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Blue Toe Syndrome featured rish academy

Blue Toe Syndrome

Newsletter Blue Toe Syndrome What is Blue Toe Syndrome? Occlusive vasculopathy, often known as blue toe syndrome, is a kind of acute digital ischemia in which one or more toes turn blue or violet in color. Petechiae or cyanosis of the soles of the feet may be present in isolated areas. There may also be scattered areas of petechiae or cyanosis of the soles of the feet. Blue toe syndrome (BTS) is characterized by painful digits with a blue or purple discoloration that does not occur as a result of direct damage. It can also result in the amputation of toes and feet, which can be fatal. Pathophysiology Acute digital ischemia manifests itself as blue toe syndrome. This means that happens when the blood supply to the toes is inadequate. One or more of the following factors can cause a reduction in blood flow: Decreased arterial flow Impaired venous outflow Abnormalities in circulating blood. The blood transports oxygen from the lungs to every part of a person’s body. To repair and multiply, each cell requires oxygen. The blood also transports waste products and provides all of the nutrients that cells require. Inadequate blood supply damages cells and the tissues that they make up. This might cause the tissue to turn blue or purple in color. The condition is known as blue toe syndrome when it affects the toes. Some people with this condition have just one discolored toe on one foot. Others might have discolored toes on both feet. Some people will find that the toes go back to their normal color when they put pressure on the skin or when they elevate their foot. Click the button below to download Pathophysiology Made Easy eBook. This eBook has 12 chapters and 234 pages. Sample of Pathophysiology Made Easy Flashcards eBook Download Now Symptoms Blue toe syndrome can cause the following symptoms in addition to blue or purple toes: Moderate or severe forefoot pain Leg muscles pain Ulcers on the feet Nodules or lesions on the feet Bruising Causes of Blue Toe Syndrome When a blockage in the small blood vessels in the foot prevents the tissues from receiving enough blood, blue toe syndrome develops. Blue toe syndrome can be caused by a variety of factors. Atherosclerosis Cholesterol is a waxy molecule that the body requires to produce hormones, vitamin D, and other digestive aids. The body produces all of the cholesterol it requires, but it is also found in foods such as eggs, beef, and cheese. When blood cholesterol levels are excessively high, it can combine with other chemicals to produce plaque. When plaque adheres to the artery walls, it narrows them, resulting in atherosclerosis. Plaque can also obstruct the flow of blood through the arteries. Embolism When something blocks a blood vessel, it is called an embolism. Plaque fragments can break out from the arterial walls and move through the bloodstream until they become lodged. Blood clots can do the same thing. Embolisms can develop spontaneously or as a result of an angiography, vascular surgery, medicine, or renal failure. Angiogram An angiogram is a form of medical imaging. Doctors use it to detect and treat blood artery blockages and atherosclerosis. A needle is inserted into an artery in the groin, and thin tubes called catheters are threaded through the arterial system. While injecting a contrast agent into the bloodstream, the team will take X-ray photographs of the person. This chemical aids in the detection of any obstructions or other difficulties. The operation can sometimes knock a fragment of plaque off the artery walls, causing blue toe syndrome, according to researchers. Vascular surgery Any procedure on the circulatory system is referred to as vascular surgery. The arteries, veins, and lymphatic system are all part of this system. Embolisms are a possible side effect of vascular surgery. A plaque fragment, blood clot, or other particles might circulate in the bloodstream until it becomes lodged in a blood vessel. Blue toe syndrome can arise when this happens in the foot. Inflammation caused by infectious and non-infectious agents Syphilis, pyogenic infection (sepsis), Behçet illness, and various types of vasculitis can all cause occlusion. Impaired venous outflow Phlegmasia cerulea dolens is caused by abnormal venous drainage along with severe venous thrombosis (a painful form of blue toe syndrome associated with leg oedema). Predisposing factors for venous thrombosis exist in many people, including: Immobility Clotting disorders Pregnancy Previous leg trauma Malignancy Circulating blood abnormalities Abnormal blood components can cause blue toe syndrome. These includes: Cryoglobulinaemia Platelet plugging Myeloproliferative disorders (eg, polycythaemia rubra vera and essential thrombocythaemia) Cryofibrinogenaemia Paraproteinaemia (which causes hyperviscosity) Cold agglutinin anaemia Paroxysmal nocturnal haemoglobinuria Medications Medicines used to thin the blood or cure blood clots, according to the European Society of Cardiology, can also cause blue toe syndrome. Cocaine and other recreational drugs can potentially cause the condition. Renal failure The kidneys play several roles in the human body: Removing waste products from the bloodstream and disposing of them in the urine Ensuring that the blood contains the proper balance of nutrients that cells require, such as sodium, potassium, and calcium Produces hormones that regulate blood pressure and red blood cell production Renal failure occurs when the kidneys are unable to function normally. According to the European Society of Cardiology, this condition can lead to blue toe syndrome Download ALL STUDY RESOURCES in Medicine & Surgery Diagnosis The clinical diagnosis of blue toe syndrome is based on the patient’s history and examination findings. To guide treatment, it’s essential to figure out what’s causing blue toe syndrome in the first place. The clinical examination usually provides clues, but more investigation in the form of laboratory blood tests, tissue biopsies, and radiographic imaging is required to confirm the diagnosis. History and examination should focus on: Hypertension or other risk factors for hypercholesterolaemia and atherosclerotic diseases Fever (indicating cholesterol emboli, infective endocarditis, myxoma, thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation) Cardiac murmur (infective endocarditis and atrial myxoma) Livedo reticularis (cholesterol emboli, myxoma, antiphospholipid syndrome,

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Graysons Syndrome Grayson Wilbrandt Corneal Dystrophy Rish Academy

Grayson’s Syndrome

Newsletter Grayson’s Syndrome (Grayson-Wilbrandt Corneal Dystrophy) What is Grayson’s Syndrome? Grayson’s Syndrome, also known as Grayson-Wilbrandt Corneal Dystrophy (GWCD), is a very rare type of corneal dystrophy characterized by varying patterns of opacification in the Bowman layer of the cornea that extend anteriorly into the epithelium, with reduced to normal visual acuity. Corneal dystrophies are a collection of hereditary diseases that affect the cornea. The cornea, the transparent outer layer of the eye, is affected. There are two purposes for the clear cornea. It bends light entering the eye onto the lens and shields the eye from germs and irritants. Corneal dystrophies are divided into three categories based on how much of the cornea they impact. In the outer cornea, anterior dystrophies are more common. The middle level is more commonly affected by stromal dystrophies. In the inner or deep corneal layers, posterior dystrophies occur. Anterior dystrophy is Grayson’s Syndrome. It’s a type of Reis-Bucklers dystrophy in which the Bowman’s layer of the cornea is affected. One of two superficial layers that make up the cornea’s outer layer is the acellular Bowman’s layer. It is located just beneath the corneal epithelium, which is the outermost layer of the cornea. You can get access to our Medical Resources Library to get access to more than 300 medical presentations and all other medical resources that will be helpful for your entire career.  Get Access to Medical Resources Library Some slides from the presentations from our Medical Resources Library Abnormal extracellular material builds up in the layers of the cornea in corneal dystrophies. Depending on the severity, this may or may not induce symptoms. The buildups in Grayson’s Syndrome produce opaque regions in the cornea. This results in varying degrees of reduced visual acuity. Grayson’s Syndrome also produces inflammation, lesions, and erosions in the eyes. The disease progresses, with symptoms getting worse over time. Grayson’s Syndrome, like all corneal dystrophies, is a hereditary disorder. It is inherited in an autosomal dominant form. If only one parent carries a faulty gene, a kid can inherit the condition. If a parent has the disease, each child has a 50% chance of developing it as well. Grayson’s Syndrome develops in children who inherit a defective gene by the age of 20. If the symptoms of Grayson’s Syndrome are minimal, therapy may not be required. Eye ointments and eye drops can aid in the healing of corneal ulcers and erosions. In some circumstances, special contact lenses, laser therapy, and corneal transplantation are also options. If you experience any vision changes or other eye complaints, see an eye doctor immediately. Routine vision examinations are usually included in well-child checkups. Seeing a doctor on a frequent basis can aid in the early detection of potential problems. Genetic testing may be able to detect corneal dystrophy if your family has a history of it. What are the symptoms of Grayson’s Syndrome? A loss in visual acuity is the most common sign of Grayson’s Syndrome. The deposition of material in the Bowman’s layer of the cornea causes this. The center of vision usually gets fuzzy, but the periphery vision may remain quite clear. Eye irritation, corneal lesions, and blister-like erosions are other symptoms of Grayson’s Syndrome. The irritation can make you feel as if something is continuously in your eye. Corneal edema and pain can result from lesions and erosions. The corneal surface becomes scarred and uneven when lesions grow and heal. This contributes to a decline in visual acuity. The condition worsens with age, and the symptoms become more severe. If you experience changes in your vision or other eye symptoms, consult your doctor as soon as possible. These problems can be caused by a variety of factors. It is critical to have an accurate diagnosis in order to effectively manage the problem. Boy with Grayson’s Syndrome Causes of Grayson’s Syndrome Grayson’s Syndrome is a hereditary condition characterized by aberrant extracellular material synthesis and buildup within the clear cornea. It is inherited in an autosomal dominant form. To put it another way, a child can be born with a condition if only one parent has an aberrant gene. A couple’s chances of acquiring the disease increase by 50% with each kid they have. Grayson’s Syndrome develops in the first two decades of life if a child inherits the gene. It results in abnormal material deposits in the Bowman’s layer of the cornea. The deposits create opaque patches that make it difficult to see clearly. They can also irritate the eyes and create other symptoms. Risk Factors of Grayson’s Syndrome. Grayson’s Syndrome is a hereditary condition, hence the risk factor for developing it is genetic. A child has a 50% chance of developing the disease if one of their parents has it. It usually appears before the age of 20. Can you reduce your risk of developing Grayson’s Syndrome? Grayson’s Syndrome cannot be prevented or reduced in any way. If you have the illness and are concerned about passing it on to your children, discuss genetic testing with your doctor. The best method to understand the danger to future children is to work with a genetic counselor. This healthcare expert can also assist you in navigating the complexities of deciding whether or not to have children. Download Pathophysiology & Clinical Medicine Flashcards eBook Sample of Pathophysiology Made Easy Flashcards eBook Treatment of Grayson’s Syndrome Treatment may not be indicated if the symptoms are minimal. Your doctor may advise that you be monitored on a regular basis to evaluate how the disease is progressing. Doctors typically prescribe lubricating eye drops, eye ointments, and antibiotics to treat irritation, sores, and erosions. While the cornea heals, special contact lenses can help protect it from irritants. Laser therapy or ablation may be used to improve eyesight and treat erosions and scarring in some circumstances. The condition, however, is progressive, and symptoms and scars will worsen over time. In severe cases, a corneal transplant may be necessary. It includes the removal of the diseased cornea and

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mechanism of action

Pharmacology – Mechanism of Action of All Drugs

Newsletter Mechanism of Action of All Drugs This is a pretty comprehensive article that explains the mechanism of action of all commonly prescribed medications.   1. Analgesics Paracetamol (Acetaminophen) Mechanism of Action Weak inhibitor of the synthesis of prostaglandins, Paracetamol also decreases prostaglandin concentrations in vivo. Aspirin Mechanism of Action Aspirin causes reduction of inflammation, analgesia, the prevention of clotting, and antipyretic. Much of this is believed to be due to decreased production of prostaglandins and thromboxane A2 by its irreversible inactivation of the cyclooxygenase (COX) enzyme, Cyclooxygenase is required for prostaglandin and thromboxane synthesis. Diclofenac Sodium Mechanism of Action Diclofenac has analgesic, anti-inflammatory, and antipyretic properties. It causes inhibition of cyclooxygenase (COX 1 and COX 2) and acts as a potent inhibitor of prostaglandin synthesis in vitro. Tramadol hydrochloride Mechanism of Action Tramadol acts on the mu-opioid receptor, blocking the neuron from communicating pain to the brain. Pethidine hydrochloride (Meperidine) Mechanism of Action Pethidine exerts its analgesic effects by acting as an agonist at the μ opioid receptor Morphine Mechanism of Action Morphine is an Opioid analgesic, activating opiate receptors that are widely distributed throughout the brain and body. Once an opiate reaches the brain, it quickly activates the opiate receptors that are found in many brain regions & produce pleasure (or reward) and pain relief. The brain itself also produces substances known as endorphins that activate the opiate receptors. Morphine mimics endogenous neurotransmitters (endorphins). Morphine binds to specific morphine-like (endorphin) receptors ( EndR). Download Pharmacology Books & Thousands of Medical Resources Sample of Pharmacology Essentials Flashcards eBook 2. Antiarrhythmics Adenosine Mechanism of Action Adenosine slows conduction time through the AV node, can interrupt the reentry pathways through the AV node, and can restore normal sinus rhythm in patients with arrhythmias. Amiodarone hydrochloride Mechanism of Action It’s primarily a class III antiarrhythmic. Like other antiarrhythmic drugs of this class, amiodarone works primarily by blocking potassium rectifier currents that are responsible for the repolarization of the heart during phase 3 of the cardiac action potential. Digoxin Mechanism of Action Digoxin increases the force of contraction of the heart muscles by inhibiting the activity of an enzyme (ATPase) that controls the movement of calcium, sodium, and potassium into the heart muscle. Inhibiting ATPase increases calcium in heart muscle and therefore increases the force of heart contractions. Digoxin also slows electrical conduction between the atria and the ventricles of the heart and is useful in treating arrhythmias. Bisoprolol fumarate Mechanism of Action Bisoprolol is a synthetic beta1 selective beta-adrenergic receptor blocker with a low affinity for beta2 receptors in bronchial smooth muscle, blood vessels, and fat cells and no intrinsic sympathomimetic activity. Therefore Bisoprolol exerts cardioselective effects include lower heart rate, decreased cardiac output, and inhibition of renin release by kidneys. At higher doses, it will lose beta1 selectivity. Atenolol Mechanism of Action It’s a Cardioselective beta 1 adrenergic antagonist, works by selectively binding to the beta 1 adrenergic receptors found in vascular smooth muscle and the heart, blocking the positive inotropic and chronotropic actions of endogenous catecholamines, thereby inhibiting sympathetic stimulation. This activity results in a reduction in heart rate, blood pressure, and decreases myocardial contractility. Diltiazem hydrochloride Mechanism of Action Diltiazem is a benzothiazepine derivative with antihypertensive, antiarrhythmic properties. It blocks voltage-sensitive calcium channels in the blood vessels, by inhibiting the ion control gating mechanisms, thereby preventing calcium levels from increase   Get Access to Medical Resources Library Some slides from the presentations from our Medical Resources Library 3. Antibiotics Amoxicillin Mechanism of Action Amoxicillin is in the class of beta-lactam antibiotics. Beta lactams act by binding to penicillin-binding proteins that inhibit a process called transpeptidation, leading to activation of autolytic enzymes in the bacterial cell wall. This process leads to lysis of the cell wall, and thus, the destruction of the bacterial cell. This type of activity is referred to as bactericidal killing. Azithromycin Mechanism of Action Azithromycin prevents bacteria from growing by interfering with their protein synthesis. It binds to the 50S subunit of the bacterial ribosome, thus inhibiting the translation of mRNA. Cefuroxime Mechanism of Action It’s a Cephalosporin group antibiotic, exerts bactericidal activity by interfering with bacterial cell wall synthesis and inhibiting cross-linking of the peptidoglycan. The cephalosporins are also thought to play a role in the activation of bacterial cell autolysins which may contribute to bacterial cell lysis. Cephalexin (Cefalexin) Mechanism of Action It’s a Cephalosporin group antibiotic, exerts bactericidal activity by interfering with bacterial cell wall synthesis and inhibiting cross-linking of the peptidoglycan. The cephalosporins are also thought to play a role in the activation of bacterial cell autolysins which may contribute to bacterial cell lysis. Ciprofloxacin Mechanism of Action Ciprofloxacin is a bactericidal antibiotic of the fluoroquinolone drug class. It acts on bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. Ciprofloxacin’s targeting of the alpha subunits of DNA gyrase prevents it from supercoiling the bacterial DNA which prevents DNA replication. Clarithromycin Mechanism of Action Clarithromycin, a macrolide antibiotic, inhibits bacterial protein synthesis by binding to the bacterial 50S ribosomal subunit. Binding inhibits peptidyl transferase activity and interferes with amino acid translocation during the translation and protein assembly process, and prevents bacterial protein synthesis. Clindamycin Mechanism of Action It is a bacterial protein synthesis inhibitor by inhibiting ribosomal translocation in a similar way to macrolides. It does so by binding to the 23S RNA of the 50S subunit of the ribosome. Clindamycin is bacteriostatic. Co-amoxiclav Mechanism of Action Co-amoxiclav is a combination of Amoxicillin and Clavulanic acid. Clavulanic acid blocks the chemical defense, known as beta-lactamase, that some bacteria produce against penicillin group antibiotics such as amoxicillin. Co-amoxiclav is active against bacterial infections that have become resistant to amoxicillin. Co-trimoxazole Mechanism of Action Co-trimoxazole, generally bactericidal, a combination of trimethoprim and sulfamethoxazole. It acts by sequential blockade of folic acid enzymes in the synthesis pathway. The sulfamethoxazole component inhibits the formation of dihydrofolic acid from para-aminobenzoic (PABA), whereas trimethoprim inhibits dihydrofolate reductase. Both drugs block folic acid synthesis, preventing bacterial cell synthesis of essential nucleic acids. Doxycycline Mechanism of Action Doxycycline is a tetracycline

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anatomicalplanes

Oblique Plane

Newsletter Oblique plane Anatomical Body Planes and Sections – Anatomy and Physiology – Oblique plane The anatomical body planes and sections help us learn the many ways in which the body can be viewed when divided into sections in anatomy and physiology. They’re extremely important to understand if you want to work in a healthcare sector where you’ll be examining images from MRI scanners and other imaging devices. Visualize an imaginary flat surface, similar to a glass rectangle, that splits the body into two parts while thinking about a body plane. Click the button below to Download 570+ High-Yield Presentations in Emergencies, Orthopedics, Gynaecology & Obstetrics, Surgery, and Clinical Medicine Get Lifetime Access to 570+ Medical Presentations Four Types of Body Planes The acronym “SOFT,” which stands for Sagittal, Oblique, Frontal, and Transverse, is an easy method to memorize the four primary types of body planes. Two of these planes (sagittal and frontal) are vertical and run from top to bottom. The horizontal plane (transverse) is one of the planes, and the oblique planes are all the “odd” angles between the horizontal and vertical planes. Sagittal Planes (Midsagittal and Parasagittal) The sagittal plane splits the body into left and right halves, running vertically from top to bottom (and front to back). This is simple to remember because your skull is divided into left and right sides by a sagittal suture. And that’s exactly what this plane does: when viewed from the anatomical position, it splits the body into right and left sides. Sagittal planes can be made even more specific by adding a prefix to aid in identifying the type of sagittal plane. A sagittal plane that properly splits the body at the midline is known as a “Midsagittal” or “median” plane. The prefix “mid” can serve as a reminder that it is in the middle. Any sagittal plane that does not completely follow the body’s midline is referred to as “parasagittal.” Oblique Planes An oblique plane is a plane that can be any angle other than horizontal or vertical. In actuality, the word “oblique” denotes “not parallel” or “at a right angle.” The phrase “obliques are odd angles” is a good way to remember this. You could also consider your oblique muscles. These muscles are placed laterally to your abdominal muscles and come down at an angle. Download Pathophysiology & Clinical Medicine Flashcards eBook Sample of Pathophysiology Made Easy Flashcards eBook Transverse Planes (Horizontal or Axial Planes) The only plane that travels horizontally, splitting the body or structure into a top (superior) and bottom (inferior) half, is the transverse plane (also known as a horizontal plane). Allow the name to assist you in remembering it: the prefix trans means “across.” Consider transatlantic flights, which will transport you over the Atlantic Ocean. Remember the direction of the horizontal (transverse) plane by thinking of the horizon, which is the horizontal boundary between the earth and the sky. Frontal (Coronal) Planes The frontal plane (also known as the coronal plane) separates the body into a front (anterior) and back (posterior) section by running vertically from top to bottom (and left to right). Allow the name to assist you once more. You’ll have a front and back section after using the frontal plane! Get Access to Medical Resources Library Share this : [Sassy_Social_Share total_shares=”ON”] Library Anatomy Anesthesiology Biochemistry Cardiology Dermatology Emergency Endocrinology ENT Examinations Forensic Med. Obs. & Gynae. Hematology Medicine Microbiology Nephrology Neurology Oncology Ophthalmology Orthopaedics Paediatrics Parasitology Pathology Pharmacology Physiology Psychiatry Pulmonology Radiology Rheumatology Surgery

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