Betaxolol - Onmeda.de

betaxolol

betaxolol - win

Betaxolol for anxiety

Betaxolol is a beta blocker that is capable of passing the blood brain barrier, and because it is selective to beta1 receptors it generally has fewer side effects than other beta blockers. Beta blockers like propranolol are commonly used to mask the physical effects of anxiety by blocking adrenaline from binding to beta receptors, but generally they're not considered to be valid anxiety treatments because they don't address the psychological component.
However, I recently came across research from 1998 that analyzed betaxolol treatment specifically for treating psychological anxiety: https://link.springer.com/article/10.1023/A:1026146528290
The results looked really promising, so I was surprised to find there was never a followup study attempting to replicate it, especially since the drug is generic. I noticed that the lead researcher filed a patent on betaxolol for anxiety, so perhaps it got lost in his myriad of other patents and no company ever pursued it.
I'm curious what what everyone thinks are about about this and if anyone has any experience.
submitted by SingularFX to DrugNerds [link] [comments]

[Article] A Double-Masked Comparison of Betaxolol vs Timolol in the Treatment of Open-Angle Glaucoma Robert C. Allen, M.D. Ellen Hertzmark, M.A. Alexander M. Walker, M.D. David L. Epstein, M.D.

DOI: https://doi.org/10.1016/0002-9394(86)90942-6
URL: https://www.ajo.com/article/0002-9394(86)90942-6/pdf
submitted by _rxdealer_ to Scholar [link] [comments]

Does anyone here take betaxolol? If so are there any side effects?

Hi, i got diagnosed with POTS a while ago (along with classical EDS, if that matters at all.) My family is pretty anti medication so this whole time I’ve been self medicating by working out, guzzling water, taking salt tablets, etc. it makes things better, but I still struggle. My parents sat me down the other day and said that if I wanted to, they would let me take medication for POTS. The medicine that was recommended by the doctor was betaxolol, 10mg, taken every morning. I can read all the scary things that could potentially happen due to taking the drug on the internet but the best way to decide to use it or not is to hear from other people that take it. Has anyone here taken betaxolol? Were there any side effects long term or short? Would you recommend it? Thanks!
submitted by ccgraves1999 to POTS [link] [comments]

Betaxolol and lysergides?

Hello. I'm planning a trip (not sure what to take yet, but I have some LSD analogues like 1p-LSD and AL-LAD) with a friend who is using a beta-blocker drug betaxolol for his arrhythmia. As far as I could find, lsd works just fine with beta-blockers, but one post mentioned that this particular medicine might have adverse effects with ergot alkaloids. No info about this other than this post. One other thing I am a bit concerned about is the fact that betaxolol is also used to tread schizophrenia symptoms.
So in short - has anyone tried combining these two substances?
submitted by eyeless_cat to askdrugs [link] [comments]

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What meds do you take for POTS?

Ive had POTS for a while, but I was officially diagnosed two years ago. Back in my teenage years my symptoms were there but a lot less severe. Im 21 now and I seem to be getting progressively worse, with short periods of improvement in between. The only noticeably helpful thing for me has been increasing my electrolyte intake. I have tried three different kinds of beta-blockers at all different doses, and they seem to either do nothing or make me feel terrible. After that i had basically given up and accepted that this is the way my body wants to work, but recently ive noticed a big “flare” in symptoms and have started looking into medications or just more effective ways to improve my quality of life outside of sports drinks and electrolyte supplements. My question is what meds have worked for you? Are there options besides beta-blockers that i may have better luck with?
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6. Glaucoma

Es una neuropatía óptica crónica progresiva, un conjunto de entidades patológicas causada por la pérdida de células ganglionares y sus axones

Generalidades

Fisiopatología

Principal: Apoptosis de Cel. Ganglionares Retinianas Adelgazamiento de capas de fibras nerviosas Pérdida axonal en el N Optico = Perdida de visión
Mecanismo continuo sobre la producción y drenaje de H. Acuoso, fluye en la Cámara anterior y drena en Schlemm Mayor resistencia al flujo, mayor presión:
G. Angulo abierto
Aumento de PIO anormalidades en el drenaje en la cámara anterior Deterioro en excreción de H. Acuoso
PIO alcanza entre 60-80 mmHg= Daño isquémico agudo de l iris + Edema + Daño N. Optico
G. Angulo cerrado
Aumento de PIO Deterioro en excreción de H. Acuoso Mal acceso de H. Acuoso al sistema de drenado
PIO no aumenta <30 mmHg= Lx Cel. Ganglionar Retiniana

Vaughan y Asbury. (2012). Oftalmología general 18e. AccesMedicina: LANGE.

Clasificación

Se caracteriza por tener alteraciones en el campo visual, se pierden las fibras nerviosas que pueden estar en relación al HT ocular
Manifestaciones: Elevación de PIO , aumento de exacerbación de N.Optico y palidez, perdida de AV progresiva y tardía.
-Excavación/Papila: Normal 0-0.3, Gaucoma 0.4 a 0.6
Diagnosticar: Tonometría, Fondo de ojo para observas la excavación, medir PA y los campos visuales.

Vaughan y Asbury. (2012). Oftalmología general 18e. AccesMedicina: LANGE.

Por cierre del ángulo primario (hay mucho abombado por parte del iris y bloquea la excreción de H. Acuoso.
Neuropátia óptica por daño estructural y afecta a la visión.
Suele ser asintomatica y es emergencia oftálmica (de la nada pierde la visión). Usualmente en los 40 años
Manifestación clínica: pérdida súbita de la visión, dolor agravante, halo glaculomatoso, nausea y vómito, cornea empañada

Vaughan y Asbury. (2012). Oftalmología general 18e. AccesMedicina: LANGE.

Diagnostico


Vaughan y Asbury. (2012). Oftalmología general 18e. AccesMedicina: LANGE.

Tratamiento

Puede ser: farmacológico, láser o quirúrgico

Bloqueador b-Adrenergico Analogo de la Prostaglandina Inhibidor de la amilasa carbonica
Solos o en combinación Bimatoprost, latanoprost y travoprost cada uno una vez al día por la noche Acetozolamida la más usada pero sus alternativas son diclofenamida y metazolamida
Timolol, betaxolol y levobunolol al 0.25% y 5% Cuando la terapia tópica es insuficiente
Metipranolol al 0.3% y Carteolol al 1% 1 x día Suprimen H. Acuoso 40-60% y se divide 125mg a 250mg 4veces al día
Contraindicación: para enfermedad obstructiva crónica del pulmón y defectos en la conducción cardiaca
Iridotomía periferica, Iridectomía e Iridoplastia Trabeculoplastia por rayos láser Cirugía de drenaje de glaucoma
Se prefiere con laser YAG Quema la malla mediante un goniolente Trabeculotomía: funciona de desviar los canales de drenaje normal y deja el paso. Tx coadyuvante: antimetabolitos como 5-fluoracilo y mitomicina C
La iridotomia es preventiva para pacientes con ángulos estrechos Facilita la salida de H. acuoso y mejoran su función Complicación: fibrosis en tej epiesclerar y acelera formación de cataratas.
Iridioplastia anillo de quemadura con rayos láser sobre el iris periférico contrae el estroma del iris. Como tratamiento inicial de glaucoma de ángulo abierto primario Visccanalostomía y Esclerotomía con implante de colágeno: evitan el espesor total del ojo

Video


https://reddit.com/link/gidbn2/video/7v2c2er90ey41/player

Referencias

Vaughan y Asbury. (2012). Oftalmología general 18e. AccesMedicina: LANGE.
Azcona-Cruz, M. I., del Carmen Ríos-Lobo, M., & Amador-Jiménez, S. (2015). Glaucoma: Aspectos relevantes para la detección oportuna. Revista Salud y Administración, 2(4), 23-35.
Maroto Jiménez, P. (2016). Glaucoma una vista al pasado con un futuro prometedor. Revista medica de Costa Rica y Centroamerica, 72(617), 741-744.
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Mint Health Benefits and Side Effects

Mint Health Benefits and Side Effects

Mint Health Benefits and Side Effects

Food Catalog / Ingredients, Herbs, and Spices / Mint
Written by: Christopher Karam | ✔️ Medically Reviewed by: Dr. Riad M., M.D - G.P and Micheal B., M.D | Last Updated: 2020 March 22
growing mint plants
Break down and Background
Mint Species and Varieties
Mint plants, also known as peppermint, pudina, and mentha, are widely regarded as a weed since its species tend to be invasive. If grown in a vegetable garden it may take nutrients and vitamins from growing vegetables that need resources to grow properly.

Mint leaves are very healthy for your digestive system as well as irritable bowel syndrome (IBS), brain function, and is an anti-inflammatory herb due to the its high vitamins, minerals, and fiber content.

It can drastically improve your overall health and is easily incorporated in many savory and sweet recipes. Mint has also been used throughout centuries as a natural medical remedy to treat many different diseases, complications, and infections.

The mint plant (genus Mentha) is part of the Lamiaceae family of herbs, which also includes:

Basil

Peppermint

Spearmint

Rosemary

Sage

Summer savory

Marjoram

Oregano

Anise hyssop

Thyme

Lavender

Perilla

Recipes That Go Well With Fresh Mint
Mint is quite popular in a large variety of beverages, foods, and recipes, include the following:

Sauces including lamb sauces, white wine vinegar mint sauce, chimichurri, yogurt sauce, and lemon-mint sauce

Salads such as Mediterranean salads and fruit salads

Desserts combined with chocolate such as puddings, cakes, brownies, ice cream, cheesecake, and cookies

Dairy products such as milk, whipped cream, cheeses, peppermint milk, and peppermint ice cream

Herbs mixed with dill, basil, peppermint leaves, oregano, and rosemary

Oils such as olive oil, coconut oil, pesto, canola oil, lemon and other essential oils

Vegetables such as cucumbers, acorns, squash, beets, parsnips, carrots, mustard and mustard seeds, zucchini, bell peppers, eggplants, onions, peas, green beans, and asparagus

Fruits such as vanilla beans, strawberries, lemons, limes, watermelon, bananas, blueberries, raspberries, blackberries, pineapple, oranges, apples, pomegranates, coconuts, and kiwis

Drinks such as alcoholic drinks, shakes, lemonade and limeade, club soda, and water

Gums using mint or peppermint

Alcoholic beverages such as mojitos, vodka mint lemonade, red and white wines, baileys, martinis, gimlets, rum, and tequila

While eating mint can offer multiple health benefits, there are other more subtle benefits that comes from applying it to your skin, inhaling vapors through diffusers or burning, or taking it through capsules and supplements.

chocolate mint plants

List of Nutrition Facts and Essential Oils
What gives mint its large list of health benefits is the high content of antioxidants, most commonly used to treat stomach issues and indigestion as it has potent antibacterial and antifungal essential oils.

Mint originated in the Asian, European, and Mediterranean areas, it’s been used for cleaning tools, tables, and their skin. Romans used to use fresh mint as a mouth freshener, whitening teeth, and as a base for their sauces.

It’s even been used for healing open wounds due to it’s blood clotting effects for soldiers during war time. Known as a high value herb that’s associated with wealth, status, good health, and cleanliness.

Mint has a calming and relaxing effect due to all of the menthol, in addition to its anti-inflammatory properties, mint reduces painful symptoms similarly to ibuprofen and pain killers.

Both mint and peppermint contain and produce a lot of menthol. Dried peppermint has around 0.3 to 0.5% of essential oils including:

Menthol (7% to 48%)

Menthone (20% to 46%)

Menthyl acetate (3% to 10%)

Menthofuran (1% to 17%)

1,8-Cineol (3% to 6%)

Menthol and menthyl both increase blood flow in the body, also activating a nervous system receptor called TRPM8 that reduces blood flow and blocks nerve receptors.

Additionally, menthol binds to kappa opiod receptors that further causes a feeling of numbness, cooling sensation, and pain reduction.

When you have a cold, having a glass of water with lemon juice as well as mint will relieve, soothe, and disinfect your throat. Mint is also great in fruit smoothies using watermelon and protein shakes, adding additional layers of flavor and all of mint’s health benefits.


100 grams of mint contains nutrients including essential vitamins and minerals such as:

Potassium (16% of the Recommended Daily Allowance)

Phosphorus (8% of the RDA)

Calcium (25%)

Vitamin C (52%)

Vitamin B6 (5%)

Vitamin A (12%)

Magnesium (20%)

Manganese (25%)

Folate (12%)

Iron (28%)

Keep in mind that mint is very low in calories, every tablespoon of dried mint is 1 calorie. This makes mint a great source of protein, fiber, and healthy essential oils which is easily included into your diet or meal plan.

Mint Health Benefits
There are hundreds of studies and research papers that have proven the large list of health benefits of mint, it has been studied thoroughly for decades.

Mint and peppermint tea is one of the most consumed herbal teas world wide. It’s brewed from peppermint leaves which has the additional benefit of releasing more phenolic compounds.

The list of phenolic compounds found in mint include:

Rosmarinic acid

Caffeic acid

The list of flavanoids found in mint include:

Eriocitrin

Luteolin

Hesperidin

Mint plants contain anti-inflammatory agent called rosmarinic acid. Rosmarinic acid has many health benefits, one of which includes reducing inflammation.

mint plants on cutting board

A research study showed that applying mint essential oil effectively relieves pain and inflammation when the patient is properly hydrated.

Peppermint oil and mint extracts can help with bad breath, breastfeeding, headaches, nausea and comes in many variations such as peppermint and mint teas, powders, oil extract capsules, applying it directly onto your skin, consuming mint supplements, or through burning it then inhaling the aroma.

The most commonly reported and scientifically proven benefits of mint includes improved digestion, helps with weight loss, relieves nausea, depression, fatigue, and headaches. Additionally, it’s also used in treatments for treating asthma, memory loss, and improving skin health.

  1. Relieves Symptoms of Irritable Bowel Syndrome (IBS)
Irritable Bowel Syndrome (IBS) is a common disorder that affects the large intestine, the side effects of irritable bowel syndrome includes:

Cramps

Bloating

Excess gas

Abdominal pains

Constipation

Diarrhea

Fatigue and difficulty sleeping

This affects the digestive tract and is usually caused by a poor diet as well as stress. Often, IBS is treated with medications such as laxatives and anti-diarrhea drugs, making healthy changes to your diet, and avoiding certain foods such as:

Dairy and lactose (milk, ice cream, cheese, yogurt)

Certain fruits (peaches, watermelon, pears, mangoes, apples, plums, nectarines)

Beans and legumes

High-fructose corn syrup, sugar, and sweeteners

Fried foods

Wheat-based and refined bread, cereals, and pasta

Gluten

Caffeinated drinks

Cashews and pistachios


There has been some research conducted surrounding mint and peppermint essential oils as well as min teas, as the anti-inflammatory and antibacterial effects of mint both help to soothe most abdominal pains, inflammation in the intestines, removes harmful bacteria, and reduces bloating.

Multiple scientific studies have proven that adding 1 to 2 drops of peppermint essential oils into your herbal teas is beneficial in treating IBS.

The list of herbal teas that can additionally reduce inflammation and symptoms of IBS:

Green tea

Chamomile tea

Ginger tea

Peppermint tea

Sage tea

White tea

Hibiscus tea

Oolong tea

This is because peppermint oil contains menthol, flavanoids, and phenolic acids. These plant-based compound helps to ease the symptoms of IBS while also providing relief. Providing calming and relaxing effects on the muscles of the entire digestive tract

  1. Relieves Indigestion
Indigestion is when your food is sitting in your stomach for a longer period of time before moving into the digestive tract, creating a sense of discomfort and fullness in the upper abdomen.

Similar to ginger and ginseng, mint is just as effective for relieving stomach-related issues such as indigestion and bloating while calming and soothing the area of discomfort.

There are multiple scientific studies that proved that mint works as a laxative due to the essential oils and insoluble fiber, moving food through the intestines at a consistent pace while increasing nutrient absorption.

mint plants growing in a garden

Peppermint essential oil’s health benefits are amplified when paired with caraway oil, reducing intestinal gas production, intestinal cramping, and soothes the digestive tract as well as an upset stomach.

Multiple clinical studies proved that supplementing with both peppermint oil and caraway oil together had similar effects to indigestion medications such as:

Omeprazole (Prilosec, Zegerid)

Lansoprazole (Prevacid)

Rabeprazole (Aciphex)

Pantoprazole (Protonix)

Esomeprazole (Nexium)

Dexlansoprazole (Dexilant)

  1. May Improve Brain Function
Ingesting mint isn’t the only way to get all of its health benefits, inhaling the aroma of essential mint plant oils may additionally benefit your brain functions.

A study conducted on 144 young adults that have been instructed to smell the aroma of peppermint essential oil and ylang ylang.

This was to be done for five minutes for each subject and have all been tested under the Cognitive Drug Research computerized assessment battery.

Peppermint was able to enhance the memory of all subjects whereas ylang ylang slightly impaired memory, and lengthened processing speeds.

Judging subjective mood, peppermint oil increased alertness whereas ylang ylang decreased alertness, but significantly increased calmness.

Another clinical study conducted on 24 participants around the age of 25, found that ingesting or breathing in the aroma equal to a total of 50 to 100 microliters of essential mint oils found these following health benefits:

Increased calcium influx in neurons

Improved performance on a cognitively demanding, Rapid Visual Information Processing task (RVIP)

Prolonged the mental fatigue associated with extended cognitive task performance in healthy adults


  1. Reduces Morning Nausea
Morning nausea is a temporary sickness that’s usually experience by pregnant mothers in their first trimester of pregnancy or through other hormonal changes.

Ingesting and smelling the aroma of a couple of mint leaves is all you’d need to alleviate symptoms of all forms of nausea.

The healthy plant-based compounds and menthol found in mint help reduce blood flow to the digestive area, numb as well as calm the nerves in the stomach area.

Having a similar effect to ginger, expecting mothers can eat mint leaves every morning and the uncomfortable feeling of nausea will be reduced, if not completely removed.

  1. Treats Cold Symptoms
Going through a cold can have drastic and uncomfortable symptoms that may have you feeling miserable, tired, aching, stuffed sinuses, or a headache.

Mint, ginseng, and ginger will all help in relieve your symptoms and get rid of a cold quicker as it’s a strong decongestant. By relaxing your lungs, muscular system, and by clearing your sinuses as well as accumulated mucus in your respiratory system.

Making colds more tolerable and reducing tension and sinus related headaches. Menthol eases other common cold symptoms such as:

Congestion

Low-grade fevers

Sore throats

Runny and stuffy nose and sinuses

Coughs

Muscle aches

Sneezing

Malaise

For optimal results, the aroma of peppermint and mint oil both help decongest your lungs and nasal passages, spreading the menthol through your respiratory tract easier.

bundle of mint herbs

  1. Reduces Breastfeeding Pains
Many mothers experience discomfort and pain when they breastfeed their babies. The pain comes from cracked as well as sore nipples and areola.

The pain can reduce the joy of breastfeeding as well as make it difficult, painful, and sometimes irritating to feed your baby comfortably.

There have been many scientific and clinical studies surrounding breastfeeding pain and breastmilk production with the consumption and application of mint. Usually caused by skin irritation, inflammation, and breast muscle soreness.

The menthol and other compounds found in mint help reduce nerve response, nerve pain, bacteria buildup, and skin dryness due to mint’s antibacterial and tissue flexibility properties. This can also be achieved by rubbing a mint leaf on the affected area.

  1. Reduces Symptoms of Asthma
Asthma is a long-term disease that affects over 305 million people worldwide. Asthma attacks and its symptoms often get worse with stress and anxiety.

Many essential plant oils help treat asthma as well as reduce some of the side effects. Peppermint oil and carrier oil can both be either diffused or applied directly onto your skin.

The plant-based compounds relaxes swollen membranes in the nose as well as the bronchial smooth muscles in the lungs, allowing for more oxygen to enter the respiratory system, loosens mucus, and reduces inflammation of lung tissues.

Here’s a list of foods and ingredients that also help treat symptoms of asthma:

Garlic

Turmeric

Honey

Ginger

Omega-3 fatty acids found in supplements or fatty fish

Coneflower (Echinacea)

Licorice Root

Vitamin D-rich foods, such as fatty fish, eggs, as well as fortified cow milk, soy milk, wheat milk, cashew milk, and almond milk

Beta carotene-rich vegetables, such as carrots, sweet potatoes, kale, spinach, squash, bell peppers, and leafy greens

Magnesium-rich foods, such as avocado, cocoa powder, chickpeas and other beans, nuts and seeds, bananas, spinach, legumes, and tofu

peppermint plants

  1. Mint Helps with Weight Loss
Mint is useful for weight loss because it’s able to more efficiently process foods into energy, this is done by intensely stimulating digestive enzymes in the stomach and colon. This process increases nutrient absorption and your metabolism.

Additionally, mint is very low in calories and is low on the glycemic index which makes it a great herb for gradually losing weight.

  1. Relieves Migraines and Headaches
Mint is a powerful adaptogenic herb that’s been scientifically proven to cure headaches and migraines. About 45% of m peppermint and mint leaves are made up of menthol.

Menthol is able to numb the area it comes in contact with and restricts nerve signals by binding to kappa opioid receptors, also slightly restricting blood flow and reduces inflammation.

When menthol gets metabolized and enters the blood stream, it’s able to pass the blood-brain barrier which allows these health benefits to have an effect on the brain.

Reducing inflammation and slightly reducing blood flow to the brain reduces the intensity of the following types of migraines and tensions:

Migraines with Aura

Migraines without Aura (Common Migraine)

Hemiplegic Migraine

Retinal Migraine

Ice Pick Headaches

Cluster Headaches

Cervicogenic headache

Sinus tension

Nausea

This type of herb is known for supporting the body's ability to accommodate emotional and physical stresses. The goal is to support the energy and assist with stress management. It is the strong aroma that seems to keep the headaches away along with alleviating unwanted stress.


  1. Gets Rid of Bad Breath
Peppermint and spearmint flavored gums are known for eliminating bad breath. This is due to the menthol and antibacterial properties of mint. Chewing parsley leaves can get the same results.

The most common reason for bad breath is due to poor oral hygiene and dry mouths from not drinking enough water. Mint’s essential oils fights off the bad breath causing bacteria on the surface of your tongue, teeth, and gums.

Many gums containing menthol will mask your bad breath as well as coats your mouth with menthol and sometimes chlorophyll.

There are other alternatives to gum, chewing mint leaves or drinking peppermint tea can both help get rid of bad breath and eliminate bacteria in the mouth.

Mint Side Effects and Detriments
Although mint has many health benefits that comes from its essential oils and plant-based compounds, there are still many side effects to using mint.

Most of the harmful effects comes from it’s plant-based compounds, flavonoids, and terpenoids such as menthol, menthone, menthyl acetate, eriocitrin, hesperidin, kaempferol 7-O-rutinoside, limonene, pulegone, caryophyllene, and pinene.

The majority of these active plant-based compounds are used in natural pesticides, herbicides, and insecticides. There have been no reported life-treatening side effects of mint.

Mint has many mild side effects, most of which comes from allergic reactions or irritants from the herb. The mild side effects of mint include:

Heartburn

Dry mouth

Nausea and vomiting

Diarrhea

Rashes, itchiness, and swelling

fresh dried mint in a bowl surrounded by leaves

  1. Reduces Breast Milk Supply
Mint leaves, peppermint, and spearmint all contribute to the reduction of breastmilk for breastfeeding mothers.

As menthol enters the blood stream it' restricts blood flow and nerve responses to multiple area, including the female breasts.

restricting blood flow and nerve responses to the breasts causes the production of milk to slow down and sometimes halt. This makes the existing breastmilk supply dry out quicker than usual.

When breastfeeding, avoid taking any mint supplements or teas for optimal production. This is even more relevant to women who already struggle with producing breastmilk.

  1. Possible Allergic Reactions On The Skin
If you’re unaware about your allergies, you should get tested at your doctor’s office or medical professional as mint may cause allergic reactions inside the mouth, on the lips, and skin.

Many people have sensitive skin, peppermint and mint essential oils could trigger additional issues such as rashes, redness, as well as blistering of dry and sensitive skin.

You may also experience mouth tingling or itching, swolen lips, tongue, and throat, as well as abdominal pains. If you begin to develop hives and/or find it difficult to breathe seek emergency medical help as soon as possible.

  1. Negatively Interacts with Certain Medications
Mint, peppermint, and spearmint can all have negative interactions with various drugs. If taking any prescription medications it’s best to consult your medical professional with any changes you make to your diet.

Here’s the full list of medications and supplements that have additional side effects when including mint into your diet:

Iron supplements

Cyclosporine: Natural immunosuppressant for preventing organ rejection

Stomach acid blockers (Histamine-2 (H2) blockers): Cimetidine (Tagamet), Ranitidine (Zantac), Nizatidine (Axid), and Famotidine (Pepcid)

Antibiotics and antifungal medicine

Antiseizure medication: Acetazolamide, Carbamazepine, and Tegretol

Heart Medications: Acebutolol (Sectral), Atenolol (Tenormin), and Betaxolol (Kerlone)

High blood pressure medications: Diuretics, Beta blockers, ACE inhibitors, Angiotensin II receptor blockers, and Calcium channel blockers


Rating and Recommendation
Highly Recommended

Mint is a healthy herb that can be added to almost any type kind of food or drink. Mostly used for relieving symptoms and issues in the digestive system.

Most of mint’s health benefits comes from mentho which is used to suppress nervous system signals, reducing sensation and numbing, reducing inflammation, and improving digestion.

In addition, the healthy plant-based compounds found in mint such as the flavanoids, flavanols, and phenolic compounds all contribute to increasing the strength of your immune system, its antibacterial, antifungal, and antiviral properties.

Here’s the full list of the health benefits of mint:

Relieves Symptoms of Irritable Bowel Syndrome (IBS)

Relieves Indigestion

May Improve Brain Function

Reduces Morning Nausea

Treats Cold Symptoms

Reduces Breastfeeding Pains

Reduces Symptoms of Asthma

Mint Helps with Weight Loss

Relieves Migraines and Headaches

Gets Rid of Bad Breath

Here’s the full list of side effects of mint:

Reduces Breast Milk Supply

Possible Allergic Reactions On The Skin

Negatively Interacts with Certain Medications

If you have suffered or are currently suffering from heart related issues, seizures, acid reflux, and high blood pressure you should consult your medical professional before adding mint or making any changes to your diet.


Frequently Asked Questions
What are the benefits of mint leaves?
Mint has many health benefits, most of which revolve around the digestive system, blood pressure, and reducing inflammation.

It can be added to many cooking, desert, and drink recipes to give a dish a lighter and fresher flavor.

Here's the full list of health benefits: 1. Relieves Symptoms of Irritable Bowel Syndrome (IBS)

  1. Relieves Indigestion

  1. May Improve Brain Function

  1. Reduces Morning Nausea

  1. Treats Cold Symptoms

  1. Reduces Breastfeeding Pains

  1. Reduces Symptoms of Asthma

  1. Mint Helps with Weight Loss

  1. Relieves Migraines and Headaches

  1. Gets Rid of Bad Breath


How to grow a chocolate mint plant?
The chocolate mint plant (Herbaceous perennial f. citrata) is a fragrant brown and green colored plant that has the appearance and flavor of chocolate.

Chocolate mint plants flourish in moist soil with partial direct sunlight, it's an invasive species so it should be planted in a restricted area.

  1. Soil: Plant your seeds in a rich, moist soil with a pH of 6.5 to 7.

  1. Light: Keep your chocolate mint plant slightly shaded, you can fully expose it to sun if you water it often.

  1. Water: Water the plant with ¼ cup of water and up to ½ a cup if fully exposed to sunlight.

  1. Fertilizer: Mint plants can use between 1 to 2 doses of balanced fertilizer every year during spring.

  1. Harvesting: You can begin harvesting your chocolate mint plant when the height reaches 4 to 5 inches tall. Do not take more than ⅓ of that bush during any harvest.

Make sure to harvest the plant as much as possible in each season, the plant will respond by growing at a faster rate taking up more space.


How to make mint julep?
To make a mint julep, you'll need the following ingredients:

  1. 4 to 5 sprigs of mint or chocolate mint

  1. 1 tablespoon of sugar, honey, sweetener, or any kind of syrup

  1. ¼ cup of bourbon whiskey

  1. Ice

Now you can assemble the ingredients to make your mint julep:

  1. Drop your mint leaves and choice of sugar at the bottom of your cup

  1. Using a pestle or spoon, crush the leaves and sugar to release the essential oils and start binding the ingredients

  1. Add the bourbon whiskey

  1. Fill the cup with ice and sir until everything's fully incorporated

  1. Garnish and enjoy!
submitted by Chris-t-fire to MyDietGoal [link] [comments]

Throwaway account: Disgusting bladder issues and just another attempt at clarifying my schizophrenia diagnosis.

I have two things I want to discuss. I'll start with the shorter, more disgusting ones -- bladder issues. The other is my diagnosis, and the "weird" behavior of the illness I've noticed lately.

Bladder Issues:

Diagnosis Talk:

Before the illness, I traumatized my lower back by falling on a string trimmer. I also traumatized my back, while stupidly doing a spin while dancing.
The first phase of my illness began in a single day, when I was 16. It was severe brain fog, followed by depression, followed by anxiety and desperation, followed by racing, low quality thoughts and some damn bad behavior.
The second phase began 3 years later after I overexerted myself mentally for a week, this showed with a feeling of mental dryness. It was complicated, so details will be lost. I remember experiencing a syncope without passing out, possibly due to shock from severe nose-bleeding. I remember I developed heart health fears and panic after this. There were terrible shoulder pains, that seemed to affect my pulse and were affected by movement of my left hand (I held my hand near my body during this time to avoid pain). I was sent to a neurologist, who didn't find anything. The psychiatrist gave me 1mg sertindole, and the shoulder pains disappeared.
I remember how I developed heart palpitations, that have been now proven by a Holter monitoring session. Basically, I was in bed and something shocked me. I jumped up, and my heart made a very strong beat, that made my spine crackle. I woke up the next morning with comparably severe palpitations (every second or third beat) and bad difficulties breathing. I was extremely panicked.
I withdrew from the sertindole on my own stupidly. Played a social game online and couldn't relax all night. That was my first psych unit visit. On the way there, in the ambulance, my legs were pulling up to my chest, this happened only once and for a comparably short time. My oxygen levels were fine. I felt "drunk" after stepping out of the ambulance.
It seems that my mental health always improves, but I'm under the impression that schizophrenia is a neuro-degenerative disease.
Now, my mental health is rapidly improving with no changes in psychiatric therapy.
About a month ago, I started physiotherapy. I went home and did the exercises and immediately felt an improvement, so I've kept doing the exercises as much as I can (every second day). I stopped doing the exercises after going to the psych unit, where my psychiatrist had promised physiotherapy. I only got one physio visit there in two weeks, sadly, so I went home. But, remarkably, my sleep during those two weeks shrunk from 10-12 hours to 6-7 hours and has remained that way. The nurses measured my blood pressure in the evening, and it was 120/80. Normally, my blood pressure climbs to ~145/80 in evenings. My mood is great, and I feel functional. My heart palpitations disappeared even though I've drunken coffee for the past 3-4 days and studied, which always summons them. (I still had palpitations at the psych unit.)
The complaint I have is that, in specific situations, I feel uneasy, dizzy, physically lacking balance, like there's no ground below my feet. I also feel my pulse strongly enough to fidget with my toes, but a new thing is rarely not feeling my pulse, unless I intentionally check for it. I feel better (but scared, uneasy) when I don't feel my pulse. My pulse feels like it's beating too strong, especially when lying down.
I'm not sure anyone will read all of this, and it's okay. I'm just very hopeful I've found something significant that could save me from more pain.
submitted by Substantial-Opinion to AskDocs [link] [comments]

Prospects of Treating Ocular Hypertension and Glaucoma with Peptidic and Non-Peptide Kinin Mimetic Drugs- Juniper Publishers

Juniper Publishers- JOJ Ophthalmology

Abstract

The endogenously generated small nonapeptide bradykinin (BK) is often associated with inflammation, edema and pain amongst many other functions and pathologies. However, the latter aspects pertain to locally produced BK from circulating plasma precursor polypeptide kinninogen (KNGN). Recent work in ocular tissues and cells have a revealed a novel local synthesis of BK and other kinins from tissue-derived KNGN via action of kallikrien enzymes, quite independent from the blood-derived polypeptide. Furthermore, the whole kininergic system machinery including local KNGN, kallikrein enzymes to generate kinins from KNGN, two sub-types of kinin receptors (Bj-and B2-receptors), and the complete signal transduction pathways coupled to these receptors have been mapped out. Additional work has highlighted a number of downstream signaling and other biological responses that ensue following activation of Ba- and B2 receptors in human ocular cells and tissues. One key aspect to be discussed in detail in this review is the novel finding that BK, peptidergic BK analogs, and especially non-peptide mimetics of kinins (e.g. FR-199097; BKA78), profoundly lower and control intraocular pressure in a number of species, including ocular hypertensive (OHT) monkeys. These novel observations strongly suggest that kinin agonists represent a novel class of ocular hypotensive agents that could be of immense value in treating OHT associated with primary open-angle glaucoma (POAG) and perhaps other forms of glaucoma.

Ocular Hypertension Associated with Glaucoma

At a simplistic level, our knowledge has advanced to a point where it is now clear that elevated intraocular pressure (IOP) results from a fundamental imbalance between the generation of aqueous humor by the ciliary body and its efflux from the anterior chamber of the eye via one of two pathways [1-3]. The most physiologically relevant mechanism of AQH drainage involves the IOP-dependent outflow via the trabecular mesh work (TM) and Schlemm's canal (SC) route [1-3]. The lesser utilized pathways under normal conditions are the uveoscleral [1-3] and ocular lymphatic [4] pathways, but the latter can be engaged by certain drugs such as FP-class prostaglandin analogs (FPGAs) like latanoprost and tafluprost [1-6]. The chronically increased IOP, a condition generally termed as ocular hypertension (OHT), caused by blockage of the AQH drainage TM/SC pathways [7] during the aging process or due to ocular inflammation and deposition of various debris, along with apoptotic death of retinal ganglion cells. can lead to a clinically defined disease called glaucoma [8-10]. This high IOP distressfully distends and traumatizes the whole Whilst, glaucoma is painless and otherwise asymptomatic globe and initiates the death of RGCs and/or breakage of RGC axons at the back of the eye. These elements then cause a retrograde demise of the RGCs leading to severing of nerve fibers connecting the retina to the brain [11-13]. Many deleterious neurotoxic elements (e.g. high levels of extruded glutamate, endothelin, inflammatory cyto-and chemo-kines, noxious gases (e.g. nitric oxide; hydrogen sulfide)) and proteolytic enzymes (e.g. caspases and matrix metalloproteinases) released by activated macrophages [12-19], injured RGCs and interneurons are the culprits responsible for such neurotoxicity/chemically-induced axotomy of the RGCs. Hypoxia and ischemia [20,21] are also involved in the initiation phase of vascular dysfunction-induced death of RGCs since the thinning of the optic nerve at the level of the optic nerve head (ONH) forces the retinal blood vessels attached to the optic nerve to bend thereby restricting blood supply to the retina. While this progressive loss of RGCs occurs over several decades, if OHT is not treated to reduce the IOP the resulting glaucomatous optic neuropathy causes severe visual impairment, reduction of visual acuity and visual field and eventually results in irreversible blindness. Although many forms of glaucoma exist (e.g. open-angle glaucoma; closed-angle glaucoma; exfoliation glaucoma; myopic glaucoma) [8,9,22-26], the most prevalent is primary open-angle glaucoma (POAG) [26-28]. Behind cataracts, POAG is the second leading cause of blindness afflicting several millions of patients. It is estimated that by 2020, the global glaucoma-related blindness will reach ~80 million [26-28]. Elevated IOP and advancing age are the two major risk factors associated with POAG even though genetic factors [26] and race (especially African and Asian heritage) [29], myopia, diabetes and oxidative stress [30-36] and various vascular irregularities and dysfunctions [20,22], and intracranial cerebrospinal pressure [37,38] have been also linked to the development of POAG. The seriousness of POAG is often underestimated since it causes no overt discomfort or pain to the patient and insidiously progresses unnoticed over time. Considerable damage to the retina [33-36] and optic nerve and optic nerve head (ONH) [14,29,39-41] continues unyieldingly leading to scotomatous damage that manifests as loss of peripheral vision followed by a "tunnel vision" syndrome, thereby finally signaling the demise of ~40% of the original million RGCsof the patient and equivalent loss of connections to the brain and visual cortex [8,9,42-45]. Those lost or dying RGCs cannot be resuscitated and their axonal connections revived [46-48], and if left untreated the glaucomatous optic neuropathy due to OHT and oxidative /neurotoxic elements would claim the remaining RGCs causing total blindness [49-53].
Data are mean±SEM uses a [Ca2+]I mobilization assay in cells derived from several different human donors' eyes. h-tNPE cells are SV40-virus- immortalized human non-pigmented ciliary epithelial cells derived from human ciliary epithelium that respond just like normal primary NPE cells. [145,146,157]
A number of treatment options have been developed to deal with POAG-associated OHT including ocular hypotensive medications [1-3,54-56], laser therapy and surgical interventions [57-64]. Unfortunately, as is the case with most drugs and surgical procedures, these treatment modalities have numerous side-effects (e.g. Burning and stinging, foreign- body sensation, brow-ache, ocular surface dryness, pulmonary hypertension and bradycardia, etc.), and adverse complications associated with them [1-3,54,55]. Additionally, poor compliance [65] and adherence to prescribed topical ocularly administrated medications by the OHT POAG patients (due to forget fulness, poor dexterity,lack of symptomatic pain or other cues due to OHT, poor understanding of the treatment regimen, and perhaps due distrust, etc.) contributes to the progression of the disease process. Similarly, laser therapies, although effective at the beginning, lose their efficacy over time [57-62]. Reports have surfaced that indicate that POAG/ OHT is only controlled in ~50% of patients who received laser treatment, and indeed due to scarring,the procedure often needs repeating within one-five years [57-64]. Indeed, such lasering and filtration procedures also have certain risks of complications and adverse events associated with them. Thus, there remains a continued unmet medical need to discover new and improved eye drop- medications and other novel surgical techniques to help the OHT/POAG patients mitigate and treat their underlying glaucomatous optic neuropathy caused by elevated IOP. To this end, a better understanding of the many complex pathways involved in AQH dynamics [4,7-10] has culminated in the discovery and development of many novel targets and ligands [13,54,55] that can modulate IOP via these targets to accomplish a level of homeostasis of AQH production and drainage. In order to address poor patient compliance, a number of innovations leading to sustained drug-release devices (e.g. implants, punctal plugs or contact lenses) [60-64,66-70] have been developed such that the patient need not remember to self-administer the medication. Likewise, a revolutionary set of novel surgical interventions [57-64] with much reduced surgical time and effort required and minimal adverse events and complications are becoming available [57-64]. These include the following: non-penetrating glaucoma surgery (NPGS), non-invasive glaucoma procedure, minimally invasive micro sclerostomy, blebless ab externo glaucoma surgery, ab externo bleb surgery, and the elegant minimally-invasive glaucoma surgery (MIGS) [60-64] that involve insertions of tiny drainage devices into the anterior chamber of the eye that appear to be highly effective in decreasing IOP [62-64]. Time will tell if indeed these innovations become mainstay treatment options for POAG/OHT patients in the near future. Regardless, however, the ordinary patient who is unable to afford the latter surgical procedures and devices, and those patients who are refractory to or cannot tolerate existing medications, will still require new topically administered drugs to lower and control the IOP in order to preserve their vision.

Present Day Pharmacotherapy for OHT

One of the earliest pharmacological agents to be used to lower elevated eye pressure is a muscarinic receptor agonist, pilocarpine [1-3]. It just happened that it promoted egress of AQH through the TM, hence pilocarpine became the first known conventional outflow promoter. Since it strongly constricted the pupil, made accommodation difficult and painful due to brow- ache, and needed to be administered up to 4-times a day, newer drugs with higher efficacy and lesser side-effects were sought and discovered over the next few decades. These included carbonic anhydrase inhibitors such as dorzolamide and brinzolamide, beta-adrenergic antagonists (e.g. timolol; betaxolol) and alpha- adrenoceptor agonists such as brimonidine and para-amino- clonidine [1-3,54,55]. Whilst these drugs lowered IOP well, they required at least twice daily dosing and they primarily inhibited the production of AQH by the ciliary processes of the ciliary body. Eventhough compliance increased and a greater efficacy was achieved, these agents had their own short-comings in terms of side-effects including ocular surface irritation (hyperemia), burning and stinging,allergy and drowsiness (a-agonists), and some pulmonary and cardiac insufficiency (with p-blockers) [13,55] Furthermore, we have learnt that AQH constituents serve important nutritional needs of the tissues inside the anterior chamber of the eye [10], and thus reducing its availability negatively impact the ciliary body, lens, corneal endothelial cells, and may in fact damage the TM and SC endothelial cells. Thus, a major breakthrough in OHT / POAG treatment occurred in the mid-90s when FP-receptor-selective prostaglandin (PG) agonists (PGAs) (e.g. latanoprost; travoprost; bimatoprost; tafluprost; unoprostone isopropyl ester) [3,5,6,71-73] were discovered and introduced into ocular clinical medicine. These PG drugs revolutionized the POAG/OHT treatment paradigm since they required once-daily ocular administration (before bed-time) and were much more potent and efficacious than the existing medications since they created new drainage pathways across the ciliary muscle and sclera (uveoscleral pathway) to help drain the AQH [1-5]. Nevertheless, these novel PGAs had some significant side-effects that included hyperemia, darkening of the iris color and increased pigmentation of the periorbital skin, growth of eye-lashes, deepening of the eye orbit, and in some cases cystoid macular edema [1-5,71-74]. Additionally, some OHT/POAG patients were quite refractory to the PGA drugs such that they required multiple drugs to control their IOPs. Not surprisingly, a multitude of fixed-dose combination products [4,75] containing different dual combinations of various ocular hypotensive drugs (and even a triple combination product) have now become available. However, due to the inherent genetic and biological variation in responses of patients to the different classes of IOP-lowering medications and their relative susceptibility to the side-effects of the drugs, there still remains a great need to hunt for and discover new drugs that are more effective, longer acting, efficacious in majority of OHT patients, and that induce fewer and milder off-target side-effects, thus having a greater therapeutic index than the existing drugs [67,76,77] (Table 3).

Future OHT/POAG Pharmacotherapy

The potential additivity of new pharmacological agents to PGAs in the treatment of OHT and POAG has spurred the recent surge in research for novel agents exhibiting IOP-lowering properties. The realization that POAG is not only caused by elevated IOP since patients with normal IOPs still lose vision [7880], but perhaps is a reflection of enhanced RGC susceptibility to oxidative stress [7-9,12,32-36,42] and apoptotic process [15,47,81-90], has stimulated a renewed interest in finding drugs that have dual or multiplicity of mechanisms of action, including direct potential neuroprotective activity. The latter aspect stems from the finding that agents like betaxolol [91-95] and brimonidine [90,96-99], whilst lowering IOP, also upregulate the release of endogenous neurotrophins [89] in retinal tissues that could heal/rescue some of the RGCs that are compromised from the elevated IOP and oxidative stress. Likewise certain PGAs stimulate blood flow at the ONH in addition to reducing IOP [5,6,100]. Additionally, as the tools to monitor IOP [98,99] have become more accessible at a lower cost and with a greater sensitivity, including round-the-clock monitoring of IOP [99,100], and as new models of OHT/POAG are introduced using various species [48,23-25,101-104], the potential for such innovations to enhance drug discovery have dramatically increased in recent years. The ability to perform AQH dynamic measurements in small laboratory animals like mice [105], and to exploit enucleated and ex-vivo perfused bovine [103,106], porcine [103] and human eye anterior segments, and even whole eye [107], has further accelerated the mechanistic approach to ocular drug discovery and characterization. Accordingly, pharmacological agents that have exhibited ocular hypotensive efficacy in some of these animal/ ex-vivo models include K+- channel openers [108], Na+-K+ -ATPase inhibitor digoxin analogs [109], angiotensin-II receptor antagonists [110,111], renin inhibitors [112], angiotensin converting enzyme (ACE) inhibitors [113-116], ACE-2 activators [117,118], cannabinoids [119], rho- kinase inhibitors [120-122], nitric oxide (NO) donors and their conjugates [123-127], serotonin (5-hydroxy-tryptamine (5-HT)) receptor agonists [103,128,129], hydrogen sulfide donors [130], dopamine receptor agonists [3], melatonin receptor agonists [13], adenosine receptor agonists and antagonists [131], guanylate cyclase activators [123,132], novel EP2 receptor agonists [133,134], dual pharmacophoric PGs encompassing FP and EP3- receptor agonistic properties [135,136], etc. The most recent unexpected discoveries of potential drug candidates for OHT/ POAG treatment pertain to the kallikrein-kinin (KNK) system which will be addressed in detail below (Table 4).
* Values are means±standard deviation. t, comparing hypertensive with contralateral normotensive eyes; �p-values: comparing baseline day with treatment day by Student's two-tailed paired t-test. ACvol, anterior chamber volume, |jl; CCT, central cornea thickness, mm; Cf| fluorophotometric out flow facility, iJl/min/mmHg; Cton, tonographic outflow facility, |j1/min/mmHg; Fa, aqueous flow, |jl/min; FuFI, uveoscleral outflow calculated with Cfl, jl/min; Futon, uveoscleral outflow calculated with Cton jl/min; Times are 30 minutes. FR-190997 (0.01%) was applied as a 30jl drop (total dose of 3jg) to each eye of each monkey Modified from Ref 155.

Conclusion

Clearly there are now several drugs approved for the treatment of OHT/POAG and a number of new AQH drainage devices either approved or on the horizon for the same purpose of lowering IOP It is the issues of compliance, and the number and relative seriousness of the side-effects, or ineffectiveness and complications of the procedures, that continue to warrant hunt for newer more efficacious and more tolerable medications. The latter quest has resulted in the recent discovery of some new ocular hypotensive agents, including the first generation Kenyan non-peptide mimetics such as FR-190997, BK2A78 and their analogs [162-164].
The studies described in this review have clearly shown the presence of various components of the kininergic system in human and monkey ocular cells and tissues using a variety of techniques. Furthermore, functionally active sub-types of BKreceptor (B1- and B2) also are present in the ocular cells involved in AQH dynamics, Hence, BK and its analogs and mimetics are able to generate a variety of second messengers such as inositol phosphates and intracellular Ca2+ in h-NPE, h-CM and h-TM cells. Activation of this signal transduction pathway, then stimulates the production and secretion of PGs from these cells. These PGs are pivotal in promoting the generation and release of MMPs from CM and TM cells that digest extracellular matrix to create new pathways for AQH to drain from the anterior chamber of the eye leading to lowering of the IOP. Such duality of action of MMPs in response to BK receptor activation probably explains the elevated TM/SC outflow and increase of uveoslceral outflow observed after treatment with FR-190997and the profound IOP-lowering that this compound produces [156,160]. These new non-peptidic kinin mimetic drugs [156,162-164] will hopefully inspire other researchers to use these as templates for synthesizing next generation of ocular hypotensive agents, perhaps with some secondary neuroprotective activity on top of the ocular hypotensive properties. We all await the results of such new discoveries.

Conflict of Interest Statement

Author is an inventor or co-inventor of some granted patents related to the use of BK agonists (peptide and non-peptide) for treatment of glaucoma and the associated OHT, and these are cited in this article. The author, is an adjunct professor at Texas Southern University (Houston, TX) and at University of North Texas Health Science Center (Fort Worth, TX), and has no other conflicts of interest to declare. The intent of this review article is simply to share and expand the knowledge of the ocular roles of Kinins and thus inspire further research in this arena for the discovery of novel drugs and treatments to help combat blinding diseases of the eye, especially OHT/POAG.
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submitted by JuniperPublishersOJO to u/JuniperPublishersOJO [link] [comments]

I can feel my heart beat, and it's making me so uncomfortable, I fidget to avoid feeling it. I had bad sleep tonight due to it.

I have documented heart palpitations (SVES, VES, and heart pauses), and I know how each of them shows or how they feel for me. But these heartbeats feel like something is different or wrong. They feel like rhytmic, powerful heartbeats. They're persistent and constant and come on when lying down, mostly. Whenever I have them, they're so uncomfortable, I fidget with my right foot, and I can't focus on anything else but avoiding them -- they're making sleep difficult. I noticed this 7 days ago, and it seems like it's coming on like an episode. I've had similar sensations before. I can usually feel them inside my solar plexus and in my abdomen, sometimes. In general, and even without this issue, I can feel my pulse when I normally shouldn't be able to, I think.
submitted by Substantial-Opinion to AskDocs [link] [comments]

What are the most effective anxiolytic and migraine-prophylaxis beta-blocker for someone with shortness of breath?

Beta-blockers without intrinsic sympathomimetic activity (ISA) provide anxiolytic properties.
Of the above, are there any beta-blockers which best target physiological anxiety and/or migraines, but has less broncho-related side effects?
submitted by thebains to AskDrugNerds [link] [comments]

Registered Dietitians, make a plan of care for my virtual patient. please.

Hi guys!
I'm a nursing student and I've read an RD's scope of practice as well as roles and responsibilities; however, I can't for the life of me figure out from an RD's perspective how to create a plan of care for this virtual patient. I need help or maybe more insight. Do RD's use some kind of templates for a nutritional assessment, diagnosis, implementation, monitoring and dx?
Here's my fake patient:

Interprofessional Standardized Patient Exercise: Case Summary
Patient Name:Brenna Jones
Presenting Problem:
Patient presents to establish care after an Emergency Department visit for a fall. Her main complaints are balance problems and fear of falling.
Actual Diagnoses:
Diabetes mellitus type 2
Peripheral neuropathy
Hypertension
Hyperlipidemia
Chronic kidney disease
Osteoarthritis
Glaucoma
Anxiety
Xerostomia
Patient Demographics:
Age: 75 years old
Sex: Female
Race: Caucasian
Height: average
Weight: Overweight
Overview of Case:
Brenna Jones is a 75 year old woman who comes to your clinic for the first time. She has not seen a doctor for about a year as it has been increasingly difficult to leave her home. Your clinic is closer to her home and easier to get to. Ms. Jones has diabetes, peripheral neuropathy, osteoarthritis, and glaucoma. She is running out of her medications and needs refills. She has fallen several times over the last several months and is very fearful of falling. The goal of the visit from the provider’s perspective is to become acquainted with the patient, to acquire relevant information about her chronic health conditions, to inquire about her adherence to her drug regimen and other health related behaviors, and to prevent future falls. The patient’s agenda is to establish care in order to get medication refills and to prevent future falls.
PRESENTING SITUATION and INSTRUCTIONS TO THE STUDENT
Brenna Jones
Brenna Jones is a 75 year old woman with diabetes, hypertension, osteoarthritis, anxiety, and glaucoma who presented to the Emergency Department (ED) two weeks ago after a fall. She complained of knee pain for which x rays were taken in the ED and showed no fractures. She has not seen a doctor for almost a year as it has been increasingly difficult to leave her home. Your clinic is closer to her home and easier to get to. She is here for follow-up of her ED visit and to establish care in your clinic. You have some records (see below) from the ED.
Vital signs: Prescription Medications:
Temperature: 37.2 C Lantus 15 units at bedtime
Pulse: 72 Glipizide 20 mg twice a day
Respiration: 14 Lisinopril 10 mg daily
Blood pressure: 152/89 Hydrochlorothiazide 12.5 mg daily
O2 Saturation: 100% on room air Aspirin 81 mg daily
Lipitor 80 mg daily
Neurontin 900 mg three times daily
Betaxolol 1 drop daily right eye
Pilocarpine 4% 1 drop four times daily right eye
Vicodin 5/500 mg 1-2 tabs two times daily as needed for pain
Lorazepam 0.5 mg three times daily as needed for anxiety
Height: 5 feet 2 inches
Weight: 155 pounds
Labs/Studies: (from ED visit 2 weeks ago)
Cholesterol 285 mg/dl (high) Na+ 140 mmol/L (normal)
K+ 4.0 mmol/L (normal)
HDL 38 mg/dl (low/normal) Cl- 101mmol/L (normal)
BUN 18 mg/dl (normal)
ALT 35 u/LCreatinine 1.3 mg/dl (abnormal)
AST 40 u/L GFR 51mL/min/1.73 m2(mildly decreased)
Total bilirubin 1.0 mg/dl (normal)
HbA1c 8 (high)
Studies: (from ED visit 2 weeks ago)
Right knee x-ray: marked tricompartmental joint space narrowing consistent with moderate degenerative joint disease
submitted by PradaC to RegisteredNurses [link] [comments]

Beta-blockers in judo competition... ethical or unethical?

I have pretty disabling social anxiety. When I compete, I get violent diarrhea pretty much until I step onto the mat. My IQ drops a few dozen points, and I'm shaky and I can't recall anything that transpires when I'm on that mat. A stark contrast to how I play in randori, even when we go tournament style. Being in front of that many eyes really fucks with me and my body.
I've checked the IJF rules, which follows The World Anti-Doping Code:
"P2. BETA-BLOCKERS
Unless otherwise specified, beta-blockers are prohibited In-Competition only, in the following sports.
 Archery (WA) (also prohibited Out-of-Competition)
 Automobile (FIA)
 Billiards (all disciplines) (WCBS)
 Darts (WDF)
 Golf (IGF)
 Shooting (ISSF, IPC) (also prohibited Out-of-Competition)
 Skiing/Snowboarding (FIS) in ski jumping, freestyle aerials/halfpipe and snowboard halfpipe/big air
Beta-blockers include, but are not limited to, the following: Acebutolol, alprenolol, atenolol, betaxolol, bisoprolol, bunolol, carteolol, carvedilol, celiprolol, esmolol, labetalol, levobunolol, metipranolol, metoprolol, nadolol, oxprenolol, pindolol, propranolol, sotalol, timolol."
It looks like it's not banned for Judo... but that doesn't mean it's entirely ethical.
Would physician-prescribed propranolol be unethical for me to take before a competition?
note: I have already been prescribed it for public speaking (at work and for my Masters studies) and general performance anxiety.
submitted by dzendian to judo [link] [comments]

POAG - Blurry Vision

Hi! I was diagnosed with primary open-angle glaucoma last October. It's advanced stage (I have lost some.vision in both eyes, more in my right than my left). I take brimonidine, dorzolomide, and latanoprost, and was put on betaxolol last month. Had SLT back in December (right) and January (left). Pressures have gone down from 40 to the high teens, but my glaucoma specialist wants to see them go down further due to the advanced stage of my glaucoma.
In late March, I noticed some blurriness, mostly in my left eye (my better eye). It has increased since, and I notice it most at work and in stores (where there is a ton of florescent lighting), and it's starting to get to the point that people's faces are fuzzy until I'm close to them.
I have seen the doctor in April and June. I had a visual fields test in June and it came back with no change since first diagnosis. I have told the doctor about my blurry vision both times, and he says it's dry eye and to take OTC preservative free drops. I've been doing that with increasing frequency for several months now with my vision getting worse.
I'm freaked out because I don't want to lose my remaining vision. I have another appointment in a week and a half. Any advice on what to do? Thanks!
submitted by marinabreeze to Glaucoma [link] [comments]

Wondering what works for some and what doesn't

I'm really glad to see that this sub exists, don't know why I didn't think to look for it earlier! Anyway, I'm 19 years old and have had POTS since I was about 15. So far, I started out on Betaxolol, that has definately helped me the most out of everything I have tried! Other than that, my doctor had me on Effexor, Mestinon, Midodrine, and Adderall, all of those really adversely affected me, Effexor made me really numb to emotions, and withdrawal from it was terrible, mestinon made my stomach problems worse and the scalp crawling from midodrine was unbearable for me, felt way too weird. I'm posting this hoping to hear from other people with POTS and hear what they've tried that's helped them and what they've struggled with.
submitted by cosmicowl29 to POTS [link] [comments]

betaxolol video

Betaxolol GC14021 Betaxolol betaxolol - YouTube Betaxolol Top # 5 Facts - YouTube Betaxolol  Wikipedia audio article - YouTube How To Say Betaxolol - YouTube Pronounce Betaxolol  SpeakMedical - YouTube

Betaxolol ist ein Wirkstoff aus der Gruppe der selektiven Betablocker, der in Form von Augentropfen zur Behandlung eines erhöhten Augeninnendrucks verwendet wird. Die Wirkungen beruhen vermutlich auf einer Reduktion der Kammerwassersekretion. Bei der Behandlung muss beachtet werden, dass der Wirkstoff in den Blutkreislauf aufgenommen werden kann. Deshalb können unerwünschte Wirkungen auftreten, welche unter anderem die Atemwege und den Herz-Kreislauf betreffen. Betaxolol is a propanolamine that is 3-aminopropane-1,2-diol in which the hydrogen of the primary hydoxy is substituted by a 4-[2-(cyclopropylmethoxy)ethyl]phenyl group and one of the hydrogens attached to the amino group is substituted by isopropyl. It is a selective beta1-receptor blocker and is used in the treatment of glaucoma as well as hypertension, arrhythmias, and coronary heart disease. Betaxolol gehört zur Wirkstoffgruppe der kardioselektiven Betablocker. Er bindet nach Einnahme also ausschließlich an Beta-1-Rezeptoren des Herzens. Dadurch verdrängt Betaxolol die aktivierenden Hormone Adrenalin und Noradrenalin von diesen Rezeptoren. Ohne deren Wirkung sinken Zahl und Kraft der Herzschläge. Dadurch wird weniger Blut durch die Gefäße gepumpt und der Blutdruck kann sinken. Betaxolol wird in Tablettenform benutzt, um bei Bluthochdruck die Blutdruckwerte zu verringern und den Blutdruck auf Dauer zu normalisieren.Außerdem wird Betaxolol in Tropfenform angewendet zur Senkung des erhöhten Augeninnendrucks bei grünem Star (Glaukom), insbesondere der Sonderform des chronischen Betaxolol ist ein Arzneimittel aus der Gruppe der Betablocker und Antihypertensiva. 2 Chemie Betaxolol hat die Summenformel C 18 H 29 NO 3 und eine molare Masse von 307,43 g/ mol . Betaxolol is a beta-blocker. Beta-blockers affect the heart and circulation (blood flow through arteries and veins). Betaxolol is used to treat hypertension (high blood pressure). Betaxolol may also be used for purposes not listed in this medication guide. Der Betablocker Betaxolol wird bei hohem Blutdruck eingesetzt. Betablocker beeinflussen das sympathische Nervensystem. Dieses reguliert zahlreiche Körperfunktionen, die nicht der willentlichen Steuerung unterliegen, z. B. die Herzfrequenz, die Weite von Blutgefäßen und Bronchien sowie die Darmtätigkeit. Diese Organe tragen bestimmte Empfangsstellen (Rezeptoren) für die Botenstoffe Adrenalin und Noradrenalin, die aus Nervenendigungen freigesetzt werden. Ein Teil dieser Rezeptoren heißt

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Betaxolol

Chemical Properties, Background of Betaxolol http://www.glpbio.com/betaxolol.html Check my animation made with #FlipaClip Download Free - https://r4x8c.app.goo.gl/avWz Betaxolol Top # 5 Facts How to pronounce Betaxolol Animated Video created using Animaker - https://www.animaker.com Peripheral Nervous System drug commercial. This is an audio version of the Wikipedia Article:BetaxololListening is a more natural way of learning, when compared to reading. Writtenlanguage only began ... Pronunciation of Betaxolol: Learn how to pronounce the word Betaxolol. Definition and meaning can be found here: https://www.google.com/search?q=define+Betax...

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