolithiasis)
** renal calculi (kidney stones)
🔹 1. Low Urine Volume
🔹 2. Urine pH
🔹 3. Rate of Solute Excretion
🔹 4. Urinary Stasis (Difficulty urinating and completely emptying the bladder.)
🔹 5. Abnormal Urothelium (Damaged epithelium )
🔹 6. Foreign Bodies / Nidus (Protein debris, bacteria, or necrotic tissue can serve as a nucleation site.)
🔹 7. Lack of Crystallization Inhibitors (prevent stone formation)
🔹 8. Genetic Factors
Nephrolithiasis (cause and effect of the factor low urine volume
cause: dehydration, low fluid intake, or excessive fluid loss (e.g., sweating, diarrhea).
effect: - Concentrates solutes (e.g. calcium, oxalate, uric acid) in a smaller urine volume. - Leads to supersaturation — when the concentration of a substance exceeds its solubility, crystals begin to precipitate. - Promotes aggregation into stones, especially in static urine.
Nephrolithiasis (cause and effect of the factor urine ph
if urine is Acidic (low pH):
cause: diet ( proteins, cranberries, ketosis) forms acidic byproducts// Physiological or Pathological Causes: Metabolic acidosis (e.g., renal tubular acidosis type 1).
=> Favors formation of uric acid and calcium oxalate stones.
if urine is alkaline (high pH):
cause : diet// pathological causes i.e. UTI, vomiting
=> Promotes phosphate stones, often struvite (magnesium ammonium phosphate), especially in UTIs caused by urease-positive bacteria (e.g., Proteus).
Nephrolithiasis (cause and effect of the factor Rate of Solute Excretion
A. Hypercalciuria / Hyperphosphaturia (Excess calcium or phosphate in urine)
→ supersaturation → crystal formation.
Causes:
Hyperparathyroidism: mobilizes calcium from bone.
Renal tubular defects: impaired reabsorption.
Chronic renal failure: disrupts mineral metabolism.
High milk/alkali intake: dietary overload.
immobilization: bone demineralization.
Genetic absorptive hypercalciuria: ↑ gut calcium absorption.
B. Hyperuricemia (Excess uric acid)
Excess uric acid → uric acid stones or acts as a nidus for calcium oxalate stones.
causes:
From gout or high-purine diets (e.g., red meat, alcohol).
Nephrolithiasis (cause and effect of the factor urinary stasis
Obstruction (BPH, strictures, tumors) slows urine flow.
==> causing urinary stasis (can’t fully pee)
Stagnant urine => longer time for crystals to aggregate and form stones.
Also promotes bacterial growth, increasing risk of struvite stones.
