Atrophy, Testis

Normal Histology
The seminiferous tubules have numerous germ cells.
Sertoli cells, with cytoplasm that extends between the germ cells,
are inconspicuous. Small dark oblong spermatozoa are seen
toward the center of the tubules.

Gross Anatomy
Bilateral atrophy may occur with a variety of conditions including
chronic alcoholism, hypopituitarism, atherosclerosis,
chemotherapy or radiation, and severe prolonged illness.

Scanner (Microscopic & Macroscopic)

Thickening of seminiferous tubule basement membrane.
Intertubular fibrosis.
Decreased sperm/no sperm present.

LPO (Treatment)
Depending on the cause of your testicular atrophy, if it
was due to a sexually transmitted disease, treatment of that
specific infection will most likely resolve the case of testicular
atrophy in time.
Hormone replacement therapy may also be prescribed
along with changes in lifestyle and regular exercise.
 HPO (Etiology)
Age: Testicular atrophy can be a consequence of natural
aging and is more commonly seen in men who have passed their
reproductive prime.
Hormone imbalance: Imbalances due to medication side
effects, radiation exposure, or even chronic steroid use can all be the
cause.
Disease: Medical conditions such as mumps virus and HIV
have been known to result in testicular atrophy. The condition may
be reversed with treatment of the disease but it depends on the
severity of the atrophy.

Heart, Myocardial Hypertrophy, Ischemic Cardiomyopathy

Normal Histology
Centrally located nucleus
The nuclei are located in the center of each fiber
Bundle of purkinje fiber

Gross Anatomy
The left ventricle, which is the main heart muscle, is usually
enlarged and dilated. This condition can be a result of a heart
attack or coronary artery disease, a narrowing of the arteries.

Scanner (Microscopic & Macroscopic)

Cardiomyocytes are hypertrophied with abundant
eosinophilic cytoplasm and box shaped nuclei
Myocytes display bizarre forms with Y shaped branching,
frequent side to side junctions or a characteristic whorled
appearance, usually around a central fibrous core
Myocardial architecture is disorganized, with bundles of
cardiomyocytes arranged at perpendicular and oblique angles to
each other (myocardial disarray)
Replacement myocardial fibrosis resulting from
microvascular ischemia and resultant cell death may be seen
 LPO (Treatment)
Surgical myectomy or alcohol septal ablation are
performed in cases with outflow obstruction to alleviate symptoms
Implantable cardioverter defibrillators (ICDs) can prevent
sudden death
Catheter based procedures can control atrial fibrillation
Heart transplantation is performed for end stage failure

HPO (Etiology)
Heterogenous genetic disease, may be familial or non-
familial
60% of familial cases are autosomal dominant with
variable expressivity and incomplete, age related penetrance
Mutations have been identified in numerous sarcomeric
protein genes; most common are the beta myosin heavy chain and
myosin binding protein C
Private mutations are unique to individual families
Identification of these mutations is important for family
screening

Hypertensive Heart Disease

Normal Histology
Nuclei are oval, rather pale and located centrally in the
muscle cell which is 10 - 15 m wide.
Cardiac muscle cells excitation is mediated by rythmically
active modified cardiac muscle cells.
Cardiac muscle is innervated by the autonomic nervous
system (involuntary), which adjusts the force generated by the
muscle cells and the frequency of the heart beat.

Gross Anatomy
Thickened left ventricle wall with increased heart weight.
The left ventricle wall thickness is usually more than 2cm
wall thickness.
The average heart weight is 500 to 600 gm. It may be as
much as 1100gm.
The papillary muscle and trabeculae carneae are rounded
and prominent and cardiac chamber is small (concentric
hypertrophy).
When cardiac failure ensues, dilatation of the chamber
also may be prominen
Scanner (Microscopic & Macroscopic)
Myocytes and nuclei are enlarged.
In long-term cases diffuse interstitial fibrosis and focal
myocyte atrophy and degeneration may develop, with left
ventricle chamber dilatation and wall thinning.
Myocardial edema and foci of necrosis characterized
either by intense eosinophilia or by complete dissolution of the
muscle fibers occur in malignant hypertension.

LPO (Treatment)
water pills to help lower blood pressure.
nitrates to treat chest pain.
statins to treat high cholesterol.
calcium channel blockers and ACE inhibitors to help lower
blood pressure.
aspirin to prevent blood clots.

HPO (Etiology)
This can cause angina (chest pain).
High blood pressure also leads to thickening of the blood
vessel walls. When combined with cholesterol deposits in the
blood vessels, the risk of heart attack and stroke increases.
Hypertensive heart disease is the
leading cause of illness and death from high blood pressure.