3rd Nerve Palsy

Home Medical Advisor Program

A geat program for doctors and medical students. It`s very nice in diagonosis and detection of diseases by some history questions.Also it provides informations about drugs and treatment.


For free DOWNLOAD:


CLICK HERE

Breast Mass Examination

Diagnosis Of Acromegaly

Clinical:
History
* Symptoms due to local mass effects of the tumor
o Symptoms depend on the size of the intracranial tumor.
o Headaches and visual field defects are the most common symptoms. Visual
field defects depend on which part of the optic nerve pathway is
compressed.
o The most common manifestation is a bitemporal hemianopsia due to
pressure on the optic chiasm.
o Tumor damage to the pituitary stalk might cause hyperprolactinemia due
to loss of inhibitory regulation of prolactin secretion by the
hypothalamus. Damage to normal pituitary tissue can cause deficiencies
of glucocorticoids, sex steroids, and thyroid hormone.
o Loss of end organ hormones is due to diminished anterior pituitary
secretion of corticotropin (ie, adrenocorticotropic hormone [ACTH]),
gonadotropins (eg, luteinizing hormone [LH], follicle-stimulating
hormone [FSH]), and thyrotropin (ie, thyroid-stimulating hormone [TSH]).
* Symptoms due to excess of GH/IGF-I
o Soft tissue swelling and enlargement of extremities
o Increase in ring and/or shoe size
o Hyperhidrosis
o Coarsening of facial features
o Prognathism
o Macroglossia
o Arthritis
o Increased incidence of obstructive sleep apnea
o Increased incidence of glucose intolerance or frank diabetes mellitus,
hypertension, and cardiovascular disease
o Hyperphosphatemia, hypercalcuria, and hypertriglyceridemia possible
o Increased incidence of congestive heart failure, which might be due to
uncontrolled hypertension or to an intrinsic form of cardiomyopathy
attributable to excess GH/IGF-I
o Increased incidence of colonic polyps and adenocarcinoma of the colon

Physical
* Typical facies of acromegaly
o Frontal bossing
o Thickening of the nose
o Macroglossia
o Prognathism
* Women can have mild hirsutism.
* The thyroid gland might be enlarged and typically manifests as multinodular
goiter.
* Enlarged extremities with sausage-shaped fingers are signs of acromegaly.
* Skin is oily and has skin tags. Skin tags are possible markers for colonic
polyps.

Causes
* Acromegaly can be either GHRH independent or GHRH dependent. Both forms cause
identical clinical syndromes.
* Most cases are GHRH independent. Elevated GH concentration suppresses GHRH
production by the hypothalamus.
o More than 95% of the GHRH-independent cases are due to a GH-secreting
pituitary tumor. The pituitary adenoma might be a macroadenoma (>1 cm)
or a microadenoma (<1 style="color: rgb(51, 102, 255);">Laboratory Studies
* Random GH measurements are often not diagnostic because of the episodic
secretion of GH, its short half-life, and the overlap between GH concentration
in acromegalic patients and healthy subjects.
* Because GH secretion is inhibited by glucose, measurement of glucose
nonsuppressibility might be useful. Two baseline GH levels are obtained prior
to ingestion of 75 or 100 g of oral glucose, and additional GH measurements
are made at 30, 60, 90, and 120 minutes following the oral glucose load.
o Patients with active acromegaly are unable to suppress GH concentration
below 2 ng/mL after a 75-g oral glucose load. With newer assays for GH
using the immunoradiometric assay (IRMA), a criterion of less than 1
mcg/L is used following oral glucose ingestion.
o A paradoxical rise in GH concentration is observed in 15-20% of patients
with acromegaly following oral glucose ingestion.
* Because IGF-I has a long half-life, its measurement is useful to gauge
integrated GH secretion, to screen for acromegaly, and to monitor the efficacy
of therapy.
o IGF-I concentrations vary with age. An assay in which reference ranges
have been stratified in such a manner is required.
o Starvation, obesity, and diabetes mellitus decrease IGF-I concentration.
o Pregnancy increases IGF-I concentration.
* Measurement of IGF-binding protein-3 (IGFBP-3), the main binding protein for
circulating IGF, is increased in acromegaly and might be useful in the
diagnosis of acromegaly. Measurement may also be helpful in following the
activity of the disease during treatment.
* GHRH concentration can be obtained if clinically indicated.
o Levels of less than 300 pg/mL usually indicate an ectopic source of GHRH.
o In pituitary disease (GHRH independent), GHRH concentration is within
reference ranges or suppressed.
* Because up to 20% of GH-secreting pituitary adenomas cosecrete prolactin, the
prolactin level may also be elevated. However, as indicated above, a rise in
prolactin can be due to stalk compression as well as co-secretion from a
pituitary adenoma.
* Pituitary adenomas can be associated with deficiencies of other pituitary
hormones. Consider evaluation of the adrenal, thyroid, and gonadal axes.
Imaging Studies: CLICK HERE
* Because of the relatively high incidence of nonfunctioning, incidentally
discovered pituitary adenomas, obtain imaging studies only after a firm
biochemical diagnosis of acromegaly.
* Because GH-secreting pituitary adenoma is the most common cause, perform
imaging of the sella turcica first.
o MRI is more sensitive than CT scan.
o MRI provides detailed information about surrounding structures such as
the optic chiasm and cavernous sinuses.
* If the MRI findings of the sella are negative, appropriate studies to localize
tumors causing ectopic secretion of GH or GHRH can be obtained.
o CT scan of the abdomen/pelvis evaluates for pancreatic, adrenal, or
ovarian tumors secreting GH/GHRH.
o Chest CT scanning evaluates for bronchogenic carcinoma secreting GH/GHRH.
source:www.emedicine.medscape.com FOLLOW PART 2

Treatment Of Acromegaly

Medical Care:

Because elevated GH/IGF-I concentration is associated with increased mortality rates, try to decrease/normalize their concentration. Most experts define cure, or adequate control, as a glucose-suppressed GH concentration of less than 2 ng/mL by radioimmunoassay (RIA) (1 mcg/L by IRMA) and normalization of the serum IGF-I concentration.

No single modality of treatment consistently achieves the above levels. A multimodality approach usually requires surgery as the first line of treatment, followed by medical therapy for residual disease. Radiation treatment is generally reserved for refractory cases.

1* Somatostatin and dopamine analogues and GH receptor antagonists are the mainstays of medical treatment and are generally used after failure of primary surgery to induce complete remission.
2* Bromocriptine is a dopamine agonist with limited effectiveness in the treatment of acromegaly. It can reduce the circulating GH level to less than 5 ng/mL in only 20% of patients and can normalize the IGF-I concentration in 10% of patients. Shrinkage in tumor size is also observed in fewer than 20% of patients. Cabergoline, another dopamine agonist, fares somewhat better with response rates of 46%.
3* Tumors that cosecrete prolactin have a better response rate to dopamine agonists. The response to these agents is often detected by a trial of the drug in suitable patients.
4* Somatostatin is a natural inhibitor of GH secretion. Because of its very short half-life, long-acting analogues have been developed. The long-acting analogue can be administered once per month but is extremely expensive (>$12,000/y in 1999).
o Octreotide is the most extensively studied and used somatostatin
analogue.
o It primarily binds to the somatostatin receptor subtypes II and V and
inhibits GH secretion.
o Treatment with octreotide reduces GH concentration to less than 5 ng/mL
in 65% of patients and to less than 2 ng/mL in 40% of patients; it
normalizes concentration IGF-I in 60% of patients.
o Tumor shrinkage is observed in 20-50% of patients.
5* Pegvisomant, a GH receptor antagonist normalizes IGF-I levels in 90-100% of patients. As expected from its mechanism of action, GH levels increase during treatment and no decrease in tumor size is seen. A minority of patients may experience an increase in tumor size; whether this is due to natural history of the disease or an effect of treatment is unclear. Periodic imaging studies are advised in patients on this medication.
6* Radiation treatment takes to reduce/normalize GH/IGF-I levels. About 60% of patients have a GH concentration of less than 5 ng/mL 10 years after radiotherapy. A similar percentage of patients develop panhypopituitarism as a result of treatment. Because of the disappointing results and adverse effects, radiotherapy is used as an adjuvant for large invasive tumors and when surgery is contraindicated. Some studies suggest that radiation is associated with the development of secondary tumors.

Surgical Care:

Even though surgery might not cure a significant number of patients, it is employed as first-line therapy. Patients with residual disease can then be offered adjuvant treatment.

* Transsphenoidal hypophysectomy has the dual advantage of rapidly improving
symptoms caused by mass effect of the tumor and significantly reducing or
normalizing GH/IGF-I concentrations CLICK HERE
* Remission depends on the initial size of the tumor, the GH level, and the
skill of the neurosurgeon.
* A remission rate of 80-85% can be expected for microadenomas and 50-65% for
macroadenomas.
* The postoperative GH concentration may predict remission rates. According to
the results of one study, a postoperative GH concentration of less than 3
ng/dL was associated with a 90% remission rate, which declined to 5% in
patients with postoperative GH concentration greater than 5 ng/dL.

Prognosis:

-Remission depends on the initial size of the tumor, the GH level, and the skill of the neurosurgeon.

* Remission rates of 80-85% and 50-65% can be expected for microadenomas and
macroadenomas, respectively.
* The postoperative GH concentration may predict remission rates. According to
the results of one study, a postoperative GH concentration of less than 3
ng/dL was associated with a 90% remission rate, which declined to 5% in
patients with a postoperative GH concentration greater than 5 ng/dL.

Cervical Spine & Upper Limb Examination

Intra-abdominal lump examination

Breast Examination

Periphral Vascular System Examination

Part 1


Part 2


Part 3


Part 4

Ischemia & Gangrene

Medicating for High Blood Pressure

THORACENTESIS

COMPLICATION OF THORACOCENTESIS:

1. Pneumothorax: There are two types of pneumothoraxes which can follow a Thoracentesis.

The first one is secondary to the introduction of air from the outside. This is benign and does not give rise to any symptoms. It should be left alone.

The second type of Pneumothorax occurs due to an accidental puncture of the lung. If the patient is asymptomatic, keep him under observation and follow the patient's progress with a serial chest x-ray. Usually, the puncture in the lung seals and air will be absorbed spontaneously. If the patient is symptomatic, chest tube drainage may be necessary.
2. Hemothorax: Bleeding is a possibility during a Thoracentesis. Fortunately, this is rare. Injury to an intercostal artery is fortunately rare since physicians seem to be aware of their location and avoid it during Thoracentesis.
3. Vaso-Vagal Syncope
4. Empyema Empyema is a dreaded complication. Follow strict surgical aseptic techniques to avoid it.
5. Laceration of the Liver or Spleen
6. Tumor Seeding Implantation of tumor cells through a Thoracentesis needle track is an infrequent complication. This occurs with a high degree of frequency in patients with Mesothelioma and may pose problems. However, with other tumors, it is of little significance.
7. Pain Pain during the procedure is due to poor technique in the use of a local anesthetic. Occasionally you may encounter a patient who is so high strung that even touching him may cause pain! Try premedication and reassurance if this should be the case. Mild pain is to be anticipated for 24 hours after the procedure. If the patient complains of shoulder pain during the procedure, it indicates that the needle is piercing the diaphragmatic pleura. The site of the tap is too low.
8. Extravasation of Fluid
Subcutaneous Seroma: If the fluid is under tension, extravasation can occur along the needle track to the subcutaneous tissue. In some patients, this is massive, disfiguring chest and abdominal wall. Anticipate this complication in massive effusions, particularly when the fluid spurts out or fills the syringe forcefully during the Thoracentesis. You may want to release the pressure by evacuating some fluid and following it up with a firm pressure bandage. Should this occur, reassure the patient. Usually, it gets reabsorbed in a matter of days.
9.Reexpansion pulmonary edema. As such, therapeutic thoracentesis is one of the most commonly performed medical procedures. Although complete drainage is generally desirable to maximize the improvement in a patient’s symptoms, to minimize the potential for subsequent procedures, to predict the success of pleurodesis for malignant pleural effusions, and to optimize postdrainage chest imaging, expert consensus suggests limiting drainage in one setting to 1 L to avoid reexpansion pulmonary edema (RPE) .

CASE OF THE WEEK

Clinical presentation:

Middle aged man, smoker, with weight loss and recent onset of cough.

The left lung is reduced in volume and its vessel-count is reduced. There is complex lobulated widening of the upper mediastinum with loss of the right para-tracheal stripe and a triangular density behind the heart on the left side. The basal artery and the hilar point have disappeared into this density and the descending aorta is not seen. The left hemidiaphragm is obscured. There is a soft tissue mass on the right side of the neck.

post your diagnosis in comments.

for more information review chest posts in the site:
http://doctorsgate.blogspot.com/search/label/CHEST

PROSTATE Cancer Explanation [3D]

A 75-Year-Old Man With Worsening Dyspnea Following Pneumothorax Treatment

A 75-year-old man presents to the emergency department with a dry cough and dyspnea on exertion. The cough began 2 weeks ago and has been progressively worsening. The patient began experiencing dyspnea approximately 1 week ago. He notes that there has also been left-sided chest pain. The patient has a history of coronary artery disease with a recent coronary bypass surgery, recurrent episodes of bilateral spontaneous pneumothoraces, and chronic obstructive pulmonary disease (COPD). He has smoked an average of 15 cigarettes daily for 40 years. His symptoms have drastically worsened by the time of presentation to the ED.

On physical examination, heart rate of 142 bpm (sinus rhythm), a respiratory rate of 41 breaths/min, a blood pressure of 170/100 mm Hg, and a pulse oximetry reading showing an oxygen saturation of 60% while breathing room air. He appears agitated, uncomfortable, and in respiratory distress. His airway is patent and he speaks single words at a time. His breathing is labored and peripheral cyanosis is appreciated. He has no breath sounds in the left hemithorax, but normal air movement is noted in the right hemithorax. Additionally, no murmurs or friction rubs are appreciated. The left hemithorax is tympanic to percussion and there is no tenderness to palpation. No tracheal deviation is noted.

The patient is immediately placed on supplemental oxygen, and he maintains an PO2 of approximately 90%. While a stat portable chest radiograph is performed, preparations are made for emergency tube thoracostomy placement. The radiograph (see 1st x-ray) reveals a left-sided tension pneumothorax. An emergency left-sided tube thoracostomy is inserted under local anaesthesia in the left fourth intercostal space at the midaxillary line. A large rush of air is appreciated. After draining the pneumothorax, the clinical picture rapidly improves. At this point the patient becomes much less dyspneic, with a respiratory rate of 22 breaths/min, a blood pressure of 124/63 mm Hg, a heart rate of 90 bpm (normal sinus rhythm), and 92% SPO2 via face mask.

10 minutes later, the patient experiences dramatic worsening of his condition,as shortness of breath. The respiratory rate rises to 32 breaths/min and the SPO2 drops to 80% despite the administration of oxygen via a nonrebreather mask. The blood pressure is maintained at 120/74 mm Hg, with a heart rate of 118 bpm (sinus rhythm). Crackles are now heard over the left lung, most prominently at the base. A blood gas analysis reveals a pH of 7.30, a PCO2 of 35.4 mm Hg, a PO2 of 52.8 mm Hg, and a bicarbonate level of 17.2 mEq/L (17.2 mmol/L), with a base excess of -7.9 mEq/L. As the patient is prepared for a new chest radiograph (2nd x-ray), empiric treatment is initiated with medications.

What is the most likely etiology of the patient’s deterioration?
Atelectasis

Pulmonary embolus

Recurrent pneumothorax

Reexpansion pulmonary edema

63 year old man with mild fever and cough

PA view of chest Xray of a 63 year old man who undergone recent renal transplant came to the hospital complaining of mild fever and cough associated with headache for more than 1 month duration.And he has had recent weight loss also.
Comment on this Xray?
What are the other Physical signs you would expect in this patient?

Dealing with a fractured humerus

SYMPTOMS OF KIDNEY STONE

Kidney Stones part 3

ElIMINATION OF KIDNEY STONE:

Initial treatment for kidney stones aims at relieving pain. This may include strong narcotic based pain relief such as morphine. If pain and other symptoms are severe, admission to hospital may be necessary so that pain relief and fluids can be given via a drip into a vein (intravenously). If infection is suspected or shown to be present, antibiotic medications may be given.

Underlying medical conditions will need to be identified and treated in order to prevent recurrence of the kidney stones.
In the majority of cases the kidney stones will pass by themselves. In these cases the only treatment required is adequate pain relief and plenty of fluids and rest.

In cases where the stones are too large to pass, the pain is excessive, there is evidence of kidney damage or infection, further treatment to remove the stones may be necessary.

SURGERY:

The different surgical techniques used to remove kidney stones include:

*Ureteric stone removal – Where a tube is passed via the urethra and bladder
into the ureter, where the kidney stones are located and removed.
*Percutaneous nephrolithotomy – Where a thin tube (nephrostomy tube) is inserted
directly into the kidney through the skin. The stone is located and removed via
the tube or shattered by ultrasonic waves.
*Open surgery – This may be necessary if the stones are large, are lodged in the
kidney, and other techniques to remove the stones are unsuitable.


LITHOTRIPSY (extracorporeal shock wave lithotripsy – ESWL):

Lithotripsy is a non-invasive alternative to surgery that uses high-energy shock waves to shatter the stones. Once the stones are disintegrated, the sand-like fragments that remain pass out of the body in the urine. Large stones may require more than one lithotripsy treatment.

Kidney Stones part 2

SYMPTOMS OF KIDNEY STONES:

A few people have and pass small kidney stones without experiencing pain.
A kidney stone attack has classic symptoms: the most agonizing pain in the lower back just below the ribs spreading around to the front of the abdomen and often extending into the groin area. The pain may come in waves as the stone tries to move through the ureter.

Sometimes there will be blood in the urine. Often there is nausea, fever and chills, and vomiting. The abdomen or lower back may be painful to touch.
The severity of the pain is no indicator of the size of the passing kidney stone. This pain is often described as the worst pain a person has ever suffered . It is reported to be more painful than gun shots, surgery, broken bones, or even burns. The pain is not a result of the stone moving or tearing the ureter as a sufferer might suspect. Rather, the pain is caused by the dilating or stretching of the urinary tract being blocked by the stone when it gets stuck in the ureter.

More than one million people in the United States are hospitalized each year because of kidney stone attacks. A suffer should call their doctor or go to the hospital emergency room if they experience severe or persistent bleeding, if the pain continues to be severe, unrelenting and persistent, or if fever and chills or nausea and vomiting develop.

During a kidney stone attack the sufferer should drink large amounts of water (two to three quarts per day). Stay active. Do not go to bed (except for normal sleep periods). Physical activity may actually assist passage of the kidney stones.

Kidney Stones part 1

There are different types of kidney stones, classified by the substances that form them. The different types include:

1.Calcium stones:
Approximately 80% of all kidney stones are calcium stones. They are composed of calcium in combination with either phosphate or oxalate. These occur when there are excess levels of calcium circulating in the blood.

2.Uric acid stones:
Approximately 10% of all kidney stones are uric acid stones. These occur when excess amounts of uric acid are present in the blood. Approximately 50% of people with this type of kidney stone also develop gout – a painful form of arthritis caused by solid deposits of uric acid in the joints.

3.Struvite stones:
Approximately 5% of all kidney stones are struvite stones. They are composed of magnesium ammonium phosphate and tend to occur in people who have repeated urinary tract infections.

4.Cystine stones:
Approximately 2% of all kidney stones are cystine stones. Cystine is a type of amino acid. People with cystine stones usually have an abnormality with the way their body processes amino acids in the diet.


CAUSES OF KIDNEY STONES:

There are many potential causes of kidney stone formation. In general they are the result of a super concentration of chemicals in the urine that results in crystals being formed. This may be brought on by one or more of the following:

* a family genetic predisposition to form stones;
* an excess of calcium or certain other minerals in the diet (sometimes due to
local geographic water or soil conditions);
* intake of excess uric acid, certain medications, Vitamin C, or Vitamin D;
* a diet of fruits and vegetables high in oxalate (a by product of metabolism);
* long term dehydration (possibly due to inadequate intake of fluids) and its
resulting concentration of urine;
* urinary infection;
* living in an area where high temperatures cause sweating and loss of fluids; or
* possibly, just leading a sedentary (low physical activity) lifestyle.

The main function of the kidneys is to eliminate byproducts of metabolism.This means they are constantly collecting the major ingredients for kidney stones - including calcium, oxalate, and uric acid.These minerals are kept in suspension until they are passed out of the body. Too much metabolic byproducts in insufficient fluid (urine) makes a person prone to kidney stone formation.

The over concentration of metabolic byproducts in the urine can cause these minerals to move out of suspension and crystallize. These small crystals that precipitate out of the super saturated urine will usually pass on out through the urinary tract, but they may begin to clump together. Any existing crystal makes it easier for other crystals to form. If they stay in the kidney very long, the crystals gradually grow larger and larger until they become a kidney stone so large that it cannot pass through the urinary tract.

Many underlying metabolic disorders may be the root cause of excessive calcium and oxalate forming stones in the kidney. Often doctors overlook the basic cause because of the attention of the sufferer being on the immediate cause of the pain leading the physician to be primarily concerned with the extraction or dissolution of the kidney stone causing the problem. The potential root causes include, but are not limited to the following:
1. A re-absorption of the calcium from the bones back into the blood system
which the kidneys then filter out (resorptive hypercalciuria or
hyperparathyroidism).
2. The intestines absorb too much calcium from the diet (absorptive
hypercalciuria).
3. The kidneys filter out calcium from the blood but do not allow the reaborption
of the calcium back into the blood as it should while it is still in the
tubule of the kidney (renal hypercalciuria).
4. Several forms of bowel disease (ulcurative colitis, regional enteritis, etc.)
which can contribute to high levels of urinary oxalate excretion.
5. Excess dietary intake of oxalate from foods such as green leafy vegatables.
(See list of high oxalate foods.)
6. High levels of uric acid in the urine can act as a breeding ground for calcium
oxalate stones.
7. Or, in a reverse manner, the lack of certain stone formation inhibitors
normally found in the urine may not be present in sufficient quantities and
thereby allow the formation of stones. One such indigredient is citrate (which
this author is deficient in); another is magnesium.
8. Infection stones are indicators of the underlying infection in the urinary
tract.

Clinical Surgery Lectures - 01 Introduction

Clinical Surgery Lectures - 03 Swellings

3D Medical Animation - What is Cancer?

Brain Anatomy and Functions