CASE 1 ➔ Final Diagnosis/ Impression: UTERINE PROLAPSE

A 65 Years old female complained of lower abdominal discomfort, The protrusion of

voiding and defacatory difficulties. the cervix of the uterus into
The patient also feels a bulge in the lower vagina of the cervix the lower part of the vagina
protruding through the vaginal introitus. close to the vestibule and
Hysterectomy was done. Grossly, the uterus was small with a thinned causes a bearing-down
out endometrial lining. sensation in the womb and
an increased frequency of
➔ Salient Features and burning sensation on
★ 65 years old urination.
★ Female The prolapse occurs
★ Lower abdominal discomfort as a result of advancing
★ Voiding age and menopause and
★ Defecatory difficulties results from weakness of
★ Lower vaginal bleeding in the cervix through vaginal introitus the muscles, ligaments, and
★ Thinned endometrial lining fasciae of the pelvic floor
that constitute the support
➔ Differential Diagnosis of the uterus and other
pelvic viscera.

Symptoms include:
★ pelvic
heaviness
★ pelvic pain
★ lower back pain
★ constipation
★ difficulty
urinating
★ urinary
frequency
★ painful sexual
intercourse
 ➔ Pathophysiology of Uterine Prolapse

Occurs when pelvic floor muscles and ligaments stretch and

weaken and no longer provide enough support for the uterus. As a
result, uterus slips down into or protrudes out of the vagina.

Factors:
★ Pregnancy
★ Delivery of a large baby
★ Being overweight or obese
★ Lower estrogen level after menopause
★ Chronic constipation or straining with bowel movements
★ Chronic cough or bronchitis
★ Repeated heavy lifting Stages of Uterine Prolapse:
★ pelvic tumors, sacral nerve disorder ★ STAGE 1 - the uterus is in the upper half of the vagina
★ STAGE 2 - the uterus has descended nearly to the opening of
the vagina
★ STAGE 3 - the uterus protrudes out of the vagina
★ STAGE 4 - the uterus is completely out of the vagina
➔ Management & Treatment During this exam, the physician inserts a device called a
speculum, that allows him to see the inside of the vagina, and
NON – SURGICAL examine the vaginal canal and uterus.
★ Kegel Exercises- to strengthen pelvic muscles
★ Weight Management ➔ Prognosis: FAIR PROGNOSIS
★ Constipation Treatment
★ Vaginal Pessary- a plastic or rubber ring inserted into the Based on the signs and symptoms the pt. experienced 3rd
vagina to support the bulging tissues degree prolapsed uterus. The patient has fair potential as condition
can be surgically repaired with the removal of uterus by hysterectomy
SURGICAL to prevent severe procidentia. But with any surgery comes the risk of
★ Hysterectomy- open abdominal, laparoscopic, vaginal complication. Vaginal vault prolapse may occur after hysterectomy
(recommended) ultimately turning the vagina inside out which often accompanied by
★ Hysteropexy- uterine suspension procedure to preserve an enterocele.
uterus;uses a strip of synthetic mesh to lift the uterus and hold
it in place. One end of the mesh is attached to the cervix and
the other to a bone (sacrum).

➔ Diagnostic Modalities/ Procedures

★ PELVIC EXAMINATION/BIMANUAL EXAMINATION

-One hand is placed midway between the umbilicus and the
symphysis pubis and pressed downwards towards the pelvic
hand
-Using the palmar surface of your fingers, palpate for the
uterine fundus while gently pushing the cervix anteriorly with
the pelvic hand

Physician may ask the patient to:

-Bear down as if having a bowel movement (to assess how far
the uterus has slipped into the vagina, to determine the degree
of prolapse)
-Tighten the pelvis muscles as if stopping a stream of urine (to
check the strength of the pelvic muscles)
CASE 2 ➔ Final Diagnosis/Impression: Alcoholic Fatty Liver

50 year old male who had been a heavy drinker for 20 years. He had Fatty Steatosis (also
been in and out of the hospital for the past year because of recurrent known as Hepatic Steatosis)
bouts of ascites associated with jaundice and emaciation. Ultrasound happens when fat is
of the liver shows hepatomegaly. Based on the above history and accumulated in the liver. It
sonographic findings, the patient was diagnosed as a case of fatty develops when the body
steatosis (fatty change of the liver). produces too much fat or is
unable to metabolize fat
➔ Salient Features efficiently.
★ Patient: 50-year old Male Alcoholic Liver
★ History: Heavy alcoholic drinker for 20 years Disease due to excessive
★ Hospitalization: In and out of the hospital for the past year due alcohol consumption.
to:
Recurrent bouts of Ascites
Jaundice
Emaciation
★ Sonographic Findings: Ultrasound of Liver showing ➔ Pathophysiology of Alcoholic Fatty Liver
Hepatomegaly

➔ Differential Diagnosis
➔ Management and Treatment

Non- Pharmacological Management

★ Weight management
★ Alcohol detoxification
★ Exercise
★ Dietary changes

Pharmacological Treatment
★ Corticosteriods ➔ Prognosis
★ Pentoxyfilline
ALCOHOL HEPATITIS is a syndrome of progressive
➔ Diagnostic Modalities/ Procedures inflammatory liver injury associated with long term heavy intake of
ethanol.
Most patient with mild alcoholic hepatitis ,short -term prognosis
is good and does not required hospitalization.
Contrary, patient with severe acute alcoholic hepatitis are at
high risk of early death. Alcohol hepatitis usually progresses to
cirrhosis if heavy alcohol use continues and mortality can be
substantial.
CASE 3
➔ Differential Diagnosis
A massively obese (5’3”, 275 pounds), 55-year old- sexually active
female, nulligravida (no pregnancies), presents to her gynecologist
because of vaginal spotting for 1 year. Her medical history includes:
non-insulin dependent diabetes mellitus, age 43, and medication
controlled hypertension. No IV drug use. Her gyn history includes:
menarche, age 11; coitarche age 20; lifetime sexual partners, 2; 6
menses/year until age 51 when she became menopausal and stopped
her menstrual periods. An endometrial biopsy yield abundant tissue.
Following biopsy, the patient is lost to follow-up for 8 years. She is
finally brought to the ER after fainting at home. Her hemoglobin is
5g/dl (ref. Range 12-16 g/dl). The endometrial biopsy is repeated,
followed by a simple hysterectomy with bilateral
salphingo-oophorectomy.

➔ Salient Features
★ 55 years old female
★ Massively obese (5’3”, 275 pounds)
★ Sexually active ➔ Final Diagnosis/Impression: Endometrial Hyperplasia
★ Nulligravida
★ Vaginal spotting for 1 year Endometrial hyperplasia occurs when the endometrium -the
lining of the uterus- becomes too thick. It is not cancer, but in some
cases, it can lead to cancer of the uterus.

➔ Pathophysiology of Endometrial Hyperplasia

Endometrial hyperplasia usually occurs after menopause,

when ovulation stops and progesterone is no longer made. It also can
occur during perimenopause, when ovulation may not occur regularly.

Hyperplasia is:
★ Bleeding during the menstrual period that is heavier or lasts
longer than usual
★ Menstrual cycles that are shorter than 21 days (counting from
the first day of the menstrual period to the first day of the next
menstrual period)
★ Any bleeding after menopause

Factors:
★ Age older than 35 years
★ Never having been pregnant
★ Older age at menopause
★ Early age when menstruation started
★ Personal history of certain conditions, such as diabetes
mellitus, polycystic ovary syndrome, gallbladder disease, or
thyroid disease
★ Obesity
★ Family history of ovarian, colon, or uterine cancer

Types of Hyperplasia:
★ Simple hyperplasia
★ Complex hyperplasia
★ Simple atypical hyperplasia
★ Complex atypical hyperplasia
 SURGICAL MODALITIES
➔ Management and Treatment ★ Hysterectomy- Considered first choice treatment for EH.

HORMONAL THERAPY ★ Thermal balloon endometrial ablation or resectoscopic

★ Progestin Therapy- synthetic progestogens with similar effects endometrial ablation therapy- feasible, safe and effective
as progesterone. Most frequently employed to induce EH treatment option for simple and complex non-typical EH.
regression in women with EH without atypia or those who wish
to retain fertility. ★ Resectoscopic surgery- is an effective treatment for EH
without atypia, especially for those at high risk for medical
➢ Medroxyprogesterone acetate (MPA) is a synthetic therapy or hysterectomy.
steroidal progestin. It is used to treat cases with absent
or irregular menstruation period, or abnormal uterine ➔ Diagnostic Modalities/ Procedures
bleeding. Prevents overgrowth in the uterine lining in
postmenopausal women receiving estrogen hormone ❖ Endometrial Hyperplasia
and decreases risk of EH progression. Endometrial biopsy shows abundant tissue associated with
prolonged estrogen stimulation of the endometrium, obesity, and
➢ Megestrol acetate (17- hydroxylated progesterone). menopause.
160-360 mg/day is effective for endometrial Non-insulin dependent diabetes mellitus. Excess insulin
malignancies w/o causing marked harmful effects on stimulates the production of androgen which is later converted to
serum lipid profiles and glucose levels. estrogen.
No pregnancies (Nulligravida). Non-ovulation due to lack of
➢ Levonorgestrel (LNG) is a 2nd generation progestin. cycling caused by high estrogen levels
LNG-impregnated intrauterine device (LNG-IUD).
2 Categories of Endometrial Hyperplasia:
➢ Norethindrone acetate or Norethisterone acetate is a
synthetic, orally active steroidal progestin with ★ Non-atypical hyperplasia
antiandrogen and antiestrogen effects. It reduces the Increased in the gland-to-stroma ratio. The gland show variation in
incidence of EH in post-menopausal women treated size and shape and may be dilated.
with estradiol.
★ Atypical Hyperplasia(Endometrial intraepithelial neoplasia)
★ Gonadotropin- Releasing Hormone Therapy- GnRH analogues Complex patterns of proliferating glands displaying nuclear atypia.
suppress the hypothalamic pituitary-ovarian axis – The glands are commonly back-to-back and often have complex
inhibiting estrogen production. Appear to have direct anti- outlines due to branching structures.
proliferative effect on endometrial cells.
*Approximately 23% to 48% of women with a diagnosis of atypical *Note: the patient was lost to follow up her condition for 8 years which
hyperplasia are found to have carcinoma when a hysterectomy is can then be presumed that no therapy or treatment of any kind was
performed. done.

*After 8 years, endometrial biopsy was repeated which may have lead
to our diagnosis of atypical type 1 endometrioid carcinoma.

*Her second endometrial biopsy would have likely yielded a localized

polyploid tumor or a tumor that diffusely infiltrates the endometrial
lining, which may proceed with myometrial invasion then direct
extension to adjacent structures/organs.

*Up to 20% of endometrioid carcinomas contain foci of squamous

differentiation.

*Squamous elements may be histologically benign-appearing when

they are associated with well-differentiated adenocarcinomas.

* Less commonly, moderately or poorly differentiated endometrioid

carcinomas contain squamous elements that appear frankly
malignant. *Current classification systems grade the carcinomas
based on glandular differentiation alone and ignore areas of solid
squamous differentiation.

*With this, her primary physician might have suggested for her to
undergo simple hysterectomy, along with bilateral
salpingo-oophorectomy.

*Sequencing of her genomes might also be considered to further

strengthen the diagnosis, which may result to her having mutations in
❖ Endometrial Carcinoma Type 1
the PTEN tumor suppressor gene (which is identified in 30% to 80%
Endometrial carcinomas, in general, usually manifest with
of endometrioid carcinomas), mutations in PIK3CA oncogene,
irregular or postmenopausal bleeding, which can tied to the patients’s
suggesting that it was invasive, mutations in KRAS which further
1 year occurence of vaginal spotting. It is slow to metastasize but if
stimulates PI3K/AKT signaling (in approximately 25% of the cases),
left untreated, it will eventually disseminate to regional nodes and
and loss of function mutations in ARID1A, occurring one-third of the
more distant sites.
tumors.
 Natural menopause occurring after age 52 years increases the
risk for endometrial cancer 2.4-fold compared with women who
experienced menopause before 49 years of age.
The risk of endometrial cancer is increased 3 times in women
who are 21 to 50 pounds overweight and 10 times in those more than
50 pounds overweight
Diabetes mellitus increases a woman’s risk for endometrial
cancer by 1.3 to 2.8 times.

➔ Prognosis

When there are no atypical cells present, the chance of

endometrial hyperplasia eventually becoming endometrial cancer is
very unlikely.
The risk of endometrial hyperplasia progressing to a
carcinoma is related to the presence and severity of cytologic atypia.
CASE 4 ➔ Differential Diagnosis

This 81-year-old man awoke one morning unable to move his right
arm or leg and unable to speak. He rang a bell with his right hand to
summon the housekeeper. She telephoned the man’s son and also
called for an ambulance. The son met the ambulance at the hospital
emergency room. The son said that his father had a “stroke” about a
year before, involving profound weakness of his left arm and leg, but
had regained nearly full use of them within a few months.
Physical examination was begun, but the patient suddenly arrested
and could not be resuscitated. An autopsy was performed.
Upon removal of the brain at autopsy, patchy parenchymal loss and
severe cerebrovascular atherosclerosis were noted. Coronal sections
of the cerebral hemispheres revealed multifocal parenchymal lesion,
some of which were centered at the depths of the sulci. Some lesions
were granular and crumbly, and some were cystic. A large lesion in ➔ Final Diagnosis/ Impression: Ischemic Stroke
the left lateral frontal lobe and nearly the entire pons were simply
softened. Characterized by the sudden loss of blood circulation to an
area of the brain, resulting in a corresponding loss of neurologic
➔ Salient Features function.
★ 81 years old
★ Male
★ Inability to move his right arm or leg
★ Inability to speak
★ Had a stroke about a year before
★ Patchy parenchymal loss and cerebrovascular atherosclerosis;
multifocal parenchymal lesion of the coronal section of
cerebral hemispheres; some lesions are granular or crumbly,
cystic, and softened.
➔ Pathophysiology of Ischemic Stroke ➔ Management & Treatment

MEDICATIONS
★ Intravenous injection of tissue plasminogen activator (tPA)

SURGERY
★ Endovascular Therapy
★ Balloon angioplasty coupled with stenting
★ Carotid endarterectomy

REHABILITATION SERVICES
★ Physical, occupational, and speech therapy

➔ Diagnostic Modalities/ Procedures

★ Computed Tomography (CT) Scan

 In this case, the patient suddenly arrested and could not be
resuscitated.
Overall mortality rate at 30 days after stroke: 28%
Mortality rate at 30 days after ischemic stroke: 19%
1-year survival rate for patients with ischemic stroke: 77%.

★ Magnetic Resonance Imaging (MRI The prognosis varies greatly depending on the stroke severity
and on the patient’s premorbid condition, age, and poststroke
complications. The National Institutes of Health Stroke Scale (NIHSS)
score was the strongest predictor of early mortality risk. Cardiogenic
emboli are associated with the highest 1-month mortality in patients
with acute stroke.

Factors increasingly associated with early stroke death includes:

★ Age
★ Stroke severity measured by the National Institutes of Health
Stroke Scale (NIHSS)
★ Pre-stroke functional disability (modified Rankin Scale > 0)
★ Pre-existing heart disease
★ Diabetes mellitus
★ Posterior circulation stroke syndrome
★ Non-lacunar stroke cause

The Predicting Early Mortality of Ischemic Stroke score,

ranging from 0 to 12 points, was developed to identify patients with a
high risk of early mortality after an ischemic stroke. Patients with a
score ≥ 10 had a 35% risk of dying within the first few days at the
stroke unit.
The presence of computed tomography (CT) scan evidence of
infarction early in presentation has been associated with poor
outcome and with an increased propensity for hemorrhagic
transformation after fibrinolytic therapy.
➔ Prognosis
Hemorrhagic transformation occur in 5% of uncomplicated
ischemic strokes in the absence of fibrinolytic therapy, although it is
not always associated with neurologic decline.
CASE 5

A 70 year old man was brought to the hospital for evaluation of chest ➔ Differential Diagnosis
pain. He described feeling weak and dizzy after a walk around the
block the morning of his admission. This episode of dizziness was
followed by 10-15mins. of chest pain that quickly resolved when he
rested. He also described a 2-month history of similar but shorter
episodes of chest pain and dizziness after working in his yard. He had
been told several years ago that he had a slight heart murmur, but
had not been evaluated further. He had been otherwise healthy all his
life.

Physical signs and auscultation suggested aortic valve narrowing. His

lungs were clear to auscultation. A chest radiograph showed an
enlarged heart and a vague area of calcification at the base of the
heart in the region of the aortic valve. Cardiac enzymes and other
laboratory tests were normal. An EKG showed atrial fibrillation and left
ventricular hypertrophy. His valve was replaced and he did well for
several years. He then began to have signs and symptoms of aortic
➔ Final Diagnosis/ Impression: Aortic Valve Stenosis
regurgitation.

➔ Salient Features
★ 70 year old man
★ Chest pain
★ Weakness and dizziness after a walk in the morning prior to
his admission
★ 10-15minutes of chest pain, resolved upon resting
★ 2 month history of shorter episodes of chest pain & dizziness
★ Slight heart murmur years ago
★ Aortic valve narrowing
★ Enlarged heart and Calcifications at Aortic valve
★ EKG= atrial fibrillation & left ventricular hypertrophy Occurs when the heart's aortic valve narrows. This narrowing
★ Valve replaced (good for several years) Aortic regurgitation prevents the valve from opening fully, which reduces or blocks blood
(later onset) flow from your heart into the main artery to your body (aorta) and
onward to the rest of your body.
➔ Pathophysiology of Aortic Valve Stenosis

Signs and Symptoms

★ Abnormal heart sound (Heart murmur)
★ Chest pain (Angina)
★ Feeling faint (Syncope)
★ Shortness of breath
★ Fatigue
★ Heart palpitations
★ Heart Failure – weakened heart that doesn’t pump well

➔ Management & Treatment

MEDICAL TREATMENT
★ Beta-blockers and Angiotensin-converting enzyme (ACE)
inhibitors

SURGICAL TREATMENT
★ Aortic Valve Replacement
 ★ Percutaneous Aortic Balloon Valvuloplasty (PABV) ➔ Diagnostic Modalities/ Procedures
- preferable operation in many children and young adults with
congenital, non calcific AS. It is performed routinely as part of TAVR. ★ Echocardiography
This test uses sound
waves to produce video
images of your heart in
motion.
This imaging
modality helps the examiner
to distinguish among
congenital, calcific, and
post- inflammatory or
rheumatic valve stenosis.
Doppler echocardiography are indices of transaortic flow
velocities, which allow the calculation of the aortic valve annulus
★ Transcatheter Aortic Valve Replacement (TAVR) (AVA) and transaortic pressure gradients. Together, these values
- most frequently performed via the transfemoral route. allow for grading the severity of aortic valve stenosis.

★ Electrocardiogram (ECG)
In this test, wires (electrodes) attached o pads on your sin
measure the electrical activity of your heart. An ECG can detect
enlarged chambers of your heart, heart disease and abnormal heart
rhythms.
 provide discordant conclusions about the severity of aortic valve
★ Chest X-ray stenosis
Can help determine whether Measurements of the left ventricle and aortic pressures and,
your heart is enlarged, which can occur sometimes, cardiac output are taken and used to calculate transaortic
in aortic valve stenosis. gradients.
It can also show whether you Additional information gleaned from cardiac catheterization
have an enlarged blood vessel (aorta) includes left atrial and pulmonary artery pressures and the
leading from your heart or any calcium assessment of other valve disease
buildup on your aortic valve
Also helps determine the ➔ Prognosis
condition of the lungs.
The onset of symptoms is a significant indication of a poor
★ Stress testing prognosis and cardiac decompensation.
Used in combination After the onset of symptoms, patients with severe aortic
with echocardiography. the test stenosis have a survival rate as low as 50% at 2 years and 20% at 5
is termed exercise - stress years without aortic valve replacement.
echocardiography. Prognosis after successful AVR symptoms and quality of life
Used in evaluating are in general greatly improved.
asymptomatic patients or For people who are younger than 65 is about five years less
patients with equivocal than that of the general population. For people older than 65, it is
symptoms. about the same.
Should not be
performed in patients with
unequivocal symptoms or in patients whose aortic valve stenosis
severity or comorbidity contraindicates strenuous activity.

★ Cardiac catherization
Provides information regarding
the presence and severity of valvular
obstruction.
Procedure is required before
aortic valve repair when either
concurrent coronary artery disease is
suspected or a patient's history,
physical examination, and/or
echocardiographic measurements
CASE 6 ➔ Final Diagnosis and Impression: Benign Prostatic Hyperplasia

A 63 year old male presented with urinary hesitancy, frequency, and Benign Prostatic
nocturia. Digital rectal exam revealed a large, nodular, and rubbery Hyperplasia also called as
prostate with no hard regions. The serum prostatic specific antigen nodular prostatic hyperplasia is
was 6 ng/ml (ref. range 0-4 ng/ml), thus transrectal ultrasound and the most common age-related
prostatic biopsies were performed, followed by a trans-urethral disease in men older than age
resection of the prostate. 50 years. It is characterized by
the formation of large, discrete
➔ Salient Features lesions in the periurethral zones
★ Age: 63 years old, Male rather than in peripheral zones.
★ Presented with urinary hesitancy, frequency and nocturia The severity of symptoms
★ Digital rectal examination revealed a large, nodular, and may vary in men but symptoms
rubbery prostate with no hard regions. tend to gradually worsen
★ Serum Prostatic Specific Antigen was 6 ng/ml (reference overtime. Patients with BPH may
range 0-4 ng/ml) experience the following:
▪ frequent or urgent need to urinate
➔ Differential Diagnosis ▪ increased frequency of urination at nigh (nocturia)
▪poor urine stream or a stream that stops and starts
▪ dribbling at the end of urination
▪ painful micturition (dysuria)
▪ increased risk of developing bacterial infections of the
bladder and kidney.
▪ inability to completely empty the bladder (acute retention of
urine)
Normally, the prostate weighs 20 gm in adult men but with
BPH it will weigh up to 60 to 100 gm. The enlargement of the prostate
gland compresses and narrows the urethral canal causing partial or
complete obstruction of urethra. This will further cause urinary
symptoms.
➔ Pathophysiology of Benign Prostatic Hyperplasia
 ➔ Management & Treatment

There are wide varieties of treatment available for an enlarged

prostate, including:

MEDICATION- most common treatment for mild to moderate

symptoms of prostate enlargement.
★ Beta Blockers – relaxes bladder neck muscles and muscle
fibers in prostate, making urination easier.
Side effects: dizziness, retrograde ejaculation
Examples: Alfuzosin (Uroxatral), Tamsulosin (Flomax),
Doxazosin (Cardura), Silodosin (Rapaflo)
★ 5-alpha reductase inhibitors – shrink the prostate by
preventing hormonal changes that cause prostate growth.
Examples: Finasteride (Proscar), Dutasteride (Avodart)
★ Combination Drug Therapy – combination of beta-blockers
and 5-alpha reductase inhibitor.
The critical mediator in this process is dihydrotestosterone ★ Tadalafil (Cialis) – treatment for erectile dysfunction can also
(DHT)- synthesized by the stromal cells of the prostate from treat prostate enlargement.
circulating testosterone via the activity of 5a-reductase, type 2.
DHT binds to the nuclear androgen receptor (AR) in stromal MINIMALLY INVASIVE THERAPIES OR SURGERY-
and epithelial cells, activating the transcription of androgen-dependent Symptoms are moderate to severe. Medication haven’t relieved
genes. symptoms. One has urinary tract obstruction, bladder stone, blood in
DHT is not a direct mitogen, but it does increase the urine/kidney. Prefer definitive treatment.
production of secondary growth factors and their receptors, ★ Trans-Urethral Resection of the Prostate (TURP)
particularly fibroblast growth factor-7 (FGF-7) by stromal cells. The surgeon removes all but the outer part of the prostate.
FGF-7 acts in a paracrine manner to stimulate stromal cell TURP generally relieves symptoms quickly. Most men have a
proliferation and inhibits epithelial apoptosis. stronger urine flow soon after the procedure. Need a temporary
Augmented FGF-1 and FGF-2 and transforming growth catheter to drain the bladder.
factor-B (TGF-B) production also contribute by driving fibroblast
proliferation.
 However, if symptoms are tolerable, one might decide to postpone
treatment and simply monitor symptoms. For some men, symptoms
★ Trans-Urethral Incision can ease without treatment.
of the Prostate (TUIP)
A lighted scope is OTHER TREATMENTS:
inserted into your urethra, and ★ Ayurvedic Medicine
the surgeon makes one or two VarunadiVati. ​The herbal tablets made from the bark of this
small cuts in the prostate tree are recommended in Ayurveda for prostate enlargement or BPH.
gland — making it easier for Ayurveda is an age old traditional medical system still in practice in
urine to pass through the India and recognized by the WHO. Herbal non-hormonal ayurvedic
urethra. This surgery might be medicine that treats BPH by reducing prostate weight.
an option if you have a small ★ Coffee Enemas
or moderately enlarged A coffee edema is a type of natural “colon cleanse” that
prostate gland, especially if involves injecting coffee and water into the rectum and colon, parts of
you have health problems that the large intestine that connect to the anal opening. While still not
make other surgeries too exactly a mainstream way to fight illness, coffee enemas are nothing
risky. new. Coffee enemas have been around since the late 1800s, used at
the time to help speed up healing following surgeries. First made
★ Trans-Urethral Microwave Therapy (TUMP) famous by the Gerson Institute in the 1950s, when it began using
Your doctor inserts a special electrode through your urethra coffee enemas as part of natural cancer treatments, others are now
into your prostate area. Microwave energy from the electrode destroys turning to this procedure for various ailments — especially those that
the inner portion of the enlarged prostate gland, shrinking it and don’t respond well to traditional treatments or prescription
easing urine flow. TUMT might only partially relieve your symptoms, medications.
and it might take some time before you notice results. This surgery is ★ Acupuncture
generally used only on small prostates in special circumstances Researchers find acupuncture and Chinese herbal medicine
because re-treatment might be necessary. effective for the alleviation of urinary retention caused by BPH.
 ★ Homeopathic Medicine Ultrasounds are used early in the diagnostic process to
Literally means “like disease”. This means that the medicine determine whether your prostate is enlarged or has an abnormal or
given is like the disease that the person is expressing. Its principle is asymmetrical shape.
Like cures like. One example is ​Chimaphillaumbellate - this remedy is ★ Prostate-Specific Antigen Blood Test
often helpful when the prostate is enlarged, with urine retention and PSA is a substance produced by the prostate gland.
frequent urging. Elevated PSA levels may indicate prostate cancer, a
noncancerous condition such as prostatitis, or an enlarged prostate.
MANAGEMENT (ref. range 0-4ng/ml)
★ Keep yourself active. Lack of physical activity can make you ★ Biopsy
retain urine. Activities like walking, jogging, and swimming can To remove small slivers of tissue for examination under a
help reduce urinary problems. microscope. If there is suspicion for prostate cancer.
★ Do ​Kegel exercises​. Stand at, or sit on the toilet and contract
the muscle that allows you to stop and start the flow of pee. ➔ Prognosis
Hold it for 5 to 10 seconds. Do this 5 to 15 times, 3 to 5 times Any type of prostate procedure can cause side effects.
a day to help with bladder control and function. Depending on the procedure you choose, complications might
★ Meditate. Nervousness and tension cause some men to include:
urinate more often. Try meditation along with exercise to help ★ temporary difficulty with urination
reduce stress. ★ urinary tract infection
★ Try double voiding. When you do urinate, go once and then try ★ bleeding
to go again a few moments later. This will help you to fully ★ erectile dysfunction
empty your bladder, lessen the feeling of constantly having to ★ very rarely, loss of bladder control (incontinence)
pee, and maybe save you another trip to the bathroom. ★ retrograde ejaculation
If left untreated, BPH can progress and cause subsequent
medical issues. When the bladder does not empty completely, you
➔ Diagnostic Modalities/ Procedures become at risk for developing urinary tract infections (UTIs). Other
serious problems can also develop over time, including bladder
★ Digital Rectal Exam (DRE) stones, blood in the urine (hematuria), incontinence, or urinary
The physician inserts a gloved finger into the rectum (located retention.
next to the prostate) and feels the back of the prostate. Urinary retention is the sudden and complete inability to
With the DRE, the examiner can assess prostate size and urinate and can occur when the obstruction from BPH progresses to
contour, evaluate for nodules, and detect areas suggestive of the point that the prostate blocks the urethra and it is no longer
malignancy. possible to completely empty the bladder. If retention occurs,
★ Prostate Ultrasound emergency medical intervention is required. In rare cases, bladder
It involves a small probe that is inserted a short distance into and/or kidney damage can develop from BPH. BPH is not a risk
the rectum. factor for the development of prostate cancer.
CASE 7 ★ Had severe unrelenting pain for 45 minutes and was not
relieved by nitroglycerine
A 40 year-old diabetic was evaluated in the emergency room for chest ★ Medications include antihypertensive and cholesterol-lowering
pain. She had a history of hypertension, and a 30 pack year smoking agents.
history. Her medications included antihypertensive and ★ PHYSICAL EXAMINATION
cholesterol-lowering agents. She had a prior admission several years HR 105
ago for a small uncomplicated myocardial infarct. She had angina for BP 100/50 (usually about 155/95)
many years, averaging one bout of angina a week. Her usual angina Temp. 100 °F
lasted 10-15 minutes and was relieved by nitroglycerine. A
cardiologist attempted angioplasty several years ago. This procedure ➔ Differential Diagnosis
relieved her symptoms for six months but eventually exercise-induced
angina returned. There were no clinical changes until two weeks prior
to her emergency room admission, when she began having daily
angina attacks that lasted 30 minutes or more. In the hour prior to her
admission she had awakened with several chest pain, nausea and
dyspnea. There had been severe unrelenting pain for 45 minutes and
it had not been relieved by nitroglycerine. HR 105. BP 100/50 (her
usual BP runs about 155/95). Temperature 100 °F . One examiner
described her as obese and diaphoretic (sweating profusely), with
pale skin and labored respirations. Rales were heard over both lung
fields. An EKG and serial cardiac enzymes were ordered.

➔ Salient Features
★ Patient was seen in her 40s with a history of diabetes,
hypertension, and a 30 pack year smoking history
★ She was described as obese, diaphoretic with pale skin and
labored respirations.
★ Prior admission for small uncomplicated myocardial infarct
★ Had angina averaging one bout a week, lasting 10-15 minutes
and is relieved by nitroglycerine ➔ Final Diagnosis/ Impression: Myocardial Infarction
★ Had angioplasty which relieved her symptoms, eventually
exercise-induced angina returned Myocardial infarction is diminished blood supply to the heart,
★ Began having daily angina attacks lasting 30 minutes or more exceeds a critical threshold and overwhelms the myocardial cellular
prior to emergency room admission repair mechanisms designed to maintain normal operating function
★ Awakened with severe chest pain, nausea and dyspnea an and homeostasis.
hour prior to admission
 A high index of suspicion for MI should be maintained,
especially when evaluating women, patients with diabetes, older
patients, patients with dementia, patients with a history of heart
failure, cocaine users, patients with hypercholesterolemia, and
patients with a positive family history for early coronary disease.

VITAL SIGNS
★ Heart rate
The patient's heart rate is often increased but depressed heart
rate may also be present in some cases.
​ NORMAL ​Shows the damage of myocytes Unequal palpable pulses can be suggestive of the presence of
aortic dissection, which commonly presents with chest pain radiating
Myocardial Infarction is the irreversible death (necrosis) of to the back, accompanied by a blood pressure difference of 15 mm
heart muscle secondary to prolonged lack of oxygen supply. Hg or greater between both arms and an aortic regurgitation murmur.
Patients with typical acute MI usually present with chest pain ★ Blood pressure
and may have prodromal symptoms of fatigue, chest discomfort, or Patient's blood pressure is initially elevated (hypertension
malaise in the days preceding the event. because of peripheral arterial vasoconstriction resulting from an
adrenergic response to pain, anxiety, and ventricular dysfunction).
Signs and Symptoms Alternatively, hypotension can also be seen.
★ Chest pain (angina) ★ Respiratory rate
★ Profuse sweating (diaphoresis) The respiratory rate may be increased in response to
★ Paleness (palor) pulmonary congestion or anxiety.
★ Labored breathing (dyspnea) ★ Temperature
★ Arrhythmia with an abnormally rapid rate (tachycardia) or Fever is usually present within 24-48 hours, with the
abnormally slow rate (bradycardia) temperature curve generally parallel to the time course of elevations
of creatine kinase (CK) levels in the blood. Body temperature may
Other symptoms include the following: occasionally exceed 102°F.
★ Anxiety, commonly described as a sense of impending doom ★ Heart
★ Pain or discomfort in areas of the body, including the arms, left On palpation, lateral displacement of the apical impulse,
shoulder, back, neck, jaw, or stomach dyskinesis, a palpable S4 gallop, and a soft S1 sound may be found.
★ Light-headedness, with or without syncope Paradoxical splitting of S2 may reflect the presence of left
★ Cough bundle-branch block or prolongation of the pre-ejection period with
★ Nausea, with or without vomiting delayed closure of the aortic valve, despite decreased stroke volume.
★ Wheezing A pericardial friction rub may be audible as a to-and-fro
★ Fullness, indigestion, or choking feeling rasping sound.
 ★ Chest
Rales or wheezes may be auscultated these occur secondary
to pulmonary venous hypertension, which is associated with extensive
acute left ventricular MI.
★ Abdomen
Patients frequently develop tricuspid incompetence,
hepatojugular reflux may be elicited even when hepatomegaly is not
marked. A pulsatile abdominal mass may suggest an abdominal aortic
aneurysm.
★ Extremities
Peripheral cyanosis, edema, pallor, diminished pulse volume,
delayed rise, and delayed capillary refill may indicate vasoconstriction,
diminished cardiac output, and right ventricular dysfunction or failure.

➔ Pathophysiology of Myocardial Infarction

 cell shape and organ structures are preserved by coagulation protein
but nucleus disappears.
Causes of Coagulative Necrosis
Hypoxia (lack of oxygen) is the most common condition that
causes cell death in a localized area that is perfused by blood
vessels. When these vessels fail to deliver oxygen and other
important nutrients there is ischemic infarction in that tissue and result
in coagulative necrosis. There is reduced blood flow results in
reduced oxygen and nutrients to the cells which results in hydrolytic
lysis of the cells. When this ischemia occurs in central nervous system
it causes liquefactive necrosis. It is caused by conditions that do not
involve trauma, toxin or immune response.

★ Discuss the Mechanism of Cell Injury and Cell Death with

Emphasis to Ischemic Cell Injury

★ Identify the Necrosis in this Case

Necrosis is death of large group of cells followed by acute

inflammation due to some underlying pathologic process but it is
never physiologic which is called apoptosis.

Coagulative Necrosis:
Coagulative necrosis is an accidental type of cell death
followed by acute inflammation in which underlying tissue architecture
is preserved for at least several days. Necrotic tissue remains firm,
 ★ Describe the Morphologic Alterations in Cell Injury Gangrenous necrosis- usually applied to a limb that has lost is
blood supply and has undergone necrosis involving multiple tissue
Cellular swelling is the first manifestation of almost all forms of planes. Ex. Necrosis of distal foot in diabetic patients
injury to cells
The ultrastructural changes of reversible cell injury include:
1. Plasma membrane alterations, such as blebbing, blunting,
and loss of microvilli.
2. Mitochondrial changes, including swelling and the
appearance of small amorphous densities.
3. Dilation of the Endomplasmic reticulum, with detachment of
polysomes; intracytoplasmic myelin figures may be present.
4. Nuclear alterations, with disaggregation of granular and
fibrillar elements.

Caseous necrosis- encountered most often in tuberculous

infection. The term “caseous”(cheese-like) is derived from the friable
white appearance of the area of necrosis
On microscopic examination the necrotic area appears as a collection
of fragmented or lysed cells and amorphous granular debris enclosed
within a distinctive inflammatory border.

Fat necrosis- refers to focal areas of fat destruction, typically

resulting from release of activated pancreatic lipases into the
substance of the pancreas and the peritoneal cavity.
★ Differentiate Patterns of Tissue Necrosis On histologic examination the necrosis takes the form of foci of
shadowy outlines of necrotic fat cells, with basophilic calcium deposits
Coagulative necrosis – form of necrosis in which the surrounded by an inflammatory reaction. Ex. Occurs in acute
architecture of dead tissues is preserved for a span of at least days. pancreatitis.
The injury denatures not only structural proteins but also enzymes
and so blocks the proteolysis of dead cells. Ex. Infarction Fibrinoid necrosis- usually seen in immune reactions involving
blood vessels.
Typically occurs when complexes of antigens and antibodies are ★ Severe Prolonged Ischemia
deposited in the walls of arteries. Severe swelling of mitochondria, calcium influx into
Deposits of these immune complexes, together with fibrin that has mitochondria and into the cell with rupture of lysosomes and plasma
leaked out of vessels result in a bright pink and amorphous membrane.
appearance in H&E stains. Death by necrosis and apoptosis due to the release of
cytochrome c and mitochondria.

➔ Management and Treatment

Non-pharmacological
★ Discuss the Clinic-Pathologic Correlation and Consequence of ★ Counseling and Education of patients
Ischemic Cell Injury in the Particular Case ★ Lifestyle measure
★ Smoking cessation
40 year old diabetic ★ Avoid alcohol intake
Hypertension ★ Diet and nutrition
30 packs a year smoking history ★ Salt restriction
10-15 min angina per week relieved by nitroglycerine
30 min daily angina attacks Pharmacological
★ Aspirin
★ Mild Ischemia ★ Thrombolytics
Reduced oxidative phosphorylation → Reduced ATP ★ Antiplatelet agents
generation → failure of Na pump → influx of sodium and water → ★ Other blood thinning medications
organelle and cellular swelling (reversible).
★ Pain reliever ➔ Diagnostic Modalities/ Procedures
★ Nitroglycerin
★ Beta blockers ★ Patient History
★ ACE inhibitors Past Medical History
History of Present Illness
Surgical and Other Procedures Family Health History

★ Electrocardiogram
An electrocardiogram (ECG) is the recording of the electrical
activity of the heart and its visible record.
Monitor evolution and resolution of MI. Determine location and
relative size of infarction
12 lead ECG can help to distinguish between ST- elevation MI
and Non-ST-elevation MI.

★ Cardiac Markers
Substances that are released into the blood when the heart is
damaged or stressed. They are the markers measured to evaluate
heart function. These BIOMARKERS are usually test by getting the
serum of the blood, placed it in the red tube and will be processed in
the Clinical Chemistry Department.
MYOGLOBIN
TROPONIN I and T
CK- MB
LACTATE DEHYDROGENASE
 Cardiac CT or MRI
These tests can be used to diagnose heart problems, including
the extent of damage from heart attacks.

➔ Prognosis

Patient has a poor prognosis and a low chance to recover with

therapy due to the following factors which include her Advanced Age,
Diabetes, Obesity, the cumulative loss of functional myocardium
caused by her uncomplicated small myocardial infarction several
years ago, the recurrence of the Disease after Angioplasty several
years ago and her unresponsiveness to treatment like Nitroglycerine.

★ Additional Tests
Chest X-ray
An X-ray image of your chest allows your doctor to check the
size of your heart and its blood vessels and it reveals the
complications of myocardial infarction such as congestive heart
failure.

Echocardiogram
An ultrasound scan of the heart, is able to visualize the heart,
its size, shape, and any abnormal motion of the heart walls as they
beat that may indicate a myocardial infarction.

Coronary Catheterization (Angiogram)

A liquid dye is injected into the arteries of your heart through a
long, thin tube (catheter) that's fed through an artery, usually in your
leg or groin, to the arteries in your heart. The dye makes the arteries
visible on X-ray, revealing areas of blockage.

Exercise Stress Test

Monitor with electrodes that are attached to chest and monitor
the heart response while an individual walks on a treadmill.
CASE 8 ➔ Pathophysiology

A 65 year old-carpenter came in for consultation due to an

enlargement of both his breast for the past six years. He has
beer-belly and had been consuming at least 5 bottles of “red horse”
beer for the past ten years. Biopsy of his breast shows increase in
extracellular matrix with quite a number of ductules.

➔ Salient Features
★ 65 years old
★ Enlargement of breast (past 6 years)
★ Beer belly
★ Consumes 5 bottles of Red Horse (last ten years)
★ Breast biopsy: Increased ECM and ductule proliferation

➔ Differential Diagnosis

➔ Final Diagnosis/ Impression: Gynecomastia Secondary to

Chronic Alcoholism
➔ Management and
Treatment

★ Corrective diet and lifestyle

★ Get more sleep
 ➔ Management and Treatment

★ Corrective diet and lifestyle

★ Get more sleep

➔ Diagnostic Modalities/ Procedures

Laboratory tests that may be considered:

★ Routine laboratory tests
Serum chemistry panel: Total testosterone, luteinizing
hormone, estradiol, and dehydroepiandosterone sulfate levels
★ Tissue biopsy

➔ Prognosis: Fair
With the removal of the primary cause of cause of
gynecomastia and through medical treatment, the patient’s condition
is reversible.
Pateient’s old age is a great factor in increase hormonal
changes (estrogen- androgen ratio) that could delay the patient’s
progress.
Men with gynecomastia have about five-fold greater risk for
developing male breast cancer when compared to the general
population.
CASE 9
➔ Final Diagnosis/ Impression: Barrett’s Esophagus
A 50-year-old security guard presents with a long standing history of
retrosternal burning and belching which he commonly gets after
meals. He has been smoking since the age of 13 and he consumes
five bottles of beer every night. A month ago he was treated for
“gastroesophageal reflux dyspepsia”. Upper gastrointestinal
endoscopy reveals streaks of red to velvety mucosa at the
gastroesophageal junction. Biopsy from this site shows the presence
of gastric and intestinal-type columnar cells.

➔ Salient Features
★ 50 years old
★ Male
★ History of retrosternal burning and belching
★ Started smoking at the age of 13
★ Consumes 5 bottles of beer every night Often diagnosed in people who have long-term
★ Treated a month ago with Gastroesophageal Reflux gastroesophageal reflux disease (GERD) — a chronic regurgitation of
Dyspepsia acid from the stomach into the lower esophagus.
★ Endoscopy: Streaks of red to velvety mucosa at the Metaplasia from squamous to columnar type — esophageal
gastroesophageal junction squamous epithelium is replaced by intestinal-like columnar cells
★ Biopsy: Presence of gastric and intestinal-type of columnar under the influence of refluxed gastric acid.
cells Appears reddish and friable on endoscopy
Presence of goblet cells in the columnar epithelium — hallmark of
➔ Differential Diagnosis disease.

Symptoms:
★ Frequent heartburn
★ Difficulty swallowing food
★ Less commonly, chest pain

Risk Factors:
★ Chronic heartburn and acid reflux
★ Age
★ Being a man
 ★ Being white
★ Being overweight
★ Current or past smoking

➔ Pathophysiology of Barrett’s Esophagus

GERD is accepted as
the primary etiologic factor for
BE.
BE is thought to be the
result of esophageal epithelial
response to injury.
- squamous cell epithelium to
columnar cell epithelium native
epithelium.
*offering greater tolerance to
low pH, but also a tendency
towards dysplastic change
predisposing to esophageal
adenocarcinoma.
Replacement of white lining
squamous mucosa to red velvety
mucosa (an intestinal type of
mucosa) at the gastroesophageal
junction.

➔ Management and Treatment

★ Chemoprevention
Once-daily PPI therapy
Once-daily dosing provides effective symptom relief and tissue
healing in 85–90% of patients; up to 15% of patients require
twice-daily dosing.
Note: Routine use of twice-daily dosing is not recommended,
unless necessitated because of poor control of reflux symptoms or
esophagitis.

PPIs (Acid-suppressing medicines) include:

★ Omeprazole (Prilosec, Zegerid)
★ Lansoprazole (Prevacid)
★ Pantoprazole (Protonix)
★ Rabeprazole (AcipHex)
★ Esomeprazole (Nexium)
★ Dexlansoprazole (Dexilant)
 ★ Endoscopic Therapy
Once Barrett esophagus has been identified, patients should ★ Biopsy
undergo periodic surveillance endoscopy to identify histologic markers The doctor will remove a sample of tissue to be examined
for increased cancer risk (dysplasia) or cancer that is at an earlier under a microscope in the laboratory to confirm the diagnosis.
stage and is amenable to therapy. Dysplasia is the best histologic The sample will also be examined for the presence of
marker for cancer risk. precancerous cells or cancer.
Intestinal metaplasia can be identified by the presence of
★ Surgical Therapy goblet cells on biopsy of the esophageal mucosa.
Antireflux surgery is not be pursued in patients with BE as an
antineoplastic measure. However, this surgery should be considered ➔ Prognosis
in those with incomplete control of reflux on optimized medical
therapy. Patients that undergo regular endoscopic surveillance with
biopsy may identify the cancer at an early stage and the risk of
★ Diet malignant progression among patients with Barrett esophagus is
Patients should avoid the following: lower.
Fried or fatty foods, Chocolate, Peppermint, Alcohol, Coffee, If carcinoma is discovered, then esophagectomy is indicated.
Carbonated beverages, Citrus fruits or juices, Tomato sauce, Generally, adenocarcinomas discovered while screening for Barrett
Ketchup, Mustard, Vinegar. esophagus are early-stage lesions and have good prognosis (5-year
Aspirin and other nonsteroidal anti-inflammatory drugs survival >85%).
(NSAIDs). Even with aggressive acid suppression, proton-pump inhibitor
Patients also should decrease the size of portions at mealtime, treatment does not lead to regression of Barrett esophagus and the
avoid eating 3 hours prior to bedtime, elevate the head of the bed 6 rate of progression to adenocarcinoma is approximately 0.25% to
inches, lose weight (if overweight), and stop smoking. 0.4% per year.
There are reports that antireflux surgery alone can lead to
➔ Diagnostic Modalities/ Procedures regression of Barrett esophagus in more than 25% of patients, and
that surgery lowers the risk for progression to adenocarcinoma.
★ Endoscopy
A nonsurgical procedure used to examine a person’s digestive
tract.
During an upper endoscopy, an endoscope is easily passed
through the mouth and throat and into the esophagus, allowing the
doctor to view the esophagus, stomach and upper part of the small
intestine.
It is used to visually inspect the lining of the esophagus.
Upper endoscopy should demonstrate displacement of the
squamocolumnar junction proximal to the gastroesophageal junction.