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**Urinary System Disorders

Chapter 18: Urinary System Disorders

1. Overview of the Urinary System Functions

  • Metabolic Waste Removal: The urinary system is responsible for removing metabolic wastes from the body.

  • Hormone Elimination: It removes hormones from circulation.

  • Excretion of Drugs/Foreign Materials: Drugs and other foreign materials are eliminated.

  • Homeostatic Regulation: It regulates water, electrolyte levels, and acid-base balance.

  • Erythropoietin Secretion: Secretes erythropoietin, which stimulates red blood cell production.

  • Vitamin D Activation: Activates vitamin D for calcium homeostasis.

  • Blood Pressure Regulation: Regulates blood pressure through the renin-angiotensin-aldosterone system.

2. Gross Anatomy of the Urinary System

  • Components:

    • Kidneys

    • Ureters

    • Urinary Bladder

    • Urethra

  • Supporting Structures:

    • Adrenal Gland

    • Liver

    • Spleen

    • Abdominal Aorta

    • Inferior Vena Cava

    • Common Iliac Artery and Vein

    • Renal Arteries and Veins

    • Kidneys:

    • Right and left kidneys are different in position and orientation.

    • Surrounded by peritoneum, renal fat pad, and peritoneal cavity.

3. Nephron: The Functional Unit of the Kidney

  • Structure: Each kidney contains over a million nephrons.

  • Components:

    • Renal Corpuscles:

    • Glomerulus

    • Bowman’s Capsule

    • Renal Tubules:

    • Proximal convoluted tubules

    • Loop of Henle

    • Distal convoluted tubules

    • Collecting duct

4. Formation of Urine

  • Process:

    • Filtration: Blood is supplied to the kidneys through two arterioles.

    • A large volume of fluid (containing wastes, nutrients, and electrolytes) passes from glomerular capillaries into Bowman’s capsule.

    • Cells and proteins remain in the blood.

    • Reabsorption:

    • Essential nutrients, water, and electrolytes are reabsorbed into the peritubular capillaries.

    • Regulation of pH and electrolytes occurs here.

5. Reabsorption Mechanisms

  • Transport Mechanisms:

    • Active Transport: For electrolytes.

    • Co-Transport: Sodium transport coupled with glucose or amino acids.

    • Osmosis: Water reabsorption occurs mainly in proximal convoluted tubules.

  • Significance:

    • Most water and glucose are reabsorbed for homeostasis.

6. Hormones Involved in Reabsorption

  • Antidiuretic Hormone (ADH):

    • Secreted by the posterior pituitary.

    • Promotes water reabsorption in distal convoluted tubules and collecting ducts.

  • Aldosterone:

    • Secreted by adrenal cortex.

    • Promotes sodium reabsorption in exchange for potassium or hydrogen ions.

  • Atrial Natriuretic Hormone:

    • Hormone from the heart that reduces sodium and fluid reabsorption.

7. Glomerular Filtration Rate (GFR)

  • Control Factors:

    • Autoregulation, sympathetic nervous system influence, and renin activity.

  • Mechanisms:

    • Autoregulation and hormones control pressure in glomerular capillaries:

    • Vasoconstriction of afferent arteriole decreases glomerular pressure and filtrate.

    • Aldosterone increases sodium and water retention, raising glomerular pressure and increasing filtrate.

    • Renin leads to vasoconstriction, thus increasing glomerular pressure and filtrate.

  • Implications:

    • Blood pressure is closely related to kidney function, increasing with renal failure.

8. Incontinence and Retention

  • Incontinence:

    • Defined as loss of voluntary control of the bladder.

    • Variants:

    • Enuresis: Involuntary urination in children older than 4 years, often related to developmental delay.

    • Stress Incontinence: Common in women due to increased intra-abdominal pressure from activities (coughing, lifting).

    • Overflow Incontinence: Occurs when detrusor muscle weakness leads to incomplete bladder emptying, prevalent in older adults.

  • Retention:

    • Inability to empty the bladder, which may accompany overflow incontinence.

    • Conditions leading to retention include spinal cord injuries and anesthesia.

9. Common Disorders of the Urinary System

  • Urinary Tract Infections (UTIs):

    • Very common.

    • Lower UTIs: Cystitis, Urethritis.

    • Upper UTIs: Pyelonephritis.

    • Causative Organism: Escherichia coli is a common pathogen.

10. Types of UTIs and Associated Organisms

  • Other Organisms Associated with UTIs:

    • Klebsiella, Proteus, Enterobacter, Citrobacter, Serratia, Pseudomonas, Enterococcus, Coagulase-negative Staphylococcus, Chlamydia, Mycoplasma.

  • Factors:

    • More common in women due to short urethra and proximity to the anus.

    • In older men, prostatic hypertrophy and urine retention are risk factors.

11. Cystitis and Urethritis

  • Definitions:

    • Cystitis: Inflammation of the bladder wall.

    • Urethritis: Inflammation of the urethra.

  • Symptoms:

    • Hyperactive bladder, pelvic pain, dysuria, urgency, frequency, nocturia.

    • Systemic signs: Fever, malaise, nausea, leukocytosis.

    • Urine often appears cloudy with unusual odor.

12. Pyelonephritis

  • Definition:

    • Inflammation of one or both kidneys, often progressing from ureter to kidney.

    • Purulent exudate fills pelvis and calyces.

  • Consequences:

    • Recurrent infections lead to scar tissue formation, loss of tubule function, hydronephrosis, and potential renal failure if untreated.

  • Symptoms:

    • Signs of cystitis plus renal disease-related pain, systemic high temperature, and urinalysis indicating urinary casts.

13. Inflammatory Disorders: Glomerulonephritis

  • Pathophysiology:

    • Forms due to an antigen-antibody complex following infection.

    • Increased capillary permeability leads to fluid and waste retention.

  • Symptoms:

    • Dark, cloudy urine, facial and periorbital edema, elevated blood pressure, flank pain, decreased urine output.

    • May lead to metabolic acidosis.

14. Nephrotic Syndrome

  • Pathophysiology:

    • Usually secondary to renal diseases or systemic disorders, such as SLE or toxins.

    • Characterized by significant proteinuria with a sequence of symptoms.

  • Symptoms:

    • Hypoalbuminemia, generalized edema, elevated blood cholesterol, lipiduria, foamy urine.

15. Urinary Tract Obstructions

  • Causes:

    • Urolithiasis, hydronephrosis, tumors can obstruct urinary flow.

16. Urolithiasis (Calculi)

  • Formation:

    • Stones can develop in urinary tract due to excessive solutes or insufficient fluid intake, often manifested with obstruction.

  • Types of Stones:

    • Calcium salts, uric acid stones, struvite, and cystine (rare) stones.

    • Formation Factors:

    • High urine calcium levels, hyperuricemia from gout or cancer chemotherapy, urinary pH levels.

  • Symptoms:

    • Often asymptomatic until obstruction presents; severe pain (renal colic) may occur during obstruction.

17. Hydronephrosis

  • Definition:

    • Condition characterized by kidney swelling due to urine buildup.

  • Secondary Causes:

    • Calculi, tumors, untreated prostatic enlargement can lead to hydronephrosis.

  • Consequences:

    • If untreated, can lead to chronic renal failure.

18. Tumors: Renal Cell Carcinoma

  • Characteristics:

    • Primary tumor arising from the tubule epithelium, usually in renal cortex.

    • Often asymptomatic in early stages and can metastasize at diagnosis.

  • Symptoms:

    • Painless hematuria, flank pain, weight loss, anemia.

19. Bladder Cancer

  • Characteristics:

    • Predominantly malignant tumors arising from bladder’s transitional epithelium.

    • Invasive tumors that may metastasize to lymph nodes, liver, and bone.

  • Predisposing Factors:

    • Chemical exposure, smoking, recurrent infections, heavy analgesic use.

20. Vascular Disorders: Nephrosclerosis

  • Definition:

    • Thickening and hardening of arterioles and small arteries walls, reducing kidney blood supply.

  • Pathophysiology:

    • Leads to renin stimulation, increased blood pressure, and chronic ischemia causing renal tissue destruction.

21. Congenital Disorders

  • Examples:

    • Vesicoureteral reflux, agenesis, hypoplasia, ectopic kidneys, and horseshoe kidneys.

22. Adult Polycystic Kidney Disease

  • Genetics:

    • Autosomal dominant condition caused by a gene on chromosome 16.

  • Clinical Manifestations:

    • Develops into multiple cysts, leading to kidney enlargement, tissue compression, and chronic renal failure.

23. Wilms' Tumor

  • Description:

    • Common pediatric tumor occurring in children 3-4 years old.

  • Symptoms:

    • Abdominal mass, clothes fitting improperly, hypertension.

24. Renal Failure

  • Types:

    • Acute Renal Failure (ARF) and Chronic Renal Failure (CRF).

25. Acute Renal Failure

  • Causes:

    • Bilateral kidney diseases, severe shock, nephrotoxins, mechanical obstruction.

  • Symptoms:

    • Oliguria, pain, edema, hypertension.

26. Chronic Renal Failure

  • Definition:

    • Gradual, irreversible destruction of kidney function over time.

  • Causes:

    • Chronic kidney diseases, congenital conditions, sustained exposure to nephrotoxins.

27. Stages of Chronic Renal Failure

  • Early Stages:

    • Decreased renal reserve with no apparent symptoms.

    • Renal Insufficiency:

    • Decreased GFR (about 20% of normal), significant nitrogen waste retention, and elevated blood pressure.

  • End-Stage Renal Failure:

    • Almost negligible GFR with various systemic effects, leading to oliguria or anuria.

28. Signs and Symptoms Across Stages of Chronic Renal Failure

  • Early Signs:

    • Increased output, general signs like anorexia, nausea, anemia, fatigue.

  • Complete Failure Signs:

    • Oliguria, systemic infections, dry skin, peripheral neuropathy, complications from electrolyte imbalances.

29. Comparison Between Acute and Chronic Renal Failure

Characteristic

Acute Renal Failure

Chronic Renal Failure

Causes

Severe shock, burns, nephrotoxins

Nephrosclerosis, diabetes, long-term exposure

Onset

Sudden, acute

Slow, insidious

Early Signs

Elevated serum urea

Polyuria, anemia, fatigue

Progressive Signs

Oliguria and increased urine output

End-stage failure with oliguria, azotemia

Conclusion

  • The urinary system plays a critical role in homeostasis, and various disorders can significantly impact its function, leading to serious health implications and requiring prompt medical attention.

1. Overview of the Urinary System Functions

  • Metabolic Waste Removal: The urinary system is responsible for filtering blood to remove metabolic wastes, such as urea (from protein metabolism), creatinine (from muscle metabolism), and uric acid (from nucleic acid metabolism), through processes of glomerular filtration and tubular secretion.

  • Hormone Elimination: It removes spent hormones (e.g., steroid hormones, certain peptide hormones) and their metabolites from circulation, preventing their accumulation and sustained action.

  • Excretion of Drugs/Foreign Materials: Drugs, environmental toxins, and other foreign materials are eliminated via filtration and tubular secretion, protecting the body from toxic buildup.

  • Homeostatic Regulation: It precisely regulates water balance, electrolyte levels (e.g., sodium, potassium, calcium, phosphate), and acid-base balance (by excreting H+ and reabsorbing bicarbonate), maintaining internal stability.

  • Erythropoietin Secretion: Secretes erythropoietin in response to hypoxia, a hormone that stimulates red blood cell production in the bone marrow, vital for oxygen transport.

  • Vitamin D Activation: Activates vitamin D by performing the final hydroxylation step (25-hydroxyvitamin D to 1,25-dihydroxyvitamin D), which is crucial for calcium absorption from the gut and calcium homeostasis.

  • Blood Pressure Regulation: Regulates blood pressure through the renin-angiotensin-aldosterone system (RAAS), by adjusting blood volume and systemic vascular resistance, as well as influencing sodium balance.

2. Gross Anatomy of the Urinary System

  • Components:

    • Kidneys

    • Ureters

    • Urinary Bladder

    • Urethra

  • Supporting Structures:

    • Adrenal Gland

    • Liver

    • Spleen

    • Abdominal Aorta

    • Inferior Vena Cava

    • Common Iliac Artery and Vein

    • Renal Arteries and Veins

  • Kidneys:

    • The right kidney is typically slightly lower than the left due to the large liver. They are retroperitoneal organs, meaning they lie behind the peritoneum.

    • Each kidney is approximately 11 cm long, 6 cm wide, and 3 cm thick, weighing about 150 grams.

    • They are surrounded by a fibrous capsule, a perirenal fat pad (adipose capsule), and renal fascia (Gerota's fascia), providing protection and anchoring.

    • Internal Structure: Divided into an outer renal cortex and an inner renal medulla. The medulla contains renal pyramids, separated by renal columns. Urine drains from collecting ducts within the pyramids into minor and major calyces, then into the renal pelvis before entering the ureter.

  • Ureters: Muscular tubes ( ilde{25-30} cm long) that transport urine from the renal pelvis to the urinary bladder via peristaltic contractions.

  • Urinary Bladder: A muscular, distensible sac located in the pelvic cavity, designed for urine storage. Its wall contains the detrusor muscle. The trigone is a smooth triangular area between the openings of the ureters and urethra, which is clinically significant.

  • Urethra: A tube that conveys urine from the bladder to the exterior. It differs significantly in length and function between males and females.

3. Nephron: The Functional Unit of the Kidney

  • Structure: Each kidney contains over a million nephrons, which are the microscopic functional units responsible for forming urine. They process blood to remove wastes and regulate fluid and electrolytes.

  • Components:

    • Renal Corpuscles: The primary site of blood filtration.

      • Glomerulus: A tuft of specialized capillaries with fenestrated endothelium, where blood plasma is filtered. Its unique structure maintains high hydrostatic pressure.

      • Bowman’s Capsule: A double-walled cup that surrounds the glomerulus. The inner (visceral) layer consists of podocytes with filtration slits, forming part of the filtration membrane. The outer (parietal) layer is simple squamous epithelium.

    • Renal Tubules: Responsible for selective reabsorption and secretion.

      • Proximal convoluted tubules (PCT): Highly convoluted, lined with cuboidal cells dense with microvilli (brush border) and mitochondria, indicating extensive active transport. This is where most reabsorption occurs.

      • Loop of Henle: Consists of a descending limb (permeable to water) and an ascending limb (impermeable to water, actively transports ions). It is crucial for establishing and maintaining the osmotic gradient in the renal medulla.

      • Distal convoluted tubules (DCT): Less convoluted and has fewer microvilli. Its functions are largely regulated by hormones for fine-tuning reabsorption and secretion.

      • Collecting duct: Receives filtrate from several nephrons and runs through the renal medulla to the renal papilla. It plays a final role in water reabsorption and urine concentration under hormonal control.

    • Associated Capillaries:

      • Peritubular capillaries: Surround the PCT and DCT, involved in reabsorption and secretion.

      • Vasa recta: Specialized capillaries that run parallel to the Loop of Henle in juxtamedullary nephrons, maintaining the medullary osmotic gradient.

4. Formation of Urine

  • Process: Urine formation involves three main steps:

    • Filtration: Occurs in the renal corpuscle (glomerulus and Bowman’s capsule). Blood plasma, excluding cells and large proteins, is forced from the glomerular capillaries into Bowman’s capsule due to high glomerular hydrostatic pressure. This forms a protein-free filtrate (primary urine) at a rate known as the Glomerular Filtration Rate (GFR), typically around 125 ml/minute, or 180 liters/day. The filtration membrane allows passage of water, wastes, nutrients, and electrolytes but restricts blood cells and plasma proteins.

    • Reabsorption: As the filtrate moves through the renal tubules, essential substances (e.g., most water, glucose, amino acids, necessary ions) are selectively reabsorbed from the tubular fluid back into the peritubular capillaries and vasa recta. Over 99% of the filtered fluid is reabsorbed, preventing nutrient loss.

    • Secretion: During secretion, waste products, excess ions (e.g., H+, K+), and certain drugs (e.g., penicillin) are transported from the peritubular capillaries directly into the tubular fluid. This process is important for supplementing waste removal and precise regulation of pH and electrolyte balance.

5. Reabsorption Mechanisms

  • Transport Mechanisms: Reabsorption in the renal tubules employs various mechanisms:

    • Active Transport: Utilizes ATP to move substances against their concentration gradients (e.g., sodium, glucose, amino acids) from the tubular lumen into tubule cells and then into the interstitial fluid and capillaries. The Na+-K+ pump is fundamental here.

    • Co-Transport (Secondary Active Transport): Involves the movement of two substances simultaneously. For instance, sodium reabsorption is coupled with glucose or amino acid reabsorption via symporters (both move in the same direction) in the PCT. The energy comes from the Na+ gradient established by primary active transport.

    • Osmosis: Water reabsorption mainly occurs in proximal convoluted tubules (AQP1 aquaporins are constitutively present) and collecting ducts (under ADH control), following the osmotic gradient created by solute reabsorption.

    • Diffusion/Facilitated Diffusion: Passive movement of lipid-soluble substances or certain ions through channels down their electrochemical gradients.

  • Significance: The careful balance of these mechanisms ensures that most water and all filtered glucose and amino acids are reabsorbed, maintaining the body's fluid balance and nutrient supply while eliminating waste products. The PCT reabsorbs about 65% of the filtered water and solutes, while the Loop of Henle reabsorbs another 20-25% of water and solutes, creating the medullary osmotic gradient.

6. Hormones Involved in Reabsorption

  • Antidiuretic Hormone (ADH) / Vasopressin:

    • Secreted by the posterior pituitary gland in response to increased plasma osmolality or decreased blood volume/pressure.

    • Promotes water reabsorption mainly in the late distal convoluted tubules and collecting ducts by inserting aquaporin-2 water channels into the apical membranes of collecting duct cells. This makes the urine more concentrated and helps conserve body water.

  • Aldosterone:

    • A mineralocorticoid hormone secreted by the adrenal cortex. It is a key component of the RAAS.

    • Promotes sodium reabsorption in the principal cells of the collecting ducts and distal convoluted tubules in exchange for potassium or hydrogen ions. Water passively follows sodium, leading to increased blood volume and blood pressure.

  • Atrial Natriuretic Hormone (ANP):

    • A hormone released by the cardiac atria in response to high blood volume or atrial stretch.

    • Reduces sodium and fluid reabsorption by inhibiting aldosterone and ADH release, suppressing renin secretion, and directly inhibiting sodium reabsorption in the collecting ducts. ANP also dilates the afferent arteriole, increasing GFR. This leads to increased excretion of sodium and water (natriuresis and diuresis), thereby decreasing blood volume and blood pressure.

  • Parathyroid Hormone (PTH):

    • Released from the parathyroid glands in response to low plasma calcium levels.

    • Primarily acts on the DCT to increase calcium reabsorption and in the PCT to promote phosphate excretion, thus playing a critical role in calcium and phosphate homeostasis.

7. Glomerular Filtration Rate (GFR)

  • Control Factors: GFR, the volume of filtrate formed per minute by the glomeruli of both kidneys, is tightly regulated to maintain constant fluid and electrolyte balance despite fluctuations in systemic blood pressure. Control involves both intrinsic (autoregulation) and extrinsic (neural and hormonal) mechanisms.

  • Mechanisms:

    • Autoregulation: Intrinsic mechanisms maintain a constant GFR over a wide range of mean arterial pressures (80-180 mmHg).

      • Myogenic mechanism: The afferent arteriole constricts or dilates in response to changes in blood pressure, maintaining constant flow to the glomerulus.

      • Tubuloglomerular feedback: Macula densa cells in the juxtaglomerular apparatus (JGA) sense changes in NaCl concentration in the distal tubule. If GFR increases, more NaCl reaches the macula densa, which then releases vasoconstrictors (e.g., ATP, adenosine) to constrict the afferent arteriole, thereby decreasing GFR.

    • Sympathetic Nervous System Influence: Strong sympathetic stimulation (e.g., severe hemorrhage, stress) causes significant vasoconstriction of afferent arterioles, markedly decreasing glomerular pressure and filtrate formation. This shunts blood away from the kidneys to vital organs.

    • Renin-Angiotensin-Aldosterone System (RAAS):

      • Juxtaglomerular (JG) cells in the afferent arteriole release renin in response to low blood pressure, decreased NaCl delivery to the macula densa, or sympathetic stimulation.

      • Renin initiates the conversion of angiotensinogen to angiotensin I, which is then converted by ACE to angiotensin II.

      • Angiotensin II is a potent systemic vasoconstrictor (raising blood pressure) and also constricts both afferent and efferent glomerular arterioles, affecting glomerular pressure. It stimulates aldosterone and ADH secretion, leading to increased sodium and water retention, which further raises blood volume and GFR.

  • Implications: GFR is the best overall index of kidney function. A persistent decrease in GFR indicates kidney damage or disease. Blood pressure is closely related to kidney function, often increasing significantly with advanced renal failure due to fluid retention and RAAS overactivity.

8. Incontinence and Retention

  • Incontinence: Defined as the involuntary loss of voluntary control over bladder emptying, resulting in accidental urine leakage. It is not a disease but a symptom of an underlying problem.

    • Variants:

      • Enuresis: Involuntary urination, particularly bedwetting, beyond the age when bladder control is usually established (typically after 4-5 years). Often related to developmental delay in bladder control, small functional bladder capacity, or psychological factors.

      • Stress Incontinence: Most common type in women, often due to weakened pelvic floor muscles (e.g., from childbirth, estrogen deficiency in menopause, surgery) that cannot withstand increased intra-abdominal pressure from activities such as coughing, sneezing, laughing, or lifting heavy objects, leading to small urine leaks.

      • Urge Incontinence (Overactive Bladder): Characterized by a sudden, strong, and uncontrollable urge to urinate, followed by involuntary leakage. It results from involuntary contractions of the detrusor muscle. Causes can include neurological disorders, bladder irritants, or idiopathic factors.

      • Overflow Incontinence: Occurs when the bladder becomes overfilled and distended, leading to urine leakage due to increasing intravesical pressure exceeding urethral resistance. This is often caused by chronic obstruction (e.g., prostatic hypertrophy in older men, urethral stricture) or weakness/underactivity of the detrusor muscle (e.g., diabetic neuropathy, spinal cord injury) preventing complete bladder emptying.

      • Functional Incontinence: Inability or unwillingness of a person with a normal bladder and urethral function to make it to the toilet in time due to physical disability (e.g., severe arthritis), cognitive impairment (e.g., dementia), or psychological barriers.

  • Retention: The inability to completely empty the bladder, leaving a significant amount of residual urine. This can be acute (sudden, painful inability to void) or chronic (gradual, often painless incomplete emptying).

    • Conditions leading to retention include urethral obstruction (e.g., prostatic enlargement, strictures, calculi), neurological damage (e.g., spinal cord injuries, multiple sclerosis, stroke affecting bladder control), and the effects of certain medications (e.g., anticholinergics, anesthetics).

    • Chronic retention increases the risk of urinary tract infections, hydronephrosis, and bladder damage over time.

9. Common Disorders of the Urinary System

  • The urinary system is susceptible to a wide range of disorders, including infections, inflammatory conditions, obstructive problems (like kidney stones), congenital abnormalities, and various tumors. These conditions can significantly impair renal function, leading to disruptions in fluid, electrolyte, and acid-base balance, and potentially progressing to severe renal failure. Early diagnosis and appropriate management are crucial for preventing irreversible kidney damage.

10. Types of UTIs and Associated Organisms

  • Urinary Tract Infections (UTIs): Very common, particularly affecting women. They are generally categorized as lower UTIs (cystitis, urethritis) and upper UTIs (pyelonephritis).

    • Causative Organism: Escherichia coli (E. coli), particularly uropathogenic strains, is the predominant pathogenic organism, responsible for 75-90% of uncomplicated UTIs.

  • Other Organisms Associated with UTIs: Other pathogens implicated include:

    • Klebsiella pneumoniae, Proteus mirabilis, Enterobacter spp., Citrobacter freundii, and Serratia marcescens (often associated with complicated UTIs, catheterization, or hospital-acquired infections).

    • Pseudomonas aeruginosa (commonly found in catheter-associated UTIs and in patients with complicated genitourinary tracts).

    • Enterococcus faecalis (gram-positive cocci, common in hospital-acquired UTIs).

    • Coagulase-negative Staphylococcus (e.g., Staphylococcus saprophyticus, a cause of UTIs in young, sexually active women).

    • Chlamydia trachomatis and Mycoplasma hominis (often cause urethritis, particularly sexually transmitted forms, less commonly affecting the upper tract).

  • Factors:

    • Gender: UTIs are significantly more common in women due to their shorter urethra and its anatomical proximity to the anus, facilitating bacterial ascent.

    • Older Men: In older men, risk factors include prostatic hypertrophy (benign prostatic hyperplasia - BPH) leading to incomplete bladder emptying and urine retention, urinary catheterization, and other instrumentation.

    • Other Risk Factors: Diabetes mellitus (compromised immunity, neurogenic bladder), immunosuppression, kidney stones, anatomical abnormalities (e.g., vesicoureteral reflux), and neurological diseases affecting bladder function (neurogenic bladder).

11. Cystitis and Urethritis

  • Definitions:

    • Cystitis: Inflammation of the bladder wall, most frequently caused by an ascending bacterial infection from the urethra. It is a common form of lower UTI.

    • Urethritis: Inflammation of the urethra, which can be caused by bacterial infection (e.g., E. coli) or sexually transmitted pathogens (e.g., Chlamydia trachomatis, Neisseria gonorrhoeae).

  • Symptoms:

    • Local Urinary Symptoms:

      • Hyperactive bladder: Characterized by frequent, strong urges to urinate.

      • Pelvic pain: Discomfort or pressure in the lower abdomen or suprapubic region.

      • Dysuria: Painful or difficult urination, often described as a burning sensation.

      • Urgency: A sudden, compelling need to pass urine.

      • Frequency: Need to urinate more often than usual, typically in small amounts.

      • Nocturia: Waking up at night one or more times to urinate.

      • Hematuria: Blood in the urine, which can be macroscopic (visible) or microscopic.

    • Systemic signs: May include low-grade fever, general malaise (feeling unwell), nausea, and leukocytosis (elevated white blood cell count). High fever usually indicates an upper UTI (pyelonephritis).

    • Urine characteristics: Urine often appears cloudy due to the presence of white blood cells and bacteria, and may have an unusual or strong odor.

12. Pyelonephritis

  • Definition: Inflammation and infection of the renal pelvis, calyces, and kidney parenchyma (tubules and interstitial tissue), typically an upper urinary tract infection. It can affect one or both kidneys, often progressing from a lower UTI via the ureters.

  • Pathogenesis: Bacteria (most commonly E. coli) ascend from the bladder to the kidneys, often facilitated by vesicoureteral reflux or urinary obstruction. This leads to an acute inflammatory response within the kidney, causing purulent exudate (pus) to fill the renal pelvis and calyces, and patchy interstitial inflammation and necrosis.

  • Consequences:

    • Acute Pyelonephritis: Can cause severe systemic illness and potentially lead to bacteremia (bacteria in the bloodstream).

    • Recurrent or Chronic Pyelonephritis: Persistent infection or repeated acute episodes can lead to scar tissue formation (fibrosis) in the renal parenchyma. This results in progressive loss of tubule function, atrophy of nephrons, and potentially hydronephrosis if there is underlying obstruction. If untreated or severe, particularly when bilateral, it can lead to chronic renal failure due to extensive kidney damage.

  • Symptoms: Patients present with signs typical of cystitis (dysuria, urgency, frequency) along with severe renal disease-related pain:

    • High temperature: Systemic fever, often accompanied by chills.

    • Flank pain: Severe, aching pain in the loin area or costovertebral angle tenderness (CVA tenderness), indicating kidney inflammation.

    • Systemic symptoms: Malaise, headache, nausea, and vomiting.

    • Urinalysis: Reveals pyuria (WBCs), bacteriuria, and characteristic urinary casts, specifically white blood cell (WBC) casts, which are indicative of kidney parenchymal inflammation.

13. Inflammatory Disorders: Glomerulonephritis

  • Pathophysiology: Glomerulonephritis is an inflammatory condition affecting the glomeruli, the filtering units of the kidney. It is often an immune-mediated disorder.

    • Antigen-antibody complex formation: Most commonly, it develops after an infection elsewhere in the body, such as post-streptococcal glomerulonephritis (PSGN), following a Group A beta-hemolytic Streptococcus infection (e.g., strep throat or impetigo). Circulating antigen-antibody immune complexes become entrapped in the glomerular basement membrane or antibodies directly attack glomerular components.

    • Inflammatory response: The trapped immune complexes activate complement and attract