A PPT from my lectures delivered at Jayoti Vidyapeeth Women's University for the BHMS III and IV year students in Practice of Medicine

1. Diseases of Urogenital
Tract
Dr.Ravi Jain M.D.(Hom.)
ravij0000@gmail.com
Assistant Professor
Department of Practice of Medicine
Jayoti Vidyapeeth Women’s University,Jaipur

2. Urogenital System
 The Genitourinary system, or Urogenital system, is
the organ system of the reproductive organs and
the urinary system.
 We study them together because :
 Proximity to each other.
 Their common embryological origin.
 Use of common pathways.

3. Kidney and Urinary Tract Diseases
 Anatomy of Kidney and Urinary Tract
 Physiology (Renal Functions)
 Renal Disorders
 Assessment of Renal Disorders.
 Examinations in cases of Renal disorders

4. Anatomy of Kidney and Urinary Tract

5. Functions of Kidney
 Maintain volume and composition of body fluids.
 Retain certain useful substances by renal threshold.
 Excrete waste products.(urea, uric acid, creatinine).
 Homeostasis of electrolytes, minerals, anions and cations,
salt and water.
 Metabolic and hormonal functions.

6. Genitalia
 Male Genitalia
 Female Genitalia

7. Functions
 Male Genitalia :
 Produce spermatozoa and testosterone – pubertal growth,
prostate and seminal vesicle, development of secondary
sexual characters.
 Female Genitalia :
 Ovaries produces ova and hormones.
 Secondary sexual characters.

8. Renal Disorders
 Acute Renal Failure
 Acute Nephritic syndrome
 Nephrotic Syndrome
 Chronic Renal Failure

9.  Asymptomatic urinary abnormalities
 Urinary Tract Infection
 Renal Tubular Defects
 Nephrolithiasis
 Urinary Tract Obstruction

10. Assessment
 Face : Puffiness
 Eyes : Oedema
 Ear : Tophi
 Neck : JVP for fluid overload
 Skin : Purpura, Bruising, Pruritis
 Extremities : Oedema, Clubbing, Peripheral Neuropathy

11. Investigations of a case with Renal
Disease
 Urine Examination :
 Volume
 Colour and Transparency
 Urine Concentration and Osmolality
 Specific Gravity
 Urine Dilution
 pH

12. Abnormal Constituents of Urine
 Proteinurea
 Haematuria
 Sugars
 Ketones
 Bilirubin
 Cells
 Casts
 Crystals
 Micro-organisms

13. Urinary Tract Infection
(UTI)

14.  UTI is defined as the presence and multiplication of
bacteria in the urinary tract.
 It cann be uncomplicated or complicated, upper or lower.
 The clinical features, diagnosis, treatment and prognosis
depends on the organism, site of infection and structural
and functional integrity of urinary tract.

15. Urinary tract infection (UTI)
 It is an infection that affects part of the urinary tract.
 Cystitis : when it affects the lower urinary tract it is
known as a bladder infection.
 Pyelonephritis : when it affects the upper urinary tract.

16. Signs and symptoms
 Burning with urination
 Frequent urination
 Pain above the pubic bone or in the lower back
 Flank pain,
 Fever
 Nausea
 Vomiting
 Rarely bloody urine
 Pus in urine

17. Causes of UTI
 E. coli
 Staphylococcus saprophyticus
 Urinary catheterization
 Intercourse
 Contraceptives : spermicides, diaphragm, etc

18. Investigations
 Urineanalysis : MSU
 Urine may be turbid, blood stained and foul smelling.
 pH depends on pathogenic bacteria.
 Mild proteinuria
 Urine microscopy shows pus cells and pus cell casts.
 USG
 Plain X Ray KUB
 Intra venous Urography
 CT
 DMSA
 Cystoscopy

19. Homeopathic Medicines
 Thuja Occidentalis
 Nux vomica
 Sarsaparilla
 Aconitum napellus
 Apis mellifica
 Belladonna
 Berberis vulgaris

20.  Borax
 Cantheris
 Staphysagria
 Clematis erecta
 Sulphur
 Lycopodium

21. Acute Renal Failure
Acute Kidney Injury (AKI)

22.  Is characterized by the sudden impairment of kidney
function resulting in the retention of nitrogenous and
other waste products normally cleared by the kidneys.
 AKI is not a single disease but, rather, a designation for a
heterogeneous group of conditions that share common
diagnostic features.
 An increase in the blood urea nitrogen (BUN)
concentration.
 An increase in the plasma or serum creatinine (SCr)
concentration.
 Associated with a reduction in urine volume.

23.  AKI is a clinical diagnosis and not a structural one.
 AKI can range in severity from asymptomatic and transient
changes in laboratory parameters of glomerular filtration
rate (GFR), to overwhelming and rapidly fatal
derangements in effective circulating volume regulation
and electrolyte and acid-base composition of the
plasma.

24.  A sudden and usually reversible loss of renal function,
which develops over days or weeks and is usually
accompanied by a reduction in urine volume.
 An abnormally high creatinine is important to establish if
this is acute, acute on chronic, or chronic kidney disease.
 Measurements of renal function should be sought for
comparison.
 A renal ultrasound demonstrating two small kidneys
indicates chronicity

25. Pathophysiological Classification
 Pre Renal
 Intrinsic renal
 Post renal

26.  Pre renal Causes : Most common.
 Renal dysfunction caused by decrease in renal perfusion.
 Restoration of renal perfusion results in rapid recovery.
 Intrinsic renal Causes : Most common cause is Acute
tubular necrosis.
 Caused by ischemic or nephrotoxic injury.
 Post renal Causes : Due to urinary tract obstruction.

28. Clinical Features
 Pre renal failure :
 Oliguria
 Symptoms of Hypovolaemia, Thirst, dizziness, orthostatic
hypotension.
 Evidence of excessive fluid loss.

29.  Intrinsic renal failure :
 ATN should be suspected presenting after a period of
hypotension, hemorrhage, sepsis, drug overdose, surgery.
 Postrenal failure : It occurs in old men with prostatic
obstruction, symptoms of urgency, frequency, hesitancy,
and obstruction to flow of urine.

30. Investigations
 Urinalysis : Daily urine output. Presence of abnormal
constituents.
 Blood urea and Serum creatinine.
 Urine electrolytes.
 Ultrasound examination. For detecting intrinsic renal
disease.
 Serologic tests. Anitnuclear antibody.
 Renal Biopsy : when diagnostic investigations are
inconclusive.

31.  Creatinine S
 Female 44–80 μmol/L 0.5–0.9 mg/dL
 Male 53–106 μmol/L 0.6–1.2 mg/dL
 Urea nitrogen S 2.5–7.1 mmol/L 7–20 mg/dL

32. Management
 Treatment of Underlying cause
 Maintenance of body fluids and electrolyte balance.
 Maintenance of Nutritional status.
 Monitor life threatening complications.
 Renal replacement when indicated.

33. Chronic kidney disease
Chronic Renal Failure

34.  An irreversible deterioration in renal function which
classically develops over a period of years.
 Initially, manifested as biochemical abnormality.
 Loss of :
 Excretory,
 Metabolic and
 Endocrine functions of the kidney leads to the clinical
symptoms and signs of renal failure referred as Uraemia.
 Normal GFR = 120+
- 25ml/min/1.73m2

35.  Uremic features includes
 Anorexia, nausea and vomiting
 Followed by
 Drowsiness, apathy, confusion, muscle twitching
 Hiccoughs, fits and coma.

36. Stages of Chronic Renal Disease
 Stage I : Kidney damage with normal or high GFR : > 90,
 Stage II : Kidney damage with slightly low GFR : 60-89
 Stage III : Moderately low GFR : 30-59
 Stage IV : Severe low GFR : 15-29
 Stage V : Kidney Failure : <15

37. Common causes :
 Any condition which destroys the normal structure and
function of the kidney.
 Congenital and inherited - polycystic kidney
disease,Alport syndrome
 Renal artery stenosis
 Hypertension
 Glomerular diseases
 Interstitial diseases
 Systemic inflammatory diseases – SLE, vasculitis
 Diabetes mellitus
 Unknown

38. Alport syndrome
 Affects adults. Autosomal recessive disease.
 Arise from mutation or deletion of Gene on X chromosome
COL4A5 which encodes Type IV collagen.
 Accumulation of abnormal collagen results in a progressive
degeneration of GBM.
 Affected patients progress from haematuria to ESRF in
late teens or twenties.
 Associated with sensorineural deafness and ocular
abnormalities.

39. Pathogenesis
 Disturbances in water, electrolyte and acid base balance
contribute to the clinical picture.
 Exact pathogenesis is unknown.
 Many substances in abnormal concentration in plasma.
 Uremia is caused by accumulation of intermediary
products of metabolism.

41. Clinical Features
 Raised blood urea and creatinine.
 Hypertension,
 Proteinuria
 Anaemia.
 Diseases is Slowly progressive and patients are
asymptomatic until GFR falls below 30 mL/min/1.73 m2
 Nocturia , due to loss of concentrating ability and
increased osmotic load.
 Tiredness or breathlessness
 Pruritus, anorexia, nausea and vomiting
 Deep respiration related to metabolic acidosis, muscular
twitching, fits, drowsiness and coma ensue.

42. Investigations
 Urea and Creatinine
 Urinalysis and quantification of proteinuria.
 Electrolytes
 Calcium, phosphate, parathyroid hormone
 Albumin
 Full blood count (± Fe, ferritin, folate, B12)
 Lipids, glucose ± HbA1c
 Renal ultrasound
 Hepatitis and HIV serology
 ECG
 Other tests

43. Retarding Progression of CKD
 Plasma creatinine above 3.4mg/dl, progressive
deterioration in kidney function irrespective of etiology.
 Control of Blood Pressure.
 Diet : restrict protein

44. Management of the adverse effect of
CRF
 Anemia
 Fluid and electrolyte balance
 Acidosis
 Infection
 Bleeding
 Renal osteodystrophy
 Myopathy
 Others

45.  Anemia : correlates with severity of CRF
 Causes :
 Relative deficiency of erythropoietin
 Diminished erythropoesis due to toxic effects of uremia
 Reduced red cells survival
 Increased blood loss due to capillary fragility
 Reduced intake and absorption.
 Rx - Iron supplementation is needed

46.  Fluid electrolyte balance : reduced ability to concentrate
urine.
 Limitation of potassium intake (70mmol/day) and sodium
intake (100mmol/day).
 Acidosis : declining renal function is associated with
metabolic acidosis.
 Sodium bicarbonate supplements.

47.  Cardiovascular disease and lipids :
 Atherosclerosis is accelerated by hypertension. Vascular
calcification develops. Hypercholestrolemia is significant
with proteinuria and increased triglyceride level.
 Treatment of these abnormalities.
 Infection : Second most common cause of death in dialysis
patient. Cellular and humoral immunity is impaired.
 Treatment of the cause.

48.  Bleeding :
 Platlet function is impaired and bleeding time is
prolonged.
 Cutaneous ecchymosis and mucosal bleeds.
 Adequate dialysis corrects bleeding tandency.
 Renal osteodystrophy : Mixture of osteomalacia,
hyperparathyroid bone disease, osteoporosis, and
osteosclerosis.
 Deficiency of 1 aplha hydroxylase enzyme
 Parathyroidectomy

49.  Myopathy :
 Generalised myopathy is due to combination of poor
nutrition, hyperparathyroidism, Vit D Deficiency and
disorders of electrolyte metabolism.
 Other adverse effects :
 Sensory neuropathy causes paresthesiae.
 Motor neuropathy causes foot drop.
 Uraemic autonomic neuropathy causes delayed gastric
emptying, diarrhoea, and postural hypotension.

50.  Gastrointestinal manifestations include anorexia, nausea,
vomiting.
 High incidence of peptic ulcer.
 Depression is most common in patients approaching renal
replacement therapy.

51. Glomerulonephritis

52.  Glomerular diseases causes :
 Proteinurea
 Haematuria
 Loss of filtration capacity (GFR)
 Hypertension

53. Acute Glomerulonephritis
 Most common in children but can occur at any age.
 Pathologically diffuse inflammatory changes in glomeruli.
 It is an immune complex mediated glomerulonephritis.
 Preceded by Streptococcal infection.

54.  Following streptococcal infection the streptococcal
antigens stimulates antibody production.
 The antigen antibody combine to form immune
complexes.
 It gets deposited in kidney tissues and initiate acute
inflammatory reaction.
 There are contributions of cellular immunity, humoral
immunity, and other inflammatory mediators.

55.  Clinically it is abrupt onset of :
 Puffiness of face
 Macroscopic hematuria
 Proteinuria
 Oedma
 Hypertension
 Impaired renal function with or without oliguria.

56. Clinical Features
 Puffiness of the face.
 Scanty and smoky urine, frank blood.
 Infection symptoms : Fever, bodyache,vomiting.
 Cerebral symptoms : Headache, convulsion.
 Weakness, anorexia, pallor.
 Accidental discovery on routine urine examination.

57. Symptoms and signs.
 Oedema : Gradual or abrupt onset.
 <morning.
 Swelling of face to generalized anasarca.
 Hypertension : Diastolic pressure 90-120mm of Hg.
 Returns to normal after diuresis.
 JVP is raised. Peripheral oedema with a picture of CHF.
 Renal functions are impaired. : oliguria

58. Lab Investigations
 Urine examination : Oliguria, reddish brown with protein.
Red cells and casts are present.
 Evidence of streptococcal infection : Presence of A Beta
hemolytic streptococcus in throat or skin lesion.
 Hematology : Polymorphoneuclear Leucocytosis, Raised
ESR.
 Osmolarity : Usually higher.
 Renal biopsy : When the diagnosis is not clear.

59. Prognosis
 90% of the children recovery is uneventful and complete.
 Proteinuria and Hematuria may persist for few weeks to
months before returining to normal.

60. Complications :
 Acute renal failure
 Acute heart failure with pulmonary edema.
 Hypertensive encephalopathy
 UTI
 Arthritis
 Some children may develop Nephrotic syndrome or
chronic glomerulonephritis.

61. Management
 Bed rest : 3 weeks to 3 months.
 Restricted fluids : Fruit juices, water with caution. Low
salt, Low protein diet.
 Antibiotics : Erythromycin, Benathine penicilline.
 Management of complications : Diazepam for
convulsion, ACE inhibitors for hypertension.
 Dialysis : in case of rapid rising serum potassium and
blood urea.
 Renal transplant.

62. Nephrotic Syndrome

63.  A clinical condition in which there is
 Oedema
 Proteinuria
 Hypoproteinemia
 Irrespective of etiology or any other additional abnormal
clinical features.

64.  A condition characterized by
 Heavy proteinuria of > 3.5gm/1.73m2 body surface area in
24 Hrs.
 It is associated with :
 Hypoalbuminemia
 Edema
 Hyperlipidemia
 Hypercoagulable state

65. Etiology
 Idiopathic
 Primary Glomerular disease
 Secondary causes

66. Primary
 Minimal change disease
 Focal segmental glumerulosclerosis.
 Membranous nephropathy.
 Membranoproliferative glomerulonephritis
 IgA Nephropathy

67. Secondary
 Infections : Bacterial, viral, protozoal, helminthic etc
 Neoplasm : Solid tumors : lung, stomach, breast,
leukemia, etc.
 Drugs : NSAID’s, Penicillamine, gold, mercury, etc
 Multisystem disease : SLE, rheumatoid arthritis,
amyloidosis.
 Familial and metabolic diseases : diabetes mellitus,
graves disease, etc
 Misc : pre-eclampsia, malignant nephrosclerosis, obesity
etc.

68. Clinical Features
 Age & Sex : Common in childhood with peak incidence 2-3
years. M:F 2.5:1. Equal in adults.
 Oedema : Peripheral. Lower limbs. Face and abdomen
affected in children. Generalized anasarca.
 GI : Anorexia with severe malnutrition. Diarrhea and
vomiting due to edema of intestinal wall.
 General : Anorexia, lethargy, tiredness, frequent
infections and muscle wasting. Dyspnoea may occur.
 Blood Pressure : Hypertension.

69. Lab Findings
 Urine :
 Oliguria
 Proteinuria : > 5gm/day.
 Casts : Fatty casts.
 Blood :
 Anemia : normochromic
 Hypoalbuminemia
 Hyperlipoproteinemia
 Renal biopsy

70. Prognosis
 90% children respond to prednisolone.
 Adult response rate is 60%.
 Relapse rate is high.

71. Management
 General management includes fluid restriction, low
sodium diet, rest. These helps in controling edema.
 Corticosteroids : produce rapid and complete remission.
 Immunosuppressive drugs : Cyclophosphamide.

72. Homeopathic Management
 Apis Mellifica
 Apocynum Cannabinum
 Arsenic Album
 Terebinthina
 Kali ars
 Phosphorus
 Plumbum met

73. Nephrolithiasis

74. • These are urinary salts bound together by a colloid
matrix of organic materials.
• Consists of nucleus around which concentric layers of
urinary salts are deposited.

77. According to location
 In the kidney - Nephrolithiasis
 In Ureter - Ureterolithiasis
 In Bladder - Cystolithiasis

78.  Renal calculi are common, affecting ~1% of the
population, and recurrent in more than half of pts.
 Stone formation begins due to supersaturated of urine
with insoluble components due to :
 Low urinary volume
 Excessive or insufficient excretion of selected compounds,
 Other factors (e.g., urinary pH) that diminish solubility.

79. Types of Stones
 Two types
 Primary stones : Appearing without any antecedent
inflammation in urinary tract.
 Occurs in acidic urine
 Secondary stones : Formed as the result of
inflammation.
 Occurs in alkaline urine

80. Primary stones
• Calcium oxalate - Mulberry stone – Single- dark - spiky –
very hard.
• Uric acid - Rare. - Radiolucent – multiple – faceted –
yellow to dark brown.
• Cystine – Young girls at puberty – multiple- soft – yellow or
pink.
• Xanthine - Extremely rare- smooth – round – brick red.
• Indigo – Blue – uncommon

82. Secondary stones
 1. Calcium phosphate (majority)
- Triple phosphate – Calcium, Ammonium, Magnesium
phosphate – smooth, soft, friable.
- Dirty white.
2. Mixed – Phosphate stone as a covering of primary stone.

85. Types of Stones
 Approximately 75% of stones are Ca-based Ca oxalate, Ca
phosphate and other mixed stones),
 15% struvite (magnesium-ammonium phosphate),
 5% uric acid,
 1% cystine,
 Reflecting the metabolic disturbances from which they
arise.

86. Signs and Symptoms
 Asymptomatic or cause hematuria alone.
 With passage, obstruction may occur at any site along the
collecting system.
 Severe pain, often radiating to the groin.
 Nausea, vomiting, diaphoresis, light-headedness.
 Hematuria, pyuria, urinary tract infection (UTI), and
hydronephrosis.

87.  Staghorn calculi may be completely asymptomatic,
presenting with loss of renal function.
 It is associated with recurrent UTI with urea-splitting
organisms.

88. Symptoms
 Pain : Ureteric colic : Cramping, sharp, often
excruciating pain, fluctuating in intensity but not
completely remitting.
 Pain is associated with vomiting and sweating.
 Pain extends from loin down the line of ureter to groin.
 Loin pain.
 Haematuria : with or without colic.

89. Signs
 Tenderness – Present at renal angle posteriorly.(Murphy’s
kidney punch test.)
 Muscle rigidity - over kidney.
 Swelling – felt in flank.
 Abdominal distension and diminished peristalsis.

90. Effect on kidney
 Same :
 Obstruction
 Infection
 Parenchymal Ischemia
 Malignancy
 Opposite :
 Compensatory hypertrophy
 Bilateral calculi
 Infection
 Calculus anuria

91. Stone Composition
 Most stones are composed of Ca oxalate.
 Associated with hypercalciuria and/or hyperoxaluria.
 Hypercalciuria : very high-Na diet, loop diuretic therapy,
renal tubular acidosis (RTA), sarcoidosis, Cushing’s
syndrome, aldosterone excess.
 Conditions associated with hypercalcemia (e.g., primary
hyperparathyroidism, vitamin D excess, etc).
 It may be idiopathic.

92.  Hyperoxaluria is seen with intestinal malabsorption
syndromes (e.g., inflammatory bowel disease,
pancreatitis),
 Due to reduced intestinal secretion of oxalate and/or the
binding of intestinal Ca by fatty acids within the bowel
lumen.
 With enhanced absorption of free oxalate.

93.  Ca phosphate stones
 Much less common and tend to occur at an abnormally
high urinary pH (7–8), usually in association with a
complete or partial distal RTA.

94.  Struvite stones form in the collecting system when
infection with urea-splitting organisms is present.
 Proteus, Klebsiella, Providencia, Morganella, and others.
 Struvite is the most common component of staghorn
calculi and obstruction.
 Risk factors include previous UTI, urinary catheters, and
instrumentation.

95.  Uric acid stones develop when the urine is saturated with
uric acid in the presence of an acid urine pH.
 Urine pH that is <5.4 and often <5.0.
 Asscociated with
 Clinical gout
 Certain drugs e.g., probenecid, high-dose salicylates.

96.  Cystine stones
 More likely to form in acidic urinary pH.
 Result of a rare inherited defect in renal and intestinal
transport of several dibasic amino acids.
 Overexcretion of cysteine.
 They occasionally lead to end-stage renal disease.

97. Investigation
 Blood examination –
Routine examination.
Blood urea, N.P.N, creatinine for renal function
Serum calcium level
Serum uric acid level.
 Urine analysis –
Physical examination – Smoky or opalescent
Chemical ex.- Ph, protien, blood.
Microscopic - RBC, pus cells, casts, crystals.
Bacteriological – highly imp. + culture and sensitivity.
Renal function tests

98.  X- Ray – KUB
 Ultrasonography.
 Intravenous pyelography (IVP)
 Computerised tomography
 Renal scan
 Examination of stone.

103. Differential Diagnosis
 Acute Appendicitis
 Cholelithiasis, Cholecystitis
 Twisted Ovarian Tumor
 Testicular Torsion
 Renal carcinoma (may give hematuria but likely not pain)
 Pancreatitis
 Ectopic pregnancy
 Aortic aneurysm
 Acute intestinal obstruction

104. Workup
 Dietary and fluid intake history.
 Careful medical history and physical examination,
focusing on systemic diseases
 Noncontrast helical CT, with 5-mm CT cuts.
 Routine UA; presence of crystals, hematuria,
measurement of urine pH
 Serum chemistries: BUN, Cr, uric acid, calcium,
phosphate, chloride, bicarbonate,PTH
 Timed Urine collections : Cr, Na, K, urea nitrogen, uric
acid, calcium, phosphate, oxalate, citrate, pH

105. Treatment
 Depends on clinical history, and the metabolic workup.
 Nncrease in fluid intake to at least 2.5–3 L/d.
 Conservative recommendations for Ca oxalate stones :
 low-salt, low-fat, moderate-protein diet.
 Specific treatment depends upon the type of stone and
managed accordingly.

106.  Calcium oxalate : Increase fluid intake Citrat
supplementation
 Moderate sodium intake
 Moderate oxalate intake
 Moderate protein intake
 Moderate fat intake
 Thiazides if hypercalciuric
 Allopurinol if hyperuricosuric

107.  Calcium phosphate :
 Increase fluid intake
 Moderate sodium intake
 Treat hyperparathyroidism if present.
 Thiazides if hypercalciuric
 Alkali for distal renal tubular acidosis

108.  Struvite stones :
 Increase fluid intake
 Methenamine and vitamin C
 Daily suppressive antibiotic therapy

109.  Uric acid stones :
 Increase fluid intake .
 Moderate dietary protein intake.
 Allopurinol.
 Alkali therapy to raise urine pH to 6.0–6.5.

110.  Cystine stones :
 Increase fluid intake
 Alkali therapy
 Penicillamine

111. Other Management
 ESWL
 Endoscopy
 Open surgery

113. Complications
 Impaction and obstruction : at PUJ.
 Infection : Pyelonephritis, cystitis.
 Stricture of ureter.
 Malignant change due to chronic irritation of renal pelvis.
 Anuria : from obstruction.
 Hydronephrosis
 Pyonephrosis
 Renal failure
 Squamous cell carcinoma

114. Homeopathic Medicines
 Acid Nit
 Acid Benzoic
 Berberis vulgaris
 Cantheris
 Hydrangea
 Lithium carb
 Lycopodium
 Tabacum
 Sarsaparilla
 Ocimum can
 Pariera brava

115. Homoeopathic management
 Acid nit. –
Urine contains oxalic acid.
Intolerable odor- horse’s urine.
Urine cold when passed
Dark brown
 2. Acid Benz –
Highly intensified urinous odor.
Deep red, dark brown
Cystits.

116.  Berberis vulgaris –
- Pains shoots radiates from a point.
- Stitching pain from left kidney following
course of ureter into bladder and urethra.
-Burning and soreness in region of kidney.
• Cantharides -
Constant urging to urinate.
Burning , cutting pain in urethra during
micturition
Useful in paroxysm of renal colic.
Violent tensemus and stangury.

117.  Hydrangea – Acts on ureter
- Sharp pain in left loin.
-Urine hard to start. Heavy deposit of mucous.
- Soreness and burning in urethra with frequent
desire.
 6. Lithium carb–
Pains in heart while urinating; when bending
over.
Sharp stitching pain in right side of bladder.
Pain from kidney, ext. along urether through
spermatic cord into testes.

118. . Lycopodium clavatum -
- Pain extends along ureter and end in bladder.
- Child cries before urniating.
- Red sand in urine.
- Backache > urinating. Right sided.
 8. Nux vom -
- Renal pain when each pain shoots to rectum
and urging to stool.
- Right sided.

119.  Ocimum can –
- Renal colic with considerable vomitting every 15
mins.
- Urine colour saffron colour, thick purulent, smell of
musk.
• Pariera brava-
- Excruciating pains radiates from left kidney to groin
down thigh.
- Must go down on all four limbs to urinate,almost
touches floor with forehead in order to be able to pass
urine.
- Violent pain in glans penis.

120.  Sarsaparilla –
Extreme pain at conclusion of urine.
Urine dribbles while sitting.
Pain from right kidney downwards.
Urine only passes freely when standing

121.  Calc renalis – Lapis renalis - gravel and renal calculi
 Cardus marianus – Prevents further formation of stones.
 Chimaphilla - unable to urinate without standing with
feet wide apart and body inclined forward.
 Cocc –c – lancinating pain from kidney to bladder.
- brick red sediments, hematuria, urates and uric acid.
 Epigea repens – Chronic cystitis with dysurea,uric acid
deposit.

122.  Fragaria - Prevents formation of calculi.
 Pichi – Vesical tensmus and buring after urination.
(Fabina imbricata)
 Rubria tinctor - Catarrh of bladder, frequent urging to
urinate at night,with great weakness, pains from kidney to
urethra.
 Ipomea – Renal colic, aching in small of back and
extremities.

123. Polycystic kidney
disease

124.  The polycystic kidney diseases are a group of genetically
heterogeneous disorders and a leading cause of kidney
failure.
 Three Types
 ADPKD (Autosomal dominant)
 ARPKD (Autosomal Recessive)
 ACKD (Acquired cystic)

125.  The autosomal dominant form of polycystic kidney
disease (ADPKD) is the most common life-threatening
monogenic disease.
 The autosomal recessive form of polycystic kidney
disease ARPKD is rarer but affects the pediatric
population.
 Acquired cystic kidney disease (ACKD) : develops in
association with long-term kidney problems, especially in
patients who have kidney failure and who have been on
dialysis for a long time.

126.  It is characterized by progressive formation of epithelial-
lined cysts in the kidney.
 The enormous growth of these cysts ultimately leads to
the loss of normal surrounding tissues and loss of renal
function.
 The cellular defects are :
 Increased cell proliferation and fluid secretion,
 Decreased cell differentiation,
 Abnormal extracellular matrix.

127.  ADPKD is caused by mutations in PKD1 and PKD2.
 These code for polycystin-1 (PC1) and polycystin-2 (PC2)
respectively.
 PC1 is a protein–coupled receptor.
 PC2 is a calcium-permeable six-transmembrane protein.
 PC1 and PC2 are widely expressed in almost all tissues and
organs.
 PC1 and PC2 are found on the primary cilium, a hair-like
structure present on the apical membrane of a cell, and
cell-cell junctions of tubular epithelial cells.

128.  Defects in the primary cilia are linked to a wide spectrum
of human diseases, collectively termed ciliopathies.
 The most common phenotype shared by many ciliopathies
is kidney cysts.

131. Clinical Manifestations
 ADPKD is characterized by the progressive bilateral
formation of renal cysts.
 Hundreds to thousands of cysts are usually present in the
kidneys of most patients in the fifth decade.
 Enlarged kidneys can each reach a fourfold increase in
length and weigh up to 20 times the normal weight.
 The clinical presentations are highly variable.

132.  Many patients are asymptomatic until the fourth to fifth
decade of life.
 It is diagnosed by incidental discoveries of
 Hypertension
 Abdominal masses,
 Back or flank pain in ~60% of patients.
 The pain results from renal cyst infection, hemorrhage,
or nephrolithiasis.

133.  Gross hematuria resulting from cyst rupture occurs in
~40% of patients with recurrent episodes.
 Flank pain and hematuria coexist if the cyst that ruptures
is connected with the collecting system.
 Proteinuria is a minor feature.
 Infection is the second most common cause of death for
patients with ADPKD.(Cardiovascular complications are
the major cause of mortality in patients with ADPKD)
 An infected cyst and acute pyelonephritis are the most
common renal infections associated with fever and flank
pain, with or without bacteremia.

134. Complication
 The complications and renal insufficiency often correlate
with structural abnormality of the renal parenchyma.
 Kidney stones occur in ~20% of patients, more than half
of the stones in patients with ADPKD are composed of uric
acid, with the remainder due to calcium oxalate.
 Hypertension is common and typically occurs before any
reduction in glomerular filtration rate (GFR).
 Hypertension is a risk factor for both cardiovascular and
kidney disease.

135.  Hypertension results from :
 Increased activation of the renin-angiotensin-aldosterone
system,
 Increased sympathetic nerve activity,
 Impaired endothelial cilium function.

136. Complication cont.
 Intracranial aneurysm (ICA) occurs four to five times
more frequently due to defects in arterial smooth muscle
cells and myofibroblasts and causes high mortality.
 Liver cysts derived from the biliary epithelia are the most
common extrarenal complication.

137. Risk Factors
 Early diagnosis of ADPKD,
 Hypertension,
 Gross hematuria,
 Multiple pregnancies,
 Large kidney size.
 The disease can present as early as in utero, but end-
stage renal disease typically occurs in late middle age.

138. Diagnosis
 Positive family history.
 Renal ultrasonography : for presence of renal cysts.
 CT scan and T2-weighted MRI, with and without contrast
enhancement, are more sensitive.
 Genetic testing by linkage analyses and mutational
analyses.

139. Treatment
 No specific treatment to prevent cyst growth or the
decline of renal function.
 Blood pressure control to a target of 140/90 mmHg.
 The treatment of kidney stones.
 Analgesics for pain relief and hydration to ensure
adequate urine flow.
 Surgical decompression of cysts.
 More than half of ADPKD patients eventually require
peritoneal dialysis, hemodialysis, or kidney
transplantation.

140.  Large polycystic kidneys and recurrent renal cyst infection
may require pretransplant nephrectomy or bilateral
nephrectomy.
 Specific treatment strategies for ADPKD have focused on
slowing renal disease progression and lowering
cardiovascular risk.

141. Homoeopathic Management
 Aconite : Incipient stage of post scarlatinal nephritis,
pain in loins, scanty urine without blood.
 Apis mellifica : oedematous swellings of the face and
extremities, paleness, ascites, oedema pulmonum, pains
in the head, back and limbs.
 Apocynum : Palliative in dropsical conditions where the
urine is scanty. Also useful for coma & convulsions in the
nephritis of pregnency.

142.  Belladonna : greatest service in inflammation of the
kidneys with piercing burning pains in the lumbar region.
 Cantharis : nephritis with cutting pains in the lumbar
region; the urine is passed in drops and is mixed with
blood, with much urging.
 Convallaria : Nephritis from heart disorders.
 Glonoine : albuminous urine and useful in acute and
haemorrhagic nephritis.
 Plumbum : Granular degenerations of the kidneys

143. Benign Prostatic
Hyperplasia

144.  The prostate is a walnut-sized gland located between the
bladder and the penis.
 The prostate is just in front of the rectum.
 The urethra runs through the center of the prostate, from
the bladder to the penis, letting urine flow out of the
body.
 The prostate secretes fluid that nourishes and protects
sperm.

146.  Normal prostate in adult males is about 11 grams, usually
ranging between 7 and 16 grams.
 Enlargement of the prostate is nearly universal in aging
men.
 Begins by age 45 years.
 A volume of over 30 cm3 is regarded as prostatomegaly
 It occurs in the area of the prostate gland surrounding the
urethra, and produces urinary outflow obstruction.

147. Symptoms
 Obstructive symptoms : urinary hesitancy, straining,
weak stream, terminal dribbling, prolonged voiding,
incomplete emptying.
 Irritative symptoms : urinary frequency, urgency,
nocturia, urge incontinence, small voided volumes.
 As the postvoid residual increases, nocturia and overflow
incontinence may develop.

148. International Prostate Symptom Score
(IPSS)
 1. Straining
 2. Weak stream
 3. Intermittency
 4. Incomplete emptying
 5. Frequency
 6. Urgency
 7. Nocturia (times per night)

149.  Each scored
 0 : Not at all
 1 : Less than 1 time in 5
 2 : Less than half the time
 3 : About half the time
 4 : More than half the time
 5 : Almost always

150.  Total IPSS score
 0–7 = mild symptoms
 8–19 = moderate symptoms
 20–35 = severe symptoms

151. Quality of life score
 Urinary symptoms
 0 Delighted
 1 Pleased
 2 Satisfied
 3 Mixed
 4 Dissatisfied
 5 Unhappy
 6 Terrible

152. Investigations
 IPSS
 Uroflometry
 DRE
 USG : Rectal , Abdominal
 MRI

153. Treatment
 Medicinal :
 Prostate < 40 cm3: α-adrenoceptor blockers
 Prostate > 40 cm3: 5α-reductase inhibitors
 Non Surgical :
 Transurethral microwave thermotherapy (TUMT) : a device
sends computer-regulated microwaves through a catheter
to heat and destroy excess prostate tissue.

154.  Surgical :
 Transurethral resection of the prostate (TURP)
 Laser surgery : Holmium laser enucleation
 Transurethral incision of the prostate (TUIP)
 UroLift system treatment : widens the urethra by placing
tiny implants that hold the enlarged prostate tissue out of
the way.
 Open surgery
 Prostate artery embolization

155. Homoeopathic Management
 Sabal Serrulata
 Conium Maculatum
 Cantharis Vesicatoria
 Sarsaparilla Officinalis
 Lycopodium Clavatum
 Baryta Carb
 lematis Erecta
 Chimaphila Umbellata
 Thuja Occidentalis

156. Prostate cancer

157.  Common in northern Europe and the USA.
 It is increasing in frequency.
 It rarely occurs before the age of 50 and has a mean age
at presentation of 70 years.
 Prostate cancers arise within the peripheral zone of the
prostate.
 Metastatic spread to :
 Pelvic lymph nodes occurs early.
 Bone metastasis, mainly the lumbar spine and pelvis, are
common.

158. Prostatic specific antigen (PSA)
 Prostatic specific antigen (PSA) is a good tumour marker.
 40% of patients with a serum PSA > 4.0 ng/mL will have
prostate cancer on biopsy.

159. Clinical features
 Lower urinary tract symptoms indistinguishable from BPH.
 Symptoms and signs due to metastases includes :
 Back pain,
 Weight loss,
 Anaemia
 Obstruction of the ureters.

160. Diagnosis
 On rectal examination the prostate often feels nodular
and stony hard.
 An ultrasound scan.
 A plain X-ray of the pelvis and lumbar spine.
 Diagnosis is confirmed by needle biopsy.
 By histological examination of tissue removed by
endoscopic resection when needed to relieve outflow
obstruction.

161. Management
 Radical prostatectomy or radical radiotherapy in confined
tumors.
 Reducing circulating testosterone levels (either by
castration or by medication) results in a 70% initial
response rate.
 Androgen receptor antagonists such as cyproterone
acetate prevent tumour cell growth.
 Radiotherapy is useful for localised bone pain.
 Chemotherapy with 5-fluorouracil, cyclophosphamide or
nitrogen mustard.

162. Prognosis
 The life expectancy of a patient with an incidental finding
of focal carcinoma of the prostate is normal.
 Tumours localised to the prostate, the 10-year survival
rate is 60–75%, .
 If metastases are present 10-year survival rate falls to
10%.

163. Renal Adenocarcinoma

164.  The most common malignant tumour of the kidney.
 M : F = 2 : 1
 Age incidence : 65 and 75 years
 The tumour arises from renal tubules.

165.  The tumour arises from renal tubules.
 Golden-yellow and red appearance due to haemorrhage
and necrosis.
 Direct invasion of perinephric tissues is common.
 Lymphatic spread occurs to para-aortic nodes.

166. Clinical Features
 Asymptomatic
 60% with haematuria,
 40% with loin pain
 25% with a mass
 15 % with Triad of
 Pain,
 Haematuria
 A mass.

167.  Fever,
 Raised ESR,
 Polycythaemia,
 Disorders of coagulation,
 Abnormalities of plasma proteins
 Abnormal liver function tests.

168. Investigations
 Ultrasound : for differentiation between solid tumour and
simple renal cyst.
 Contrast-enhanced CT of the abdomen and chest for
staging.
 CT-guided biopsy

169. Management
 Radical nephrectomy and ipsilateral para-aortic lymph
nodes.
 Small tumours are treated percutaneously by :
 Radiofrequency ablation
 Tissue-sparing surgery
 Cryoablation.

170. Prognosis
 Tumour is confined to the kidney 5-year survival is 75%.
 In case of Distant metastases this falls to 5%.