Alagille syndrome (AS) is an autosomal dominant disorder (OMIM 118450) associated with abnormalities of the liver, heart, skeleton, eye, and kidneys and a characteristic facial appearance. In 1973, Watson and Miller reported 9 cases of neonatal liver disease with familial pulmonary valvular stenosis.

Anatomy of The Gastrointestinal Tract GIT

Anatomy of The Superficial Dissection of The Upper and Lower Limbs

TRANSUMBILICAL SINGLE SITE LAP CHOLYCYSTECTOMY

Your stomach must be empty, so you should not eat or drink anything for approximately 8 hours before the examination. Your physician will be more specific about the time to begin fasting depending on the time of day that your test is scheduled. Your current medications may need to be adjusted or avoided. Most medications can be continued as usual. Medication use such as aspirin, Vitamin E, non-steroidal anti-inflammatories, blood thinners and insulin should be discussed with your physician prior to the examination as well as any other medication you might be taking. It is therefore best to inform your physician of any allergies to medications, iodine, or shellfish. It is essential that you alert your physician if you require antibiotics prior to undergoing dental procedures, since you may also require antibiotics prior to ERCP. Also, if you have any major diseases, such as heart or lung disease that may require special attention during the procedure, discuss this with your physician. To make the examination comfortable, you will be sedated during the procedure, and, therefore, you will need someone to drive you home afterward. Sedatives will affect your judgment and reflexes for the rest of the day, so you should not drive or operate machinery until the next day.

Watch that video of an Ingrown hair turned into 140-pound tumor in man’s stomach

Histology of Thymus

Nursing skills lab procedure for IV insertion.

Histology of Testis

Basic Respiratory Clinical Exam Video

Assisted Birth Delivery HD

Ellis demonstrates how to administer an intradermal, subcutaneous, and intramuscular injection.

Our Critical Nursing Skills video tutorial series is taught by Ellis Parker MSN, RN-BC, CNE, CHS and intended to help RN and PN nursing students study for your nursing school exams, including the ATI, HESI and NCLEX.

#NCLEX #ClinicalSkills #injections #HESI #Kaplan #ATI #NursingSchool #NursingStudent⁠ #Nurse #RN #PN #Education #LVN #LPN #nurseeducator

00:00 What to expect
00:20 Intradermal injections
00:35 Cleaning site
00:54 Explaining bevel up
1:40 Inserting needle
2:00 Injecting medication
2:16 Withdrawing needle
2:29 Subcutaneous Injections
2:39 Selecting site for subcutaneous injections
3:08 Cleaning subcutaneous injections site
3:18 Pinching subcutaneous injections site
3:30 Inserting needle subcutaneous injections
4:13 Injecting medication subcutaneous injections
4:23 Post injection
4:36 Intramuscular injection
4:54 Locating intramuscular injection site
5:18 Cleaning intramuscular injection site
5:38 Inserting needle intramuscular injection
6:28 Anchoring needle intramuscular injection
6:44 Injecting medication intramuscular injection
6:55 Withdrawing needle intramuscular injection
7:05 Disposing of needle
7:43 Cleaning site
8:00 Displacing with Z-track
8:10 Inserting needle
8:23 Releasing tissue

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Watch that video of the Worlds largest Face Abscess Draining

Homocystinuria is an inherited disorder that affects the metabolism of the amino acid methionine. Amino acids are the building blocks of life. Causes Homocystinuria is inherited in families as an autosomal recessive trait. This means that the child must inherit a non-working copy of the gene from each parent to be seriously affected. Homocystinuria has several features in common with Marfan syndrome, including joint and eye changes. Symptoms Newborn infants appear healthy. Early symptoms, if present, are not obvious. Symptoms may occur as mildly delayed development or failure to thrive. Increasing visual problems may lead to diagnosis of this condition. Other symptoms include: Chest deformities (pectus carinatum, pectus excavatum) Flush across the cheeks High arches of the feet Intellectual disability Knock knees Long limbs Mental disorders Nearsightedness Spidery fingers (arachnodactyly) Tall, thin build

Primary sclerosing (skluh-ROHS-ing) cholangitis (koh-lan-JIE-tis) is a disease of the bile ducts, which carry the digestive liquid bile from your liver to your small intestine. In primary sclerosing cholangitis, inflammation causes scars within the bile ducts. These scars make the ducts hard and narrow and gradually cause serious liver damage. In most people with primary sclerosing cholangitis, the disease progresses slowly and can lead to liver failure, repeated infections, and tumors of the bile duct or liver. Liver transplant is the only known cure for primary sclerosing cholangitis. The search for other treatments to slow or stop primary sclerosing cholangitis is ongoing, and scientists have turned up many promising leads. Until better treatments are proved safe and effective, though, care for primary sclerosing cholangitis focuses on monitoring liver function, managing symptoms and, when possible, doing procedures that temporarily open blocked bile ducts.

The hepatitis E virus, responsible for major epidemics of viral hepatitis in subtropical and tropical countries, was cloned only 7 years ago.1 Hepatitis E was found to belong to the family of Caliciviridae, which includes the Norwalk virus—a common cause of gastroenteritis in humans—and consists of a single, plus-strand RNA genome of approximately 7.2 kb without an envelope (Fig. 1). The virus contains at least three open reading frames encoding viral proteins against which antibodies are made on exposure. These antibodies, especially those against the capsid protein derived from the second open reading frame2 and a protein of unknown function derived from the third open reading frame, are detected by currently available serologic assays. Retrospective studies on stored sera of past epidemics of viral hepatitis in Mexico, Africa, Afghanistan, Pakistan, India, Bangladesh, Burma, Nepal, and Borneo have revealed that all were caused by strains of hepatitis E. In addition, hepatitis E was found to be responsible for the hepatitis epidemic in the southern part of Xinjiang, China, in which 120,000 persons became infected between September 1986 and April 1988.3 Hepatitis E predominantly affects young adults (15 to 40 years old). The symptoms of hepatitis E are similar to those of hepatitis A. Frequently, a prodrome consisting of anorexia, nausea, low-grade fever, and right upper abdominal pain is present 3 to 7 days before jaundice develops. Aminotransferase levels peak (usually between 1,000 and 2,000 U/L) near the onset of symptoms; bilirubin levels (10 to 20 mg/dL) peak later. Jaundice usually resolves after 1 to 2 weeks. In about 10% of cases, the disease is fulminant—especially in pregnant women, among whom mortality rates as high as 20% due to hemorrhagic and thrombotic complications have been reported. No evidence has suggested that hepatitis E can cause chronic infection. Transmission is by the fecal-oral route, predominantly through fecally contaminated drinking water supplies. In addition, however, preliminary reports have suggested transmission of the hepatitis E virus through blood transfusions. Volunteer studies confirmed the presence of the virus in serum and feces before and during clinical disease.4 The virus is shed into feces approximately 1 week before symptoms develop. The incubation period varies from 2 to 9 weeks (mean duration, approximately 45 days). Until now, a few reports had described symptomatic hepatitis E acquired in Europe;5, 6 all patients with symptomatic hepatitis E in the United States were travelers returning from Mexico, Africa, or the Far East, in whom hepatitis E developed after their return home.7 In this issue of the Mayo Clinic Proceedings (pages 1133 to 1136), Kwo and associates describe a case of hepatitis E in a man who had not left the United States during the previous 10 years. Specific serologic tests for hepatitis E virus IgG (enzyme immunoassays and a fluorescent antibody blocking assay) and IgM8 (US strain-specific enzyme-linked immunosorbent assay with use of synthetic polypeptides deduced from the viral genome, as shown in Figure 1), developed at Abbott Laboratories (IgG and IgM) as well as at the Centers for Disease Control and Prevention (IgG), were used to prove that the patient indeed had acute hepatitis E. Researchers at Abbott Laboratories have prepared a report that describes most of the viral genome in this patient (Fig. I).8 Their results are interesting because this strain from the United States differs considerably from hepatitis E strains isolated in Mexico, Burma, Pakistan, or China. Furthermore, the sequence of the US strain is highly homologous (98% and 94% homology at the amino acid level to the second and third open reading frames, respectively) to a recently isolated hepatitis E strain from American swine.9 This finding suggests that, in the United States, hepatitis E is a zoonosis with the swine population as one of its hosts. This relationship would confirm earlier studies in Asia, where swine were also found to carry variants of the hepatitis E virus.10 Why are these two recent discoveries important for medicine in the United States? First, other sporadic, locally acquired cases of acute hepatitis may be caused by hepatitis E. Second, these back-to-back discoveries strongly suggest that a common natural host for hepatitis E is present in countries with more moderate climates. Because swine do not seem to experience any symptoms associated with infection and because symptoms in humans can be minor or absent, we now may also have an explanation for the 1 to 2% of positive hepatitis E serologic results in blood donors in the United States,11 Netherlands,12 and Italy,6 countries with large swine staples. Clearly, more research needs to be done to confirm this hypothesis. Third, in countries with more moderate climates, hepatitis E may often result in a subclinical infection. Is this variation in manifestation due to less virulent strains, and do sequence variations determine virulence? Fourth, swine may be used as an animal model for study of the disease as well as vaccine development.

Repair Deviated Nasal Septum, Endoscopic Septoplasty, endoscopic surgery, Stapler repair of nasal septum, Dr B. Todd Schaeffer.