COMPOSITION OF SEMEN

5% Spermatozoa Seminiferous tubules (testes)

 Spermatogenesis – production of the sperm cells
 Produced in the TESTES  Sertoli cells = serve as “nurse cells” for
developing sperm cells
= secrete enzyme called INHIBIN –
inhibit follicle stimulating hormone synthesis to
develop sperm cells
 Inactivated sperm cells/immature cells

Epididymis
 Sperm Maturation (Sperm become MOTILE)

60-70% Seminal Fluid Seminal Vesicle

- Main fluid present in the semen  Provide nutrients for sperm and slightly alkaline
- Produced by the SEMINAL VESICLE fluid but will be neutralize by prostatic fluid
 Rich in FRUCTOSE for sperm motility
o Fructose – energy source of sperm cell to
remain motile

20-30% Prostatic Fluid Acidic fluid

- From the PROSTATE GLAND  Contains ACP (Acid phosphatase), Zinc, Citric
acid and other enzymes (Proteolytic Enzymes)
 PROTEOLYTIC ENZYME is used for
coagulation and liquefaction

5% Bulbourethral gland Thick alkaline mucus (Pre-cum)

(Cowper’s Gland) Neutralize acidity from prostatic secretions and vagina
during intercourse

STRUCTURE FUNCTION
Seminiferous Tubules Spermatogenesis
– present in testes
– coiled tubules

Epididymis Sperm Maturation

Ductus Deferens (Vas Deferens) Propel sperm to ejaculatory ducts
Seminal Vesicles Provide nutrients for sperm and fluid
Prostate gland Provide enzymes and proteins for coagulation and
liquefaction
WHERE SEMEN AND URINE MEET

Bulbourethral glands Acid alkaline mucus to neutralize prostatic acid and

vaginal activity
Antisperm Antibodies

- if the patient and his wife does not have the ability to conceive a baby
- detect antibodies:
o semen
o cervical mucosa
o serum
- Destruction of cell

 Mixed Agglutination Reaction

 Detects the presence of IgG antibodies
 Semen sample + AHG (antihuman globulin) + Latex particles or treated RBCs coated with IgG
o Check for agglutination
o IgG will detect the presence of antisperm antibies
 Normal= <10% motile sperm attached to the particles
 Immunobead Test
 Detects the presence of IgG, IgM and IgA
 Demonstrates what area of the sperm the antibodies affecting
 Reporting: IgG tail antibodies, IgM head antibodies
 Gelatin Agglutination Test
 Sperm + 10% gelatin + patient’s serum
o Patient with antibody that will attack the sperm
 White particles in clear surrounding

Terminology Definition
Aspermia No Ejaculate / No semen
Azoospermia Absence of sperm cells
 With fluid
 Underdeveloped sperm cells
 Obstruction from previous operation or
traumatic procedures
 Infection with gonorrhea
Necrospermia Immotile or dead sperm cells (50% viability)
Oligospermia Decrease sperm concentration, decrease number of
sperm cells or presence of few motile sperm seen
in
 Hypotropic lesions
 Hypothyroidism

Microbial testing
Round cells (WBC and SPERMATIDS look alike)
 WBC and spermatids (immature sperm cells/ no tail)
 Normal value: < 1 million/mL
o > 1 million WBC/mL = INFECTION
o > 1 million spermatids/mL = disruption of spermatogenesis
o Problem in the epididymis
Test for
 Chlamydia trachomatis
 Mycoplasma hominis
 Ureplasma urealyticum

Medico-Legal Test

- Test for sperm cells and seminal fluid

- Used for Forensic Analysis

1. Microscopic Examination
2. Fluorescence under the UV light
3. Acid Phosphatase determination
4. Glycoprotien p30= more specific (protein specific for sperm cell)
5. Florence Test
 Test for choline (normal constituent of seminal fluid)
 Reagents: iodine crystal + potassium iodide
 (+) Dark brown rhombic crystals
6. Barbiero’s Test
 Test for spermin (present in seminal fluid)
 TCA + Pitric Acid
 (+) Yellow leaf-like crystals

Post-vasectomy Semen Analysis

Vasectomy
 Cutting the vas deferens so that the ejaculate will not contain any sperm cell
 Sperm cell should DECREASE until no more sperm cell are present in the sample
 The only concern is the presence or absence of sperm
 Done 2 months after vasectomy and continued until 2 consecutive monthly specimens show no sperm
 Centrifuge first to double check

Normal Values for Semen Analysis

Volume 2 – 5 mL
Viscosity Pour in droplets
pH 7.2 – 8.0
Sperm Concentration ≥ 20 million/mL
Sperm count ≥ 40 million/mL
Motility ≥ 50 within 1 hour
Quality ≥ 2.0 or a, b, c
Morphology > 30% normal forms (routine criteria)
> 14% normal forms (strict criteria)
Round cells < 1 million/mL

Additional Testing for Abnormal Semen Analysis

Abnormal Result Possible Abnormality Test
Decreased motility with normal Viability Eosin-nigrosin stain
count
Decreased count Lack of seminal vesicle support Fructose level
medium
Decreased motility with clumping Male antisperm antibodies Mixed Agglutination
reaction and immunobead
test
 Sperm agglutination with
male serum

Normal analysis with continued Female antisperm antibodies Sperm Agglutination with female
infertility serum

Sperm Function Test

- Check if the sperm cell have the capability to penetrate the egg
Test Description
Hamster egg penetration Sperms are incubated with species-non specific
hamster eggs an penetration is observed
Cervical mucus penetration Observation of sperm penetration ability of partner’s
midcycle cervical mucus
- Problem with the acrosomal cap
Hypo-osmotic swelling Sperms exposed to low-sodium concentration are
evaluated for membrane integrity and sperm
viability
Integrity of the sperm wall (hypotonic or isotonic
solution)
In vitro acrosome reaction Evaluation of the acrosome to produce ezymes
essential for ovum penetration

Renal Diseases
GLOMERULAR
 Most often immune mediated
TUBULAR
 Result from infectious or toxic substances
INTERSTITIAL
 Result from infectious or toxic substances
VASCULAR
 Caused a reduction in renal perfusion that subsequently induces both morphologic and functional changes in
the kidneys

Classification of Renal Disease

Type of Renal Disease Comment

 Disorders associated with the glomerulus
 Immunologic disorder
 Glomerulo Nephritides - collection of different
Glomerular Disorders glomerulo nephritis

 Infectious or toxic substances

 Affecting the renal tubules include those in which
tubular function is disrupted as a result of actual
damage to the tubules and those in which a
metabolic or hereditary disorder affects the
Tubular Disorders intricate functions of the tubules
 damage in RTE cells; renal tubular dysfunction

 Disorders affecting tubular function may be

caused by systemic conditions that affect or
Hereditary and Metabolic Tubular Disorder override the tubular reabsorptive maximum (Tm)
for particular substances normally reabsorbed by
the tubules or by failure to inherit a gene or
genes required for tubular reabsorption

 Disorders affecting the interstitium also affect

the tubules (tubulointerstitial disease) due to
Interstitial Disorders close proximity

 exists in both acute and chronic forms

o Acute Renal Failure
 sudden decrease in glomerular filtration
rate
 AZOTEMIA
 INCREASED BUN
 INCREASED CREATININE
  OLIGURIA

 Microscopically:
 nephron - normal morphology
but FUNCTION IS
ABNORMAL
Renal Failure
o Chronic Renal Failure
 decrease glomerular filtration rate,
slowly.
= < 25 mL/min GFR
 evident in 80 - 85% renal function
has been LOSS

 "SLOW AND SILENT"

 Microscopically: Nephron is destroyed

morphologically and functionally
 Renal calculi (kidney stones)
o Renal Lithiasis condition in favor
1. pH - acidic crystal will accumulate
and forms stone
2. Chemical Concentration - 70% of
kidney stones contain CALCIUM.
3. Urinary stasis - decrease urine;
Renal Lithiasis dehydration

Ex: calcium oxalate, triple phosphate, uric acid,

phosphate crystals

 Lithotripsy → procedure using high-energy

shock waves, used to break stones located in the
upper urinary tract into pieces that can then be
passed in the urine

Summary of Glomerular Disorders

Disorder Etiology Clinical Course

Acute glomerulonephritis  Deposition of immune  Rapid onset of hematuria
complexes, formed in and edema Permanent renal
conjunction with group A damage seldom occurs
Streptococcus infection, on
the glomerular membranes

 Because complement proteins

that was activated

 Seen 1-2 weeks after infection

  Required time to produce
enough antibodies
Rapidly progressive  Deposition of immune  Rapid onset with glomerular
glomerulonephritis complexes from systemic damage and possible
immune disorders on the progression to end stage renal
glomerular membrane failure

 Presence of
AUTOANTIBODY – directed
to nuclear antigens/ anti
nuclear antigens

 Antinuclear antibody (ANA)

– antigen directed to the
nucleus of any nucleated cells
in the body (ex: Leaukocyte)

 Seen in LUPUS/SYSTEMIC
LUPUS ERYTHEMATOSUS
(SLE)
 SLE – deposition of antigen-
antibody reaction within the
glomerular membrane causing
damage

 Leukocytic Infiltration-
ANA affects WBCs causing to
be seen; antibody binded with
antigen

Disorders Primary Urinalysis Result Other Significant Tests

Acute glomerulonephritis  Macroscopic hematuria  Antistreptolysin O titer –
 Proteinuria check presence of
 RBC casts streptococcus infection
 Granular casts  Anti–group A streptococcal
enzymes
Rapidly progressive  Macroscopic hematuria  BUN
glomerulonephritis  Proteinuria  Creatinine
 RBC casts  Creatinine clearance

- Checking for AZOTEMIA

Disorders Etiology Clinical Course

Goodpasture Syndrome  Attachment of a cytotoxic  Hemoptysis – sputum with
antibody formed during viral blood streak like patients with
respiratory infections to tuberculosis and dyspnea
glomerular and alveolar followed by hematuria
basement membranes
  Possible progression to
 Deposition of antiglomerular endstage renal failure
basement membrane antibody

 Antibody directed to the basal

lamina, not just in the kidney
but also in lungs. Lung cells
that line in the alveoli have the
presence of basement
membrane; will be attacked
and destruction

Wegener’s granulomatosis  Antineutrophilic cytoplasmic  Pulmonary symptoms

autoantibody (ANCA) binds including hemoptysis develop
to neutrophils in vascular walls first followed by renal
producing damageto small involvement and possible
vessels in the lungs and progression to endstage renal
glomerulus failure

 The cytoplasm of the

neutrophils we have the
antibody against that.

 Also in the lungs

Disorders Primary Urinalysis Result Other Significant Tests

Goodpasture Syndrome  Macroscopic hematuria  Antiglomerular basement
 Proteinuria membrane antibody
 RBC casts
Wegener’s granulomatosis  Macroscopic hematuria  Antineutrophilic cytoplasmic
 Proteinuria antibody
 RBC casts
 FANA testing – fluorescent
antinuclear antibody test –
check the pattern of the
antinuclear antigens in the
tissues

Other Glomerular Disorders

 Occur in CHILDREN following viral infection.

 Respiratory infection, specially in females,
disrupts the vascular integrity; easy destruction of
the blood vessels because of the DECREASE
Henoch-Schonlein purpura PLATELET COUNT
 RED PATCHED – LEAKED RBCS
 Thickenning of glomerular membrane –
deposition of IgG antibody → IgG binds in the
 basal lamina → INCREASE thickness
Membranous glomerulonephritis  Because of immunoglobulin and complement
protein
 Marked by 2 alterations in the cellularity of the
glomerulus
Membranoproliferative glomerulonephritis
 Having proliferation of basement membrane.

 Cellular proliferation affecting the capillary walls

of the glomerular basement membrane; immune
mediated.
 Irreversible condition; marked decrease in the
renal function
Chronic glomerulonephritis
 Untreated acute glomerulonephritis; can lead to
Renal failure
 Deposition of Immunoglobulin IgA on the
glomerulus

IgA nephropathy  IgA complexes or aggregates that is being trapped

or engulf by the mesanglial cells
 Loss the shield of negativity
 Albuminuria and lipiduria

Nephrotic syndrome  Presence of EDEMA; oncotic pressure – prevent

the leakage of water in the blood vessels
 Little change in the glomerulus

 Disruption of podocytes present in the layer of

Minimal change disease glomerulus

 Seen in children after allergic reaction or

immunization
 Disruption of podocytes in the certain number
and areas of the glomerulus but the other parts or
areas are still NORMAL OR INTACT
Focal segmental glomerulosclerosis
 Affected area is localized not all area is affected
 Genetic disorder

 Glomerular basement membrane is lamilated

Alport syndrome (may butas butas); thinning of basal lamina

 Can cause presence of RBC, albumin not

normally seen.
Summary of Metabolic disorder and Tubular Disorders

Disorders Etiology Clinical Course

 Most common  Acute onset of renal
dysfunction usually resolved
Acute tubular necrosis  Characterized by destruction of when the underlying cause is
the renal epithelial cells corrected

 Damage to the renal tubular

cells caused by ischemia or
toxic agents

 ISCHEMIC – changes in the

renal tubule because
DECREASE in OXYGEN

 DECREASE perfusion of
blood into the kidney → leading
to SHOCK – caused by
TOXIN PRODUCING
BACTERIA, CONGESTIVE
HEART FAILURE

 Odorless Urine

 Antibiotics or certain
chemicals

 Nephrotoxic drug –
VANCOMYCIN – form gram
(+) organism

 Massive hemorrhage – causing

shock

Fanconi Syndrome  Used to characterize any  Generalized defect in renal

condition that present tubular reabsorption requiring
generalized loss of proximal supportive therapy
tubular function

 PCT – reabsorption and

secretion

 Inherited in association with

cystinosis and Hartnup disease
or acquired through exposure
to toxic agents
 Disorders Primary Urinalysis Result Other Significant Tests
Acute tubular necrosis  Microscopic hematuria  Hemoglobin (12.5 g/dL)
 Proteinuria  Hematocrit (33%)
 Renal tubular epithelial cells  Cardiac enzymes (decreased
 RTEcell casts cardiac output; decrease
 Hyaline, granular, waxy, broad amount blood pumped)
casts
Fanconi Syndrome  Glucosuria  Serum and urine electrolytes
 Possible cystine crystals  Amino acid chromatography

Disorder Etiology Clinical Course

Nephrogenic diabetes insipidus  Problem with  Requires supportive therapy to
ANTIDIURETIC HORMONE prevent dehydration

 Inherited defect of tubular

response to ADH or acquired
from medications

 Type of DI:

 Hypothalamic – deficiency in
production of ADH

 Nephrogenic – Normal amount

of ADH; cells present in the
collecting duct is not
responsive with the ADH
stimulation

 Polyuria but very low specific

gravity – very diluted urine
Renal glucosuria  Inherited autosomal recessive  Benign disorder
trait

 Problem with the reabsorption

of glucose in the proximal
convoluted tubules

 Amount of glucose present in

the urine – INCREASED

 Because no enzyme necessary

for the reabsorption of glucose

Disorders Primary Urinalysis Result Other Significant Tests

Nephrogenic diabetes insipidus  Low specific gravity  ADH testing
 Polyuria
Renal glucosuria  Glucosuria  Blood glucose

= HIGH GLUCOSE IN URINE

= NORMAL IN BLOOD

Summary of Interstitial Disorders

- Caused by urinary tract infection; upper or lower urinary tract
Lower UT
Urethra - URETHRITIS
Urinary bladder - CYSTITIS
- Can move the upper urinary tract
CYSTITIS → PYELITIS (RENAL PELVIS) → ACUTE PYELONEPHRITIS (kidney)
Disorders Etiology Clinical Course
Cystitis  Ascending bacterial infection  Acute onset of urinary
of the bladder frequency and burning
resolved with antibiotics
 UTI
 most often in FEMALE (10
times)
 short urethra
 close proximity of vagina and
rectum
 ↑ Hormones = produce
MUCUS → enhancing the
bacteria adherence to bacteria
mucosa
 No prostatic fluid

 E.coli = cause contamination

and infection

Acute pyelonephritis  Infection of the renal tubules  Acute onset of urinary

and interstitium related to frequency, burning, and lower
interference of urine flow to back pain resolved with
the bladder, reflux of urine antibiotics
from the bladder, and untreated
cystitis

 Hematogenous infection =
blood to kidney

Disorders Primary Urinalysis Result Other Significant Tests

Cystitis  Leukocyturia  Urine culture
 Bacteriuria
  Microscopic hematuria
 Mild proteinuria
 Increased pH
 Transitional epithelial
cell
Acute pyelonephritis  Leukocyturia  Urine culture
 Bacteriuria  Blood culture
 WBC casts
 Bacterial casts
 Microscopic hematuria
 Proteinuria
 RTE

Disorders Etiology Other Significant Tests

Chronic pyelonephritis  Recurrent infection of the renal  Frequently diagnosed in
tubules and interstitium caused children; requires correction of
by structural abnormalities the underlying structural defect
affecting the flow of urine
 Possible progression to renal
 Causing PERMANENT failure
SCARRING to renal pelvis or
renal calyx

 Renal calyx DILATION OR

DEFORMITY
Acute interstitial nephritis  Allergic inflammation of the  Acute onset of renal
renal interstitium in response dysfunction often accompanied
to certain medications by a skin rash

 IMMUNE RESPONSE  Resolves following

because of various drugs or discontinuation of medication
conditions and treatment with
corticosteroids
 Drug Induced – methicillin,
cephalosphorin, rifampin, INCREASED WBC
sulfonamide – PRESENCE OF WBC CAST
INFLAMMATION or NO BACTERIA
ALLERGY within the
KIDNEY

 Other medications – Non-

steriodal drugs, ibuprofen, or
alaxan

 Most common cause:

 ACUTE ALLOGRAFT
REJECTION – body rejects
 the transplanted kidney;
immune system will produce
cells to attack the transplanted
organ; INCREASE
EOSINOPHIL

Disorders Primary Urinalysis Result Other Significant Tests

Chronic pyelonephritis  Leukocyturia  Urine culture
 Bacteriuria  Blood cultures
 WBC casts  BUN
 Bacterial casts  Creatinine (azotemia)
 Granular, waxy, broad  Creatinine clearance
casts
 Hematuria
 Proteinuria
Acute interstitial nephritis  Hematuria  Urine eosinophils (Hansel
 Proteinuria stain)
 Leukocyturia  BUN
 WBC casts  Creatinine
 Creatinine clearance