1) PUBLIC HEALTH
MALE REPRODUCTIVE SYSTEM
PROSTATIC PATHOLOGY
1) PROSTATE FUNCTIONS:
-It liquefies the semen to facilitate transport of the sperm - Neutralizes the acidity of the semen & vagina
- 30% of semen comes from Prostate - Secretes Acid Phosphatase, Alkaline Phosphatase & most importantly Prostatic Specific Antigen (PSA)
2) PROSTATITIS
|PATHOLOGY |DESCRIPTION & CLINICAL PRESENTATION |
|Acute prostatitis |• Occurs in young males & is caused by N.gonococci or E. coli (Dr. Seva said always due to a Bacteria). Initially begins as Urethritis & then moves to the |
| |Prostate. |
| |( Clinically we see pain during micturition (dysuria) or ejaculation [ALWAYS present are Perineal/rectal pain & Fever] & Enlarged, soft/tender prostate. |
| |( With an “initial & final micturition Cup analysis” we have the following presentation: |
| |- 1st Cup will have “thread like fibres called PROSTATIC Threads” - 2nd Cup will “Cloudy Urine” |
| |( NB: If both 1st & 2nd cup have “Cloudy Urine” then we have a Urinary system problem & not Prostatitis |
| |( If abscess formation occurs then there may be a rupture into the following areas: |
| |- ischiorectal fossa - urethra (pus with urine) - rectum |
|Chronic Prostatitis |• There is no specific cause for this pathology (For sure not caused by a Bacteria) |
| |( The Patient presents with Vague symptoms & an irregularly enlarged & firm prostate (Think CANCER) |
3) HYPERPLASIA OF PROSTATE (NOT PREMALIGNANT):
• 4 Stages of Prostate growth are as follows:
1. Enlarged at birth due to ( Maternal Estrogen 2. Regression to normal size btwn birth to puberty
3. Normal size btwn 12-45/50 yrs age 4. Benign Prostatic Hyperplasia after 50 yrs of age in 50% of males
• It is AKA Benign Prostatic Hyperplasia & generally occurs IDIOPATHICALLY in 50% of males over 50 years of age.
• Present theory is that there is a ( in androgens (testosterone) when compared to estrogen
( There is presence of nodules made up of hyperplasitc stroma & glands involving the PERIURETHRAL ZONE of the MEDIAN LOBE (above the seminal vesicle) of the Prostate gland.
( Patient presents with the following problems which occur at a slow rate (as compared to carcinoma):
- Obstruction of urinary flow due to vesicourethral sphincter obstruction (acts as a Ball & Valve mechanism) LEADING to:
1. difficulty in initiating urination & maintaining a stream 2. difficulty stopping micturition with dripping at the end 3. nocturia
- Prostate is firm & rubbery on palpation
( Complications include the following symptoms:
- Chronic retention of urine leading to repeated UTI & ( hypertrophy of smooth muscles of bladder (ultimately dilatation of bladder)
- This is followed by nodule infarction & hematuria. As the process continues we have hydronephrosis (dilatation of ureters, bladder, calyx’s) leading to pyelonephritis &
KIDNEY FAILURE
MALE REPRODUCTIVE SYSTEM
PROSTATIC PATHOLOGY
4) CARCINOMA OF THE PROSTATE
• Arise mostly from the Subscapular part of the posterior lobe of the prostate & involves the peripheral glands & ( is an ADENOCARCINOMA
• The cancer spreads via three mechanisms:
1. Direct extension via the bladder, urethra, seminal vesicle 2. Hematogenous; mainly bone (pelvis, femur, lumbar spine) but also to the lung & liver
3. Via lymphatics to other nodes
( It is seen in patients above 50 yrs of age. Patients have rapid onset (unlike BPH which is slow development) of the following symptoms:
- dysuria - urinary retention - terminal hematuria - urinary dripping - frequency & urgency of urination
( The prostate is Hard, Stony & Craggy (having many steep & rugged projections)
( Bone metastasis leads to bone pain, pathological fractures & anemia (due to infiltration of bones & reduced hematopoetic capacity)
( Diagnosis is made mainly by P/R screening & checking the blood for the following:
- Serum Prostate Specific Antigen will be elevated above its normal value of 4nmol/ml blood to 15nmol/ml (cancer) & 30nmol/ml (metastatic cancer)
- ( Serum Acid Phosphatase & Alkaline phosphatase - Xray will reveal metastasis to lung & bone etc
TESTICULAR PATHOLOGY
1) CRYPTORCHIDISM
• This is undescended or ectopic testes at birth or within 1st year of life. Descent may also be abnormal thru femoral canal instead of the inguinal canal.
• Complications include Neoplasia & then infertility
2) ORCHITIS
• Acute: - Infection caused by bacteria (most common E.coli, N. gonnococci or paramyxovirus) reaching the peididymis & testis via reflux of infected urine from prostatic urethra.
- If parayxovirus (mumps) occurs after puberty & bilaterally this will cause sterility
( Fever, PAIN, tenderness & redness of scrotum (possible complication is abscess formation ). Actual testes are enlarged & tender
• Chronic: - Occurs due to TB of kidney & is called Tuberculous orchitis
( Enlarged scrotum, NO PAIN & casseous granuloma
3) TESTIS TORSION
• This is due to congenital abnormality (inversion of the testes) or due to a severe blow to the scrotum. Commonly seen in 10-15 yr olds & RARE after 25 yrs
( There will be SUDDEN agonizing pain in groin & lower abdomen with testes hanging higher in the scrotum. Testes SO TENDER ,Patient will not let you touch it
( Scrotum is RED, HOT & TENDER & EDEMATOUS
MALE REPRODUCTIVE SYSTEM
TESTICULAR PATHOLOGY
4) TESTICULAR TUMOURS
• Most common tumour of males btwn 20-45 years age & is commonly due to:
- maldescent of the testes - DES (dietheylstillbesterol, AKA morning after Pill. Abortion should occur within 5 days) . If female conceives a male then testicular cancer is possible. If she conceives a female then Vaginal cancer is possible.
• 2 types of cancer depending on Cellular origin:
1. Germ Cell Tumour: - Seminoma (Most common type of testicular tumour & BEST PROGNOSIS because it is Radiosensitive) or Teratoma
2. Non Germ Cell Tumour: - May be from Sertoli or Leydig cells
( Clinically all tumours present with the following symptoms:
- painless unilateral enlargement of smooth, firm & heavy testes secondary to hydrocele, gynecomastia & retroperitoneal mass
- Very common to see metastasis to Lymph nodes (esp.: Left supraclavicular node: VIRCHOW’s Node), lung & liver
( The tumours secrete HCG (Human Chorionic gonadotrophin ) & AFP (Alpha fetoprotein; normally secreted by the fetal liver).
( After removal of any suspected tumour the levels of HCG & AFP need to be measured to ensure that they drop off. If they don’t this could indicated metastasis.
• Metastatic Staging is as follows:
Stage 1: Only Testis Stage 2: Testes & nodes below diaphragm
Stage 3: Stage 2 & nodes above diaphragm Stage 4: Stage 3 & pulmonary & liver metastasis
PENILE PATHOLOGY
1) CONGENITAL ANOMALIES
• Hypospadia: - Abnormal urethral opening onto the ventral or undersurface of the penis that can lead to infertility
• Epispadias: - Abnormal urethral opening on the dorsal surface of the penis that may cause infertility
• Phimosis: - Foreskin or prepuce is abnormally tight & does not retract over the glans. (physiologically normal until 6 yrs age)
• Paraphimosis: - When tight foreskin is retracted & sometimes does not return, then veinous/lymphatic return is obstructed & glans swells.
2) INFLAMMATION
• Balantitis: - inflammation of the glans • Posthitis: - Inflammation of the prepuce due to Psoriasis, penile carcinoma, diabetes, phimosis or STD
• Herpes: - painful vesicles along the penis • Chlamydia: - Granuloma venerum is painless ulcer on penis then lymph node involvement along inguinal ligament
3) TUMOURS OF PENIS
• Benign Type: - Condyloma acuminatum - HPV - Sexually transmitted - Involves mucocutaneous surface (sessile/pedunculated warts)
- involves coronal sulcus or prepuce
• Malignant: - Squamous cell carcinoma (skin involvement)
4) HYDROCELE
• Collection of fluid btwn the two layers of tunica vaginalis due to trauma, infection or testicular tumour
FEMALE REPRODUCTIVE PATHOLOGY
1) OVARY PATHOLOGY:
|PATHOLOGY |DESCRIPTION |
|Polycystic Ovary |• Occurs due to abnormal (insufficient) secretion of pituitary gonadotrophins. Therefore Estrogen & Androgen are elevated & Progesterone is |
| |depressed. |
| |( Patient presents with bilateral enlarged ovaries with multiple follicular cysts in the subcapsular region. The Corpora Lutea is absent & there is a |
| |thick capsule & hyperplastic ovarian stroma. |
| |( Clinically there is Endometrial Hyperplasia (gives rise to menstrual like bleeding) & the following symptomatology: |
| |- Hirsutism - Obesity (due to ( estrogen) - Anovulation (( ( incidence of endometrial adenocarcinoma) |
| |- Secondary Amenorrhea (irregular menstrual periods) - Infertility |
|Ovarian Tumours (malignant) |• Etiology is unknown but classification depends on histogenesis as follows: |
| |- Epithelial cell tumours: arise from the coelomic epithelium |
| |- Germ cell Tumours: arise from the follicles and may be one of the following: Teratoma (most common small tumour affecting all 3 |
| |embryological layers, Dysgerminoma, Embryonal carcinoma, Choriocarcinoma |
| |- Stromal Cell Tumours: arise from stroma of the ovaries and can be one of the following types: |
| |- Granulosa Theca Cell tumour that secretes excess estrogen, with endometrial hyperplasia & abnormal uterine bleeding |
| |- Sertoli-Leydig Cell tumour that secretes excess androgen & leads to virilization, breast atrophy, deepening of voice, |
| |clitoral enlargement, & temporal hair recession |
| |( Malignant tumours remain silent until metastisize has occurred. If very large ma lead to pressure in lower abdomen & ( freq. of micturation. |
| |Hormone secreting ovarian neoplasms present with manifestations of excess hormones. |
| |( The tumour may spread: locally (within peritoneal cavity & present as Ascites), via the blood (go to lungs), & via Lymphatics (para-aortic & iliac |
| |lymph nodes) |
2) PELVIC INFLAMMATORY DISEASE (PID)
|PATHOLOGY |DESCRIPTION |
|Salpingitis |• This is inflammation of the uterine tubes & may be : |
| |- Acute (unilateral, ascending infection from endometrium). The tube is enlarged, erythematous, with abscess formation & many PMN WITH FEVER |
| |- Chronic (often bilateral). Most often caused by IUCD (most common being Copper T), Endometriosis, TB. Very often complication is ectopic |
| |pregnancy |
|Endometriosis |• There is ectopic endometrial tissue other than the lining of the uterine cavity & may present as follows: |
| |- Endometriosis Interna (adenomyosis) due to the abnormal down growth of endometrium into myometrium |
| |- Endometriosis Externa occuring in the ovary, uterine tube, parametrium, urinary bladder & rectum |
| |( In either case the cysts (AKA chocolate cysts) undergo cyclical bleeding with ovarian hormonal activity. |
| |( The clinical features are: - crippling dysmenorrhea - severe dyspareunia ( painful intercourse) - chronic pelvic pain with irregular periods |
| |- infertility |
| |• If the Endometriosis is inflamed then we have ENDOMETRITIS & may be Acute (ascending gonococcal infection) or Chronic (TB, IUCD) |
FEMALE REPRODUCTIVE PATHOLOGY
3) NEOPLASIA OF UTERUS:
|PATHOLOGY |DESCRIPTION |
|Endometrial Polyp (BENIGN) |• This occurs around menopause & may be asymptomatic or have excess bleeding. It is located near the cervix & rarely becomes carcinomatous. |
|Leiomyoma (BENIGN) |• AKA Fibroid of uterus mainly composed of muscle with fibrous CT in it. This is the MOST common tumour of Female Genital tract |
| |They occur as single or multiple tumours & vary from 1-10 cm in size. They are only found between Menarche & Menopause (estrogen |
| |dependent) |
| |( There are 3 types commonly seen as described below: |
| |- Intramural : ? |
| |- Submucous: found beneath the endometrium & cause HEAVY bleeding & may hang down into the Cervical OS. |
| |- Subserous: Also connected by a pedicle & may attach to the mesentery or omentum |
| |( Macroscopically they are pale, round nodules with a whorl appearance. May have a pseudocapsule of fibrous/muscle tissue. Central part is |
| |vulnerable to degenerative changes due to external vasculature. |
| |( Microscopically there are groups of smooth muscle fibres. There is hyaline degeneration with fibrous overgrowth & later calcification. They |
| |may become Cystic (due to liquefaction after hyalinization) or Necrotic (due to lack of blood supply) |
| |( Symptomatology includes all the following: |
| |- Hyperamenorrhea due to necrosis - dysmenorrhea - pain due to complicated or infarcted myoma |
| |- Impaired fertility (difficult conception, abortion, preterm delivery) - Large ones cause urinary freq., urinary retention or constipation |
|Endometrial Carcinoma (MALIGNANT) |• AKA Adenocarcinoma of the uterus & is not affecting the cervix. Generally seen in Post Menopausal women (genetic predisposition) |
| |( Cancer presents with asymmetrical enlargement of the uterus & post menopausal bleeding. |
| |( Increased risk factors are (NB: SMOKING IS NOT A RISK FACTOR): |
| |- Prolonged unopposed stimulation of estrogen (ie Polycystic ovary) - Obesity - Diabetes Mellitus - Hypertension |
| |- Polycystic Ovary - Infertility |
| |( Clinically we see post menopausal bleeding (A syndrome “CORPUS Cancer” has Endometrial cancer , Obesity, DM & HT) |
| |( The cancer spreads to urinary bladder, parametrium, ovary, vagina & may spread hematogically to liver & lung |
FEMALE REPRODUCTIVE PATHOLOGY
4) CERVIX PATHOLOGIES:
|PATHOLOGY |DESCRIPTION |
|Cervicitis |• May be: - Acute (sexually transmitted by gonococci , trichomonos, herpes or after childbirth). There is Pain & purulent vaginal discharge |
| |- Chronic ( associated with thickening of the cervix). It leads to infertility. Mucus becomes viscous but not purulent. |
|Neoplastic Lesions |• Non Neoplastic lesions are called Polyps. In the Neoplastic lesions we will look at: |
| |- Condyloma Acuminatum that is a wart like lesion caused by the HPV virus & transmitted sexually |
| |- Cervix Cancer (squamous Cell carcinoma) that has a number of risk factors associated with it as follows: |
| |( 1st intercourse during adolescent years ( conception at early age ( multiple sex partners ( multiparity |
| |( cigarette smoking ( viruses (HSV, HPV) ( Male partner with previous multiple sex partners |
| |• May be divided into different stages as follows: |
| |1) Precancerous (carcinoma insitu) that is common at the squamocolumnar junction (Do PAP SMEAR) |
| |2) Mild Dysplasia with only a few layers of the stratified squamous being affected |
| |3) Moderate dysplasia with the lower half of the layers showing some sort of dysplastic changes |
| |4) Severe dysplasia with all the layers except the upper most being affected |
| |5) Carcinoma In situ has all the layers being affected with pleomorphic & hyperchromatic cells/nuclei |
| |6) Microinvasive carcinoma has the cancer invading the basement membrane & entering the lamina propria/muscular layer |
| |( Initially do PAP smear & then follow up with a Colocscopic exam of cervix. Removal is via cryotherapy & electrocautery |
| |• Staging is as follows: |
| |- Stage I: Cancer in cervix only (80% 5 yr survival) - Stage II: cancer beyond cervix but not to pelvic sidewall & into vagina (60%, 5yr survival) |
| |- Stage III: Cancer to pelvic sidewall & into lower vagina (45% 5yr survival) - Stage IV: Spread to bladder & rectum (14%, 5 yr survival) |
| |In stages II, III, & IV need to do radiotherapy & surgery to remove cervix & uterus |
5) BREAST PATHOLOGIES:
a. Gynacomastia:
• Gynacomastia is the benign enlargement of male breast tissue due to increase in estrogen & decrease in androgen. Liver schirrous may predispose to this problem.
There is a firm, mobile & unilateral (75% of time) disc beneath the nipple line with proliferation of Ductal tissue only.
b. Differential Diagnosis btwn Benign & malignant Breast cancers:
|Type of Pathology |Margins |Consistency |Fixity |Location on breast |Contour |
|Fibrocystic Dz |Ill defined |Firm & diffuse | | |Smooth Bilateral breasts |
|Fibroadenoma |Well defined Regular |Smooth & encapsulated | | |Smooth Unilateral breasts |
|Carcinoma |Well defined Irregular |Stony Hard |fixed to skin, bone, muscle|60% upper axillary quadrant |Uneven contour |
| | | | |12% each areolar & upper Inner Quad | |
| | | | |10% lower outer quad. | |
| | | | |6% lower inner quad | |
FEMALE REPRODUCTIVE PATHOLOGY
5) BREAST PATHOLOGIES:
c. Congenital anomalies:
• Milk line generally extends from axilla to the ventral surface of trunk near the inguinal region. Occasionally we may see breast arise along this line & give rise to Polymastia (axillary breast) or polythelia (supernumerary nipples)
d. Acute Mastitis:
• This is inflammation of the breast tissue & can occur during first few weeks of lactation (cause is staphyloccus from infant)
( We see swollen erythematous & painful breasts
e. Fibrocystic Breast changes:
• This is a painful condition that occurs BILATERALLY in response to cyclic hormonal changes & improves after the menstrual cycle.
We see fibrosis, cyst formation & epithelial cell hyperplasia
f. Fibroadenoma of the Breast (BENIGN):
• Commonly occuring in 20-30 age range due to focal area of estrogen
( Presentation is a solitary, smooth, painless bump not attached to skin or muscle (( mobile tumour). Difficult to palpate because it moves around
( Microscopically we see proliferation of fibrous & ductal epithelial cells. Two conditions are possible:
1) Pericanicular that has small round undistorted ducts lined with cuboidal cells surrounded by a wavy fibrous tissue
2) Intracanilicular that has ducts that are elongated & compressed by fibrous tissue
g. Breast Carcinoma:
• One in ten females will develop this pathology & is 2nd cause of cancer death in females. Occurs after age 25 & increases after 30 years.
• Cause is unknown but certain risk factors are attributable as follows:
- nulliparous female - early menarche & late menopause - 1st pregnancy after 30 yrs - presence of lobular & ductal hyperplasia
- family history - prolonged exposure to estrogen - high fat diet
• Spread is via “direct” through intraepithelial spread to ducts & lobules, via lymphatics & blood (bone, lung, liver)
|TYPES OF INVASIVE CARCINOMAS |DESCRIPTION |
|Scirrhous |• Most common in pre & post menopausal women |
| |( It looks like an unripe pear that is gritty, hard & has a white infiltrative mass. There is much CT & surface shows “orange |
| |Peel “ appearance. In later stages the Nipples retract |
|Medullary |• This is seen in post menopausal women |
| |( There are large pleomorphic cells of various shapes & sizes with marked lymphocytic infiltration. NOT as much CT as above |
| |( Not as aggressive |
URINARY TRACT PATHOLOGY
1) DEFINITIONS:
Loin pain: - dull pain felt in back side at junction of T12 & 12th ribs (due to stretching of the renal capsule)
Anuria: - Less than 100ml/24hrs. of urine due to obstruction
Oliguria: - Between 400 - 1000ml/24hrs due to renal failure
Polyuria: - Greater than 2500ml/24 hrs due to Diabetes mellitus/insepidus
Normal output: - 800 - 2500 ml/24 hrs.
Hematuria: - Blood in the urine
WBC in Urine - due to infection (acute pyelonephritis)
RBC in urine: - Glomerular disease
Casts in Urine: - protein coagulum (proteinuria)
Dysuria: - painful micturation (burning pain) due to Acute pyelonephritis or UTI
Hypertension: - due to kidney disease
Azotemia: - Nitrogen in the urine (uremia). There is ( BUN (blood urea nitrogen), ( serum creatine, ( Glomerular filtration rate (GFR)
Ureteric pain: - pain is intermittent colicky type due to stone obstruction
2) CONGENITAL ANOMALIES:
a. Agenesis:
• This is absence of a kidney (bilateral absence is not possible) & is often asymptomatic
b. Horse shoe Kidney:
• There is fusion of the lower poles of the kidneys across the midline. This causes an increase in infection & renal calculi (urolithiasis)
c. Polycystic Kidney:
• There are two types as seen here:
- Infantile Polycystic: This is an autosomal recessive disease that causes there to be no connection between secreting & collecting ducts of the kidney. Incompatible with life.
- Adult Polycystic: This is an autosomal dominant disease with bilateral involvement. The cysts fill with serous/hemorrhagic fluid & press on the calyces & ureter destroying the functional nephrons. This condition appears in late 20’s with Bilateral Loin pain. & leads to Chronic Renal Failure
( Clinically we see: - hypertension - enlarged kidney (flank pain) - Hematuria (blood in urine when cysts burst)
- repeat urinary infection - Anemia (due to (erythropoeitin)
- Uremia (( BUN)
( Complications include: - Chronic renal failure - Dialysis/renal transplant - Berry Aneurysms & Liver Cysts
URINARY TRACT PATHOLOGY
3) GLOMERULAR DISEASES:
• Glomerular diseases are characterized by functional & morphological abnormalities & are named for the amount of lesions seen (ie: focal glomerulonephritis FGN, Diffuse DGN, Segmental SGN, Global GGN). Suspect immune system dysfunction .
• 2 Syndromes exist. One is Nephrotic & the other is Nephritic.
a. Nephrotic Syndrome:
• There is loss of selective protein retention in the blood due to abnormal glomerular basement membrane leading to:
- proteinuria - hypoalbuminemia - edema (generalized pitting) - Hypercholesterolemia
• Also the following diseases have features of Nephrotic syndrome to them:
1) Minimal Change: - No lesions present. Affect children. There is fusion of foot processes of the epithelial cells under EM.
2) Henoch-Schnolein purpura:- Affects children mainly & characterized by systemic vasculitis, involving skin, kidney, abdomen & joints
( Clinically we see rash on gluteal region, arthritis, abdominal pain, mild proteinuira & diarrhoea
3)Membranous GN: - Commonest form of GN in adults & has all the characteristics of nephrotic syndrome
b. Nephritic Syndrome:
• Due to disturbance of glomerular structure involving reactive cellular proliferation resulting in:
- oliguria - hematuria - uremia - hypertension - periorbital edema
• The following diseases have features of Nephritic Syndrome:
1) Post Streptococcal GN: - Common in kids appearing 1-2 weeks after throat/skin strep. infection. Antigen/Antibody complex builds up in glomerular basement membrane.
2) Rapidly Progressing GN: - AKA RPGN & is the end result of post strep. GN or Goodpasture’s syndrome. There is severe glomerular destruction
3) Goodpasture’s GN: - There is an Antibody/Antigen reaction with kidney’s & lungs affected. May have hemopytsis of lung
URINARY TRACT PATHOLOGY
4) TUBULO INTERSTITIAL DISEASES (BOTH TUBULAR & VASCULAR):
a. Tubular disease:
• Essentially three types of causes exist for Tubular disease:
- Infectious - Toxic - Metabolic
|PATHOLOGY |CAUSE |DESCRIPTION |
|Acute Pyelonephritis |INFECTIOUS |• Most often in females due to short urinary tract (E.coli from rectum/vagina) |
| | |( There is suppuration in the cortex with inflammation of tubules filled with PMN. Only the Tubules are involved. |
| | |( Patient presents with high fever, rigor (shivering), dysuria & complications may arise, such as: |
| | |- bacteremia - pyelonephrosis - perinephric abscess - renal papillary abscess in DM patients |
|Chronic Pyelonephritis |INFECTIOUS |• Most often in males that are diabetic or patients with nephrolithiasis & associated with hydronephrosis (dilated ureters) |
| | |( Kidney is contracted, irregularly scarred & both tubules/glomeruli involved. |
| | |( Microscopically there is peeriglomerular & interstitial fibrosis & glomerular sclerosis. Tubules are filled with protein |
| | |(thyroidization) & chronic inflammatory cells |
| | |( Clinically we see chronic renal failure |
|Analgesic Nephritis |TOXIC |•Aspirin & similar drugs will cause damage to renal papillae leading to necrosis with necrotic papillae being shed in urine causing |
| | |ureteric colic & hematuria |
|Metal Toxicity |TOXIC |• Mercury, lead etc can result in coagulative necrosis & damage to the tubules |
|Gout |METABOLIC |• Urate crystals are deposited in the tubules causing obstruction & fibrosis |
|Multiple Myeloma |METABOLIC |• Malignant plasma cells cause toxic tubular injury from Bence Jones proteinuria. There is a ( RBC (Anemia), |
| | |( WBC (leucopenia), ( Platelets (thrombocytopenia) with osteoclast activated & fracture/osteopenia |
|Hypercalcemia |METABOLIC |• Increased calcium excretion in the urine leads to Renal failure |
b. Vascular diseases:
• 2 conditions exist as follows:
1) Nephrosclerosis: It may be Benign or malignant. It is hardening of the kidney blood vessels & may be unilateral.
- Benign is slow/progressive & relates to essential hypertension. There is thickening of small arteries/arterioles walls
- Malignant is sudden & occurs in malignant hypertensive patients. There is intimal cellular proliferation of small arteries/arterioles
(Bilateral)
2) Renal Artery Stenosis: It is commonly seen in elderly people. Atherosclerosis causes renal ischemia & ( ( GFR. This causes an ( in renin & ( (aldosterone leading to sodium retention & hypertension
URINARY TRACT PATHOLOGY
5) MALIGNANT TUMOURS OF KIDNEY:
a. Nephroblastoma (Wilm’s tumour):
• Most common in children (before 4 yrs) & genetically determined (equal between males/females) & of Bilateral presentation. (2nd cause of death in kids)
( There is Bilateral Loin mass with Hematuria with possible metastasizes to lungs. There is excess epithelial & CT that arises from embryonic nephrogenic tissue
b. Renal Adenocarcinoma (Hypernephroma):
• More common in Adult males without a known etiology. However risk factors such as: - Smoking - obesity - Bleeding may have a connection.
Unilateral Presentation
( There is a solid mass anywhere in the kidney & we see clear & pink granular oncocytic cells arranged in glandular/tubular form
( Metastasis to lung, liver & bone may occur. Locally it invades the perinephric fat or renal vein. Invasion of scrotum leads to Varicocele. Invasion of IVC leads to lower extremity edema.
6) NEPHROLITHIASIS (RENAL STONES):
• More common in White males 20-50 yrs of age. Renal stones are closely linked to the following factors:
- Diet (insufficiency of Vit A causes desquamation of epithelium. Cells form nidus & stone is deposited). - Dehydration increases solute concentration
- Decreased urinary citrate (due to chronic diarrhoea or ( animal protein) - Renal infarction
- Inadequate urinary drainage & urinary stasis (prostate pathology) - Prolonged immobilization (paraplegia)
- Hyperparathyroidism (hypercalcemia)
• Stones are composed of oxalate, phosphate, uric acid, cystine, calcium
( Clinically, may be asymptomatic or there may be fixed renal pain or ureteric colic pain or Strangury (painful desire to micturate)
( Stone in upper 3rd = referred pain in testes Stone in middle 3rd = pain mcburney’s point or diverticular pain) Stone bottom 3rd = medial side of thigh
Stone in bladder = ( freq. micturation, pain at tip of penis upon ending micturation, hematuria Stone in prostate = vague perineal pain
7) CARCINOMA OF THE URINARY BLADDER:
• 90% is transitional cell carcinoma & 10% is squamous cell carcinoma
• The following risk factors relate to Transitional cell carcinoma: cigarette smoking, certain dyes, analgesic abuse
• The following risk factors relate to Squamous cell carcinoma: Schistosoma
( Presents like a complicated fern like growth most often in the Trigone area of bladder. There are connective tissue stalks covered by transitional epithelium with malignant features.
( Clinically there is painless hematuria with frequency, urgency & dysuria for micturation
URINARY TRACT PATHOLOGY
8) RENAL FAILURE:
• Renal failure (failure to excrete urea & other byproducts) occurs for a number of reasons. There may be Acute failure (over days or weeks & reversible) or Chronic ( developing over months/years & related to DM, Hypertension, glomerulonephritis & all body systems affected)
• The normal BUN is 8.5 mg/dl. The kidneys have to be 50% failed before the BUN goes above this value
• Failure may be due to different causes in the 3 categories Pre / Renal / Post:
1) Pre Renal: - Cause is Blood supply decreases to kidney due to ( cardiac output (shock such as hypovolemic [burns], cardiogenic[ heart failure], septiciemia [diarrhoea])
2) Renal: - chronic pyelonephritis - diabetes - polycystic disease - hypertensive nephrostenosis
- Acute Tubular necrosis (damage to tubules due to NSAID or Gentamycin or Crush injury to muscles with ( in Myoglobin in blood)
3)Post Renal: - Stones in prostate or bladder
( In the Gastrointestinal tract we will see nausea, vomiting & diarrhoea due to ( BUN
In the Bones we will see renal osteodystrophy due to ( 1,25 dihydroxy production & ( anemia
In the heart there will be Uremic pericarditis with hypercalcemia & arrhythmia’s followed by cardiac arrest
In the CNS there will be mental confusion, seizure & coma due to ( BUN
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