Histology of Epidydymis

Histology of Corpus Luteum 2

Histology of Thick Skin

Drawing Blood Sample Venipuncture

Renal Failure Treatment Options

Eye Lid Partial Tarsectomy Surgery

The Respiratory System

The impacts of infertility from the bedroom to the bank account – options to support the journey to parenthood.

A pneumothorax (noo-moe-THOR-aks) is a collapsed lung. A pneumothorax occurs when air leaks into the space between your lung and chest wall. This air pushes on the outside of your lung and makes it collapse. In most cases, only a portion of the lung collapses. A pneumothorax can be caused by a blunt or penetrating chest injury, certain medical procedures, or damage from underlying lung disease. Or it may occur for no obvious reason. Symptoms usually include sudden chest pain and shortness of breath. On some occasions, a collapsed lung can be a life-threatening event. Treatment for a pneumothorax usually involves inserting a flexible tube or needle between the ribs to remove the excess air. However, a small pneumothorax may heal on its own.

LBD is not a rare disease. It affects an estimated 1.4 million individuals and their families in the United States. Because LBD symptoms can closely resemble other more commonly known diseases like Alzheimer’s and Parkinson’s, it is currently widely underdiagnosed. Many doctors or other medical professionals still are not familiar with LBD. LBD is an umbrella term for two related diagnoses. LBD refers to both Parkinson’s disease dementia and dementia with Lewy bodies. The earliest symptoms of these two diseases differ, but reflect the same underlying biological changes in the brain. Over time, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. While it may take more than a year or two for enough symptoms to develop for a doctor to diagnose LBD, it is critical to pursue a formal diagnosis. Early diagnosis allows for important early treatment that may extend quality of life and independence. LBD is a multisystem disease and typically requires a comprehensive treatment approach. This approach involves a team of physicians from different specialties who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms. Many people with LBD enjoy significant improvement of their symptoms with a comprehensive approach to treatment, and some can have remarkably little change from year to year. Some people with LBD are extremely sensitive or may react negatively to certain medications used to treat Alzheimer’s or Parkinson’s in addition to certain over-the-counter medications.

Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal, temporal and parietal lobes, the corona radiata, globus pallidus, caudate and putamen. The MCA is the most common site for the occurrence of ischemic stroke.[1] Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal.[1] In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the oedematus cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion. Contralateral hemiparesis and hemisensory loss of the face, upper and lower extremities is the most common presentation of MCA syndrome.[1] Lower extremity function is more spared than that of the faciobrachial region.[2] The majority of the primary motor and somatosensory cortices are supplied by the MCA and the cortical homunculus can, therefore, be used to localize the defects more precisely.it is important to note that middle cerebral artery lesions mostly affect the dominant hemisphere i.e. the left cerebral hemisphere.

What is polycystic kidney disease? Polycystic kidney disease (also called PKD) causes numerous cysts to grow in the kidneys. These cysts are filled with fluid. If too many cysts grow or if they get too big, the kidneys can become damaged. PKD cysts can slowly replace much of the kidneys, reducing kidney function and leading to kidney failure. How common is PKD? In the United States about 600,000 people have PKD. It is the fourth leading cause of kidney failure. It is found in all races and occurs equally in men and women. It causes about 5% of all kidney failure. What other organs besides the kidney are affected by PKD? PKD can affect other organs besides the kidney. People with PKD may have cysts in their liver, pancreas, spleen, ovaries, and large bowel. Cysts in these organs usually do not cause serious problems, but can in some people. PKD can also affect the brain or heart. If PKD affects the brain, it can cause an aneurysm. An aneurysm is a bulging blood vessel that can burst, resulting in a stroke or even death. If PKD affects the heart, the valves can become floppy, resulting in a heart murmur in some patients. What are the clues that someone has PKD? Most people do not develop symptoms until they are 30 to 40 years old. The first noticeable signs and symptoms may include: Back or side pain An increase in the size of the abdomen Blood in the urine Frequent bladder or kidney infections High blood pressure High blood pressure is the most common sign of PKD. Occasionally, patients may develop headaches related to high blood pressure or their doctors may detect high blood pressure during a routine physical exam. Because high blood pressure can cause kidney damage, it is very important to treat it. In fact, treatment of high blood pressure can help slow or even prevent kidney failure. Fluttering or pounding in the chest About 25% of PKD patients have a so-called floppy valve in the heart, and may experience a fluttering or pounding in the chest as well as chest pain. These symptoms almost always disappear on their own but may be the first hint that someone has PKD. How is PKD diagnosed? Ultrasound is the most reliable, inexpensive and non-invasive way to diagnose PKD. If someone at risk for PKD is older than 40 years and has a normal ultrasound of the kidneys, he or she probably does not have PKD. Occasionally, a CT scan (computed tomography scan) and MRI (magnetic resonance imaging) may detect smaller cysts that cannot be found by an ultrasound. MRI is used to measure and monitor volume and growth of kidneys and cysts. In some situations, genetic testing might also be done. This involves a blood test that checks for abnormal genes that cause the disease. Genetic testing is not recommended for everyone. The test is costly, and it also fails to detect PKD in about 15% of people who have it. However, genetic testing can be useful when a person: has an uncertain diagnosis based on imaging tests has a family history of PKD and wants to donate a kidney is younger than 30-years old with a family history of PKD and a negative ultrasound, and is planning to start a family

Interstitial cystitis is a clinical syndrome characterized by daytime and nighttime urinary frequency, urgency, and pelvic pain of unknown etiology. Interstitial cystitis has no clear etiology or pathophysiology, and diagnostic criteria for the syndrome remain undefined. Despite considerable research, universally effective treatments do not exist; therapy usually consists of various supportive, behavioral, and pharmacologic measures. Surgical intervention is rarely indicated. The International Continence Society has coined the term painful bladder syndrome (suprapubic pain with bladder filling associated with increased daytime and nighttime frequency, in the absence of proven urinary infection or other obvious pathology) and reserves the diagnosis of interstitial cystitis for patients with characteristic cystoscopic and histologic features of the condition.[1] An international consensus panel was able to generally agree on the following definition of interstitial cystitis/bladder pain syndrome (IC/BPS): unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder and associated with lower urinary tract symptoms of more than 6 weeks duration, in the absence of infection or other identifiable causes. American Urological Association (AUA) guidelines published in 2011 and amended in 2014 use an evidence-based approach to provide a clinical framework for the diagnosis and management of this condition.[2, 3, 4] In 1887, Skene initially described a condition characterized by inflammation that destroyed the urinary bladder "mucous membrane partly or wholly and extended to the muscular parietes." Guy Hunner popularized the disease with the description of characteristic bladder wall ulcers in association with a symptom complex of chronic bladder inflammation.[5] The first comprehensive epidemiologic description of interstitial cystitis is credited to Hand, who in 1949 described the widespread, small, submucosal bladder hemorrhages and the significant variation in bladder capacity characteristic of the condition. Despite years of intensive research, there are no specific clinical or urinary markers currently clinically available; no absolutely specific radiographic, laboratory, or serologic findings; and no biopsy patterns that are pathognomonic for interstitial cystitis. Some research suggests that the following may all play a role in the disease pathophysiology: (1) pelvic floor dyfunction, (2) dysregulated immune or inflammatory signals, (3) neural hypersensitivity, and (4) disruption of the proteoglycan/glycosaminoglycan (GAG) layer.[6] Interstitial cystitis, howerver, remains a diagnosis of exclusion (see Presentation, DDx, and Workup.) Intensive study has been done to attempt to identify biomarkers for IC/BPS. Some interesting studies have shown that bladder nitric oxide is an accurate marker for Hunner lesions, but these are not present in all patients, and the test requires specific equipment, which has limited widespread clinical use.[7] Differences in levels of cytokines and chemokines, specifically CXCL-10, have shown some ability to differentiate patients with and without Hunner lesions.[8] Other studies of ulcerative IC/BPS have shown that numerous other cytokines and chemokines are up-regulated as well, heralding a possible urinary test to identify patients.[9] An additional substance shown to be up-regulated in IC/BPS patients is antiproliferative factor (APF). This small 8–amino-acid peptide has been associated with suppression of cell growth, increases in transcellular permeability, and lowering of levels of proteins that form intercellular junctional complexes. It is synthesized and secreted from bladder epithelial cells from patients with IC/BPS and may play a key role in pathophysiology.[10] In vitro studies have shown that removal of APF from cell culture media restored cell proliferation and membrane integrity.[11] Studies have also suggested APF in the therapeutic effect of hydrodistension in patients with IC/BPS, although further confirmatory studies are necessary.[12] The most important element in treating patients with interstitial cystitis is education and emotional support. Periodic exacerbations are managed as they occur because no long-term therapy has been shown to prevent or delay recurrent episodes. Therefore, the purpose of treatment is to palliate and alleviate symptoms. Because no discrete pathognomonic pathologic criteria exist for assessing and monitoring disease severity, indications and goals for treatment are based on the degree of patient symptoms. Assessing patient response to treatment is also complicated because of the subjective nature of symptoms; the waxing and waning nature of symptoms without treatment; and the lack of objective serologic, physical, or histopathologic findings. Conservative measures and oral or intravesical treatments are considered first-line treatment. (See Treatment.)

Tetralogy of Fallot (teh-TRAL-uh-jee of fuh-LOW) is a rare condition caused by a combination of four heart defects that are present at birth. These defects, which affect the structure of the heart, cause oxygen-poor blood to flow out of the heart and to the rest of the body. Infants and children with tetralogy of Fallot usually have blue-tinged skin because their blood doesn't carry enough oxygen. Tetralogy of Fallot is often diagnosed during infancy or soon after. However, tetralogy of Fallot might not be detected until later in life, depending on the severity of the defects and symptoms. With early diagnosis followed by appropriate surgical treatment, most children who have tetralogy of Fallot live relatively normal lives, though they'll need regular medical care and might have restrictions on exercise.

The incidence of digitalis toxicity has declined in recent years, due to decreased use of this drug along with improved technology for monitoring of drug levels and increased awareness of drug interactions. Nevertheless, cardiac glycoside toxicity continues to be a problem in the United States because of the wide use of digoxin (a preparation of digitalis) and its narrow therapeutic window. Digitalis is a plant-derived cardiac glycoside commonly used in the treatment of chronic heart failure (CHF), atrial fibrillation, and reentrant supraventricular tachycardia.[1, 2] Digoxin is the only available preparation of digitalis in the United States. (See Etiology and Epidemiology.) Cardiac glycosides are found in certain flowering plants, such as oleander and lily-of-the-valley. Indigenous people in various parts of the world have used many plant extracts containing cardiac glycosides as arrow and ordeal poisons. The ancient Egyptians used squill (Urginea maritime) as a medicine. The Romans employed it as a diuretic, heart tonic, emetic, and rat poison. Digitalis, or foxglove, was mentioned in the year 1250 in the writings of Welsh physicians. Fuchsius described it botanically 300 years later and named it Digitalis purpurea. William Withering published his classic account of foxglove and some of its medical uses in 1785, remarking upon his experience with digitalis. He recognized many of the signs of digitalis toxicity, noting, "The foxglove, when given in very large and quickly repeated doses, occasions sickness, vomiting, purging, giddiness, confused vision, objects appearing green or yellow; increased secretion of urine, slow pulses, even as low as 35 in a minute, cold sweats, convulsions, syncope, death." (See Presentation and Workup.) During the early 20th century, as a result of the work of Cushny, Mackenzie, Lewis, and others, the drug was gradually recognized as specific for treatment of atrial fibrillation. Only subsequently was the value of digitalis for treatment of CHF established. Cardiac glycosides enhance cardiac contractility and slow conduction through the atrioventricular (AV) junction by increasing vagal tone.[3] (See Etiology.) Cardiac glycoside toxicity has been known to result from ingestion of some plants, including yellow oleander (Thevetia peruviana) and foxglove, and a similar toxidrome has been associated with the use of herbal dietary supplements that contain cardiac glycosides. Digoxin is among the top 50 prescribed drugs in the United States.[4] In 2011, the American Association of Poison Control Centers reported 1601 single exposures to cardiac glycoside drugs.[5] Cardiac glycosides account for 2.6% of toxic plant exposures in the United States.[6, 7] Most of these exposures are in children.[7] (See Epidemiology.) Digoxin-specific fragment antigen-binding (Fab) antibody fragments have contributed significantly to the improved morbidity and mortality of toxic patients since their approval in 1986 by the US Food and Drug Administration (FDA). (See Prognosis, Treatment, and Medication.)

6 Weird Things That Happen To Us During Sleep

A traumatic brain injury (TBI) is defined as a blow or jolt to the head, or a penetrating head injury that disrupts the normal function of the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate or severe, depending on the extent of damage to the brain. Mild cases (mild traumatic brain injury, or mTBI) may result in a brief change in mental state or consciousness, while severe cases may result in extended periods of unconsciousness, coma or even death. The 4th International Conference on Concussion in Sport held in Zurich, Switzerland in 2012 defined concussion, a subset of mTBI, as the following: Concussion is the historical term representing low velocity injuries that cause brain ‘shaking’ resulting in clinical symptoms and that are not necessarily related to a pathological injury. Concussion is a subset of TBI and will be the term used in this document. It was also noted that the term commotio cerebri is often used in European and other countries. Minor revisions were made to the definition of concussion, which is defined as follows: Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include: 1. Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an "impulsive" force transmitted to the head. 2. Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously. However, in some cases, symptoms and signs may evolve over a number of minutes to hours. 3. Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury and, as such, no abnormality is seen on standard structural neuroimaging studies. 4. Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. However, it is important to note that in some cases symptoms may be prolonged. To view peer reviewed literature related to sports concussions, the Sports Concussion Library can be found here. Incidence The U.S. Consumer Product Safety Commission (CPSC) tracks product-related injuries through its National Electronic Injury Surveillance System (NEISS). According to CPSC data, there were an estimated 446,788 sports-related head injuries treated at U.S. hospital emergency rooms in 2009. This number represents an increase of nearly 95,000 sports-related injuries from the prior year. All of the 20 sports noted below posted increases in the number of injuries treated in 2009, except for trampolines, which posted 52 fewer injuries in 2009. Sports that exhibited substantial increases from 2008 to 2009 included water sports (11,239 to 28,716*), cycling (70,802 to 85,389), baseball and softball (26,964 to 38,394) and basketball (27,583 to 34,692). *Four categories were tabulated by the AANS in the current analysis that were not reflected in the 2008 injury data analysis, but together, these account for only 1,397 injuries. The actual incidence of head injuries may potentially be much higher for two primary reasons. 1). In the 2009 report, the CPSC excluded estimates for product categories that yielded 1,200 injuries or less, those that had very small sample counts and those that were limited to a small geographic area of the country; 2). Many less severe head injuries are treated at physician's offices or immediate care centers, or are self-treated. Included in these statistics are not only the sports/recreational activities, but the equipment and apparel used in these activities. For example, swimming-related injuries include the activity as well as diving boards, equipment, flotation devices, pools and water slides. The following 20 sports/recreational activities represent the categories contributing to the highest number of estimated head injuries treated in U.S. hospital emergency rooms in 2009.

Endometriosis (en-doe-me-tree-O-sis) is an often painful disorder in which tissue that normally lines the inside of your uterus — the endometrium — grows outside your uterus. Endometriosis most commonly involves your ovaries, fallopian tubes and the tissue lining your pelvis. Rarely, endometrial tissue may spread beyond pelvic organs. With endometriosis, displaced endometrial tissue continues to act as it normally would — it thickens, breaks down and bleeds with each menstrual cycle. Because this displaced tissue has no way to exit your body, it becomes trapped. When endometriosis involves the ovaries, cysts called endometriomas may form. Surrounding tissue can become irritated, eventually developing scar tissue and adhesions — abnormal bands of fibrous tissue that can cause pelvic tissues and organs to stick to each other.

Lung Sounds - Rales, Rhonchi, Wheezes

A hemangioma (he-man-jee-O-muh) is a birthmark that most commonly appears as a rubbery, bright red nodule of extra blood vessels in the skin. A hemangioma grows during the first year of life, and then recedes over time. A child who had a hemangioma during infancy usually has little visible trace of the growth by age 10.