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abybweisse · 5 years

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LONG VENT POST: Family issues, part 1 of ?

So, a bit ago I said I’m not as active right now, due to family issues. I didn’t want to fill the thread of that post with all the long, sordid details.

Right now I’m trying to get my mother into an “assisted living and memory care” community (nursing home, basically) and doing everything I can to stop her credit union accounts from hemorrhaging from all her incompetence (she’s been scammed a bunch and generally taken advantage of).

Yesterday’s biggest takeaway was the discovery of numerous scams she fell for over the past few years... plus three months worth of fraudulent Uber and Uber Eats charges... and the fact that she pays about $550/mo on car insurance but the last couple times (at least, maybe more) she got collision repairs done? She didn’t file claims and pay a $500 deductible. No, she paid in full, out of pocket. Out $7k instead of $1k for two repairs in just a few months’ time. How can you pay huge insurance premiums and never notify them when you need collision repairs?!

Found out just recently that about a couple years ago, someone scammed her for an easy $5k. Found out she never deposits the full amount on car payments I send her. She never makes full deposits on the rent a tenant pays her. Instead, she cashes much of them out, and I have no idea what she does with the cash.

She buys stuff in bulk but cannot use most of it before it goes bad, but she refuses to toss out expired foods. Her hoarding tendencies have gotten worse. Even though she tells my sister and I not to send her gifts that would add to the clutter in the house, I found out yesterday she’s been dropping $200-$300 on random stuff from places like TJ Maxx and Tuesday Morning just because they made her “happy”. She hasn’t even unpackaged the hanging glass butterflies or other things. I told her she can take them to the “home”....

She’s wrecked two brand new Priuses (about $30k each, each paid up front/in full with inheritance money from my dad, who died five years ago) within about two years’ time. The first was “totaled”, but I have yet to verify whether she ever opened a claim to get money for it. This one hasn’t been officially declared totaled or repairable. I had to file the claim on it on her behalf. For all I know, the $550/mo premium might be on both cars. I’ll know for sure soon. If she’s been paying insurance on a car that was “totaled” two years ago instead of getting market value of about $22k, I will definitely break down and cry. For at least the 50th time in the past few days. Seriously, if she just found out the previous one couldn’t be fixed and walked away from it without filing a claim and getting the huge payout... and is therefore also still paying for insurance on it? I’ll probably scream, too.

The latest (and last ever) car wreck was last Wednesday. We’ve been telling her for over a year she shouldn’t be driving. Her doctors have told her the same for at least 6mo. My sister and I were planning to visit her and take away her keys, but the wreck happened before we could even finalize our travel plans.

This time, she was trying to get to dialysis (she goes three days a week), and she couldn’t use Uber anymore, so she was determined to drive herself. Just before 5 am, she was driving down her own residential street and blacked out (apparently) and hit three parked (and unoccupied) vehicles. Police showed up and she got out of her car and told them she needed a ride to dialysis. One of the officers took her. She can’t recall hitting three cars. Told me she hit a curb and one car. Later told someone else she only hit a curb. I don’t know anything about the curb, but probably. However, I definitely believe the police report that three parked cars were hit badly and had to be towed away, too. After the police spoke to her tenant, they said they’d make things easier for us and revoke her license. Phew.

I convinced dialysis staff (actually, they completely agreed without question) to send her to hospital afterwards instead of letting yet another friend take her home. Good thing, too, because before dialysis was even up that morning, she was in a lot of pain; she had told them earlier she didn’t need to be looked at. Well... no broken bones, no major injuries, and her labs were ok except slightly low potassium. However, a brain scan showed something I already knew just by dealing with her: it showed ischemic changes associated with dementia. Monday of that week, I had called her renal doctor to tell him I worried about her mental health and wondered if it had anything to do with the renal failure. He said he didn’t think so; it’s got to be something else causing the mental decline we are seeing. When I told him she’s still driving sometimes, he became furious and said he’d refer her to get a full dementia evaluation. Well, before he could even get the referral to her, she’d wrecked again. He’s seen her now, but I haven’t heard any updates from him. Mom says she hasn’t done the evaluation (that she knows of), and she heard someone at the hospital mention “dementia”, but she doesn’t recall what they said about it. 😔

I didn’t take photos when I finally saw her car, but I’m going back up to Dallas tomorrow and staying in a Motel 6 overnight (with my dog) to take care of as much financial matters for her as I can in these next two days. I’ll get another chance to see the car (to clean out items), so I’ll take pics then. I might not get back to Austin until sometime Wednesday. Not sure about Wednesday yet, but I already requested Monday and Tuesday off from work by email and left a vm with coworkers. I’m about to run out of annual leave because of this. I know I’ll be making many weekend trips coming up until my sister and I have gotten her moved into the nursing facility. And for a while afterwards, too, since we have to clean out the house, put some of her stuff into a storage unit, and sell the house ASAP. Plus, we need to visit often, at least at first, to make sure she’s settled in, isn’t hating it too much, and is being taken care of properly.

It’s a good thing my sister is paying for my hotel charges and has also offered gas money (though I haven’t asked for gas money... yet). This is still way cheaper for her than booking herself flights back and forth between Olympia, WA and Dallas, TX. The more leg work I do on this, the happier my sister is to help with my travel costs. Honestly, she really doesn’t want to come down here until it’s time to move our mom, clean the house, and put it up for sale.

And, since we have so little time to get her affairs in order, we are placing her in the only community my mom and I have toured, so far. I told her if it turns out to not be a good place (at all) once she moves in, we can keep looking at others (while she still lives at that one) and move her again. But, honestly, this place does seem nice enough, and none of these places are perfect. Plus, it’s right next to the hospital where she always goes... the one where her doctors are associates. I joked that if they needed to send her to the hospital, they could put her on a gurney and wheel her down the street. She laughed at that and said the location is perfect.

Sigh. She’s being compliant and has even said thanks for us (her two daughters) stepping up to help her and get things taken care of. We were afraid she would refuse to leave her house of almost 40years. She’s not even batting an eye at us deciding to sell the house to make sure she can afford the rent and services (the suites at the community are rented out like apartments, but with three meals a day and unlimited snacks, weekly cleaning service, weekly laundry service, landline phone, cable, and internet included. We will have to pay more for “memory care” and probably for medical transport they provide (unless that’s included, too), plus whatever else. She might take her cat with her, or she might leave him with a friend of the family. But it’s a one-time, non-refundable fee of $500 if she keeps him. I kind of hope she gives him up, and they just bring him along on visits to her. She would have trouble taking care of him.

She’s never shown me her finances before. We had no idea how bad (completely uncontrolled) her spending was. It was probably bad enough before our dad died, but afterwards, she started going downhill fast. Now she’s in renal failure and requires dialysis three days a week. She’s recently lost an unhealthy amount of weight in a very short time, apparently because she can’t remember to eat and sometimes she’s too disoriented to get up. She can’t cook anymore, and she’s hardly done cleaning chores since she had kids (that’s what us kids were for: housework). So she’s a money-wasting hoarder in a house full of dirty dishes, dirty clothes, clutter everywhere, and $100’s — maybe $1000 worth — of groceries she can’t get through but won’t throw out when they go bad. And she won’t let anyone else touch them while she’s still living there.

I have so much to do the next couple days, I had to write a list of each thing I need to look into and take care of before I return home. I still have some stuff to get ready for the trip, so this is the end of the first vent post.

I hope I get more sleep tonight than I have the past week....

#off topic #PLEASE DO NOT REBLOG #will reblog to off topic #might delete later #venting #family problems #dementia #assisted living #nursing home #memory care #long post #personal post

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yuki-urameshi · 2 years

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TL;DR: Marilyn Monroe, my 14 year old cat, has a mass in her stomach. I need help paying the other $500. I am paying $100 every two weeks, but would love to pay it all up front. There's a lot more that goes with the story, but this is the TL;DR version

Donations can be made at: paypal.me/bronzecoffee Reblogs are MORE than welcomed.

Marilyn Monroe has been with me for 13-14 years now. She's at least 14 because she was already a fully grown cat when I got her. She's never had a heat and has only been around neutered males as long as I've owned her. A couple of week ago my sister, that I live with, said she thought Marilyn lost weight, and she was right. She did look really slender. Marilyn's always been round. To the point people asked me a lot if she was pregnant, and I always said no. About a week ago she stopped eating all her dry treats. Then she didn't eat any of them. I was concerned, but also thought maybe she got tired of the flavor. It's been the same one for a while now. This past Thursday, Jan. 6, we took her to the vet for a senior screening, which is blood work, her vaccines, and rabies shot. I tried to warn the vet we took her two that she doesn't like being handled. I mentioned they could use a muzzle and gloves, even a blanket. They didn't, and it took two of the techs to hold her down while scruffed. They stressed her so badly she urinated all over herself, bit the clippers while scruffed, and it was a mess. The stress elevated her kidney levels for the exam enough for them to call me and tell me she had 'elevated levels'. I didn't really understand what she was talking about, it was so fast and over the phone. Didn't really give me time for questions. She mentioned the words 'renal' and KD diet, which I had to Google just meant a kidney diet. Took her home and she was mad but seemed OK. She didn't eat Thursday, Friday, or Saturday. I called the emergency vet in the area and asked if that was normal, and they said no. I should probably bring her in. So I did that. They sedated her after I told them what happened at the first vet. They retook her blood work and ran a urinalysis. Her kidney levels were well within normal, but her blood looked like she was fighting an infection/inflammation. They found a hard mass her in abdomen. They also gave her under the skin fluids, a pain relief shot that would last a few days, because it is squishing up her organs, and a nausea medication because she was throwing up prior to when she stopped eating. (Also had her claws clipped so she stopped taking out the techs.) Told me to go back to the vet for an xray because it would be cheaper than at their hospital. The first vet that stressed her out so much was the only one that could take her in today. So I did that. They said it went a lot better than normal. Today they found what looks like a couple of calcified/mummified kittens in her abdomen/uterus. They're not 100% sure that's what it is. She's having surgery tomorrow, Jan. 11, 2022. It needed to be done quickly since it was clearly impacting her eating and drinking. I paid $480 on a $1000 bill today. They let me set up a payment plan, but I can only do $100 every two weeks. I don't get paid much. Any and all help is appreciated, from reblogs to donations.

#cat post #vet bills #need help #donations #reblogs are appreciated

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bepejojag · 2 years

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Abstract algebra an introduction 3rd edition solutions pdf

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siva3155 · 4 years

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300+ TOP MEDICAL SCIENCE Objective Questions and Answers

MEDICAL SCIENCE Multiple Choice Questions :-

1) Regarding serratus anterior muscle which is incorrect? A. Multipinnate muscle B. Lifts arm above the shoulder C. Supplied by long thoracic nerve D. Originates from lower eight ribs Ans: D 2) The treatment of choice for atticoantral variety of chronic suppurative otitis media is: A. Mastoidectomy B. Medical management C. Underlay myringoplasty D. Insertion of ventilation tube Ans:A 3) All of the following are the complications in the new born of a diabetic mother except? A. Hyperbilirubinemia B. Hyperglycemia C. Hypocalcemia D. Hypomagnesemia Ans:B 4) The correct line of management in child who has swallowed a coin is? A. Fiber optic endoscopy B. Rigid endoscopy C. Laparotomy D. Wait and Watch Ans: D 5)Helper cells belong to? A. T cells B. Macrophages C. B cells D. Monocytes Ans:A 6)Mac Ewen's triangle can be felt through the? A. Superior conchae B. Cymba conchae C. Middle conchae D. Posterior part of auricle Ans:B 7)Most common strain of E.coil giving rise to traveller's diarrhoea is? A. Entero-invasive E.coil B. Entero-pathogenic E.coil C. Entero-toxigenic E.coil D. Entero-aggregative E.coil Ans:C 8)With urine turning green on ferric chloride test, the diagnosis is: A. Phenylketonuria B. Alkaptonuria C. Multiple carboxylase deficiency D. Glutaric aciduria Ans:A 9)For assessing the ability of protein utilisation the best index is? A. Urea B. Uric acid C. Blood ammonia D. Urinary nitrogen content Ans:D 10)Screening test is not useful when? A. Incidence of the disease B. Incidence is low in the community C. Early detection leads to favorable outcome D. The disease has a lead time Ans:B

MEDICAL SCIENCE MCQs 11)Nerve not related to humerus is? A. Radial B. Median C. Axillary D. Musculocutaneous Ans:D 12)What is the percentage of chances of hydatidiform mole to develop choriocarcinoma? A. 5% B. 15% C. 50% D. 80% Ans:B 13)Vasomotor reversal of Dale is because of? A. Block of alpha receptors B. Block of alpha & beta receptors C. Agonistic action on alpha receptors D. Adrenaline only Ans:A 14)Primary visual field is situated around the ______ sulcus? A. Central B. Calcarine C. Superior temporal D. Inferior occipital Ans:B 15)Medical treatment for BPH includes? A. Finesteride B. Methyl testosterone C. Oestrogens D. Osmic acid Ans:A 16)Anterior dislocation of shoulder causes all except? A. Circumflex artery injury B. Avascular necrosis head of humerous C. Brachial plexus injury D. Chip fracture scapula Ans:D 17)HIV is a? A. Retrovirus B. Flavivirus C. Oncovirus D. Arbovirus Ans:A 18)In shigella dysentery associated hemolytic uremic syndrome, the false statement is? A. Leucocytosis B. Neurological abnormalities C. Hepatic failure D. Thrombotic angiopathy Ans:C 19)Dengue hemorrhagic fever is caused by? A. Type I secrotype B. Re-infection with the same serotype of dengue virus C. Re-infection with the different serotype of the dengue virus D. Re-infection in immunocompromised host Ans:C 20)When the sample size is less than 30, one of the following modifications is made in the formula of standard deviation? A. Numerator is increased B. Denominator is decreased C. Both numerator and denominator are changed D. Numerator is decreased Ans:B 21)Oesophagus receives blood supply from all except? A. Inferior thyroid artery B. Inferior phrenic artery C. Internal mammary artery D. Bronchial artery Ans:C 22)All are pencillinase resistant except? A. Methicillin B. Nafcillin C. Penicillin D. Dicioxacillin Ans:C 23)Mild hemolyti anaemia is associated with vitamin.. . Deficiency? A. B6 B. E C. A D. C Ans:B 24)Trimethoprim acts by? A. Inhibiting DHFR B. Inhibiting cell metabolism C. Inhibiting DNA D. Inhibiting RNA Ans:A 25)Paradoxically split second heart sound signifies severe? A. Pulmonary stenosis B. Mitral stenosis C. aortic stenosis D. tricuspid stenosis Ans:C 26)Riboflavin nutritional status is assessed by? A. Xanthine oxidase levels in RBC's B. Glutathione reductase activation in RBC's C. Urine excretion of Riboflavin D. Cytochrome- C-reductase levels in kidneys Ans:B 27)Provision of free medical care to the people at government expense is known as? A. State medicine B. Social therapy C. Social medicine D. Social insurance programme Ans:A 28)Shortest sacrocotyloid diameter causing narrowing of pelvis is a feature of which type of maternal pelvis? A. Android B. Gynaecoid C. Platypelloid D. Anthropoid Ans:C 29)What is Bennett's fracture? A. Fracture dislocation of base of first metacarpal B. Fracture dislocation of base of first metatarsal C. Fracture of first metatarsal D. Fracture of first metacarpal Ans:B 30)All the following techniques are helpful in the diagnosis of haemoglobinopathies, except? A. Alkali denaturation test B. Cellulose acetate electrophoric C. Sickling test D. Osmotic fragility test Ans:D 31)Which of the following is not likely in patients taking amiodarone? A. Pulmonary fibrosis B. Hypothyroidism C. Hyperthyroidism D. Gynaecomastia Ans:D 32)Which of the following helps in preventing colon cancer? A. High fiber diet B. Selenium C. Antioxidants D. Fatty food Ans:A 33) Size of ovary, above which considered to be malignant? A. 2 cm B. 5 cm C. 8 cm D. 10 cm 34)Cadaveric spasm A. Instant in onset B. Confined to small group of muscles C. Occurs only in voluntary muscles D. All of the above Ans:D 35)The radionuclide used for ventriculography is A. Thallium B. Technetium C. Gallium D. Pottasium Ans:B 36)"Signet ring cells" are seen in? A. Carcinoma cervix B. Carcinoma endometrium C. Krukkenberg tumour D. Carcinoma vulva Ans:C 37)Cimetidine was synthesized by? A. Black B. Upjohn C. Lindsay D. Lilly Ans:A 38)Nutritional status of children between 0-4 years in a community can be assesed by all except? A. Mortality in 0-4 years B. Birth weight of less than 2.5 gm C. Maternal Hb D. Height and weight of all preschool children Ans:C 39)Pulmonary fibrosis in Bronchogenic carcinoma of lung may follow exposure to? A. Coal dust B. Silica C. Asbestos D. Bagasse Ans:C 40)Ejection fraction increases with? A. Decrease end-systolic volume B. Decrease end-diastolic volume C. Decreased peripheral resistance D. Venodilation Ans: A 41)Which is NOT visualized on posterior rhinoscopy? A. Eustachian tube B. Inferior meatus C. Middle turbinate D. Posterior border of nasal septum Ans:B 42)Which one of the following would cause a metabolic acidosis is with a normal anion gap? A. Renal tubular acidosis B. Acute renal failure C. Diabetic ketoacidosis D. Aspirin overdose Ans: A 43)All of the following organs contain aneurysm in polyarteritis nodosa except? A. Liver B. Lung C. Kidney D. Pancreas Ans: C 44)Diphtheria toxin acts by? A. Inhibiting Acetyl Choline release B. Inhibiting glucose transport C. Increasing levels of Cyclic AMP D. Inhibiting protein synthesis Ans:D 45)Smokeless gun powder is composed of? A. KMno4 B. HCN C. Nitrocellulose D. Sulphur Ans:C 46)Cetuximab (an EGFR antagonist) can be used in? A. Palliation in head and neck cancer B. Anal canal carcinoma C. Gastric cancer D. Small cell lung carcinoma Ans:A 47)The formula showing relations of pressure, thickness and radius? A. Laplace formula B. Ohm's law C. Pascal's law D. Poisseulle's formula Ans:A 48)Dapsone is useful for treating all except? A. Leprosy B. Dermatitis Herpetiformis C. Madura Foot D. Lymphoma Ans:D 49)The most important factor to overcome protein energy malnuntrition in children less than 3yrs is; A. Suply of subsidized food from ration shop B. Early supplimentation of solids in infants C. immunization to the child D. Treatment of anaemia and pneumonia in infant and toddlers Ans:B 50)The binding of 2,3 BPG to Hemoglobin is to? A. Carboxyterminal B. Amino terminal C. Sulphydryl groups D. None of the above Ans:B MEDICAL SCIENCE Objective type Questions with Answers 51)Dissociate anaesthesia is described with which of the following? A. Propofol B. ketamine C. Thipental D. Halothane Ans:B 52)In colour Doppler the colour depends upon? A. Strength of returning echo B. Relation of transducer to blood flow C. Frequency of Doppler used D. Type of Doppler machine used Ans:B 53)The commonest cause of breech presentation is: A. Prematuarity B. Hydrocephalus C. Placenta praevia D. Polyhydramnios Ans:A 54)Which of the following pathologic processes in an example of dysplasia? A. Actinic keratosis B. Chronic cystitis C. Chronic bronchitis D. Ulcerative colitis Ans:A 55)True regarding tubercular meningitis: A. Generally occurs as dissemination of a miliary tuberculosis B. The cranial nerves frequently are involved C. The most common affected leptomeninges are at the base of the brain D. Communicating and obstructive hydrocephalus cortical abscesses, and empyemas are very uncommon complications Ans:D 56)Haemostasis means? A. Coagulation B. Maintenance of electrolyte balance C. Sufficient hydration D. Arrest of bleeding Ans:D 57)The average coronary blood flow in human being at rest is _ % of cardiac output ? A. 4.5% B. 5-10% C. 10-15% D. 15-20% Ans:A 58)Rigor mortis first starts in? A. Upper eyelids B. Lower eyelids C. Lower limbs D. Fingers Ans:A 59)Madura foot is caused by? A. Blastomycosis B. Nocardia C. Candida albicans D. Tinea versicolor Ans:B 60)Population of 10000, birth rate 36 per 1000, 5 maternal deaths, the MMR is? A. 14.5 B. 13.8 C. 20 D. 5 Ans:B 61)Which of the following is not in WHO surveillance? A. Rabies B. Influenza C. Malaraia D. Varicella Ans:D 62)The cause of breech presentation are all except? A. Previous caesarean section B. Placenta previa C. Contracted pelvis D. Oligohydramnios Ans:A 63)True about minoxidil is? A. Increases hair growth B. Antihypertensive C. Both D. None Ans:C 64)Cold agglutinins are seen in? A. Mycoplasma pneumonia B. Psittacosis C. Legionella pneumonia D. TB Ans:A 65)No. of negative stools mandatory to release a case from isolation in typhoid? A. 3 samples same day B. 2 samples on first day and 1 sample on the second day C. 1 sample of first day and 2 samples on the second day D. 3 samples on 3 separate days Ans:D 66)The most specific feature of death due to hanging is? A. Tardieu spots B. Ligature mark C. Fracture of thyroid cartilage D. Dribbling of saliva Ans:D 67)Cauliflower ear is due to? A. Haematoma B. Carcinoma C. Fungal infection D. Herpes Ans:A 68)Following agents have effects on the NMJ, EXCEPT A. Curare B. Decamethonium C. Succinylcholine D. Hexamethonium Ans:D 69)Entamoeba, which is not found in gut? A. E.coli B. E.histolytica C. E.gingivalis D. E.nana Ans:C 70)most deaths involving placenta previa result from? A. Infection B. Toxemia C. Hemorrhage D. Thrombophlebitis Ans:C 71)Tympanic plexus is formed by? A. Tympanic branch of glossopharyngeal nerve B. Vagus nerve C. Facial nerve D. mandibular nerve Ans:A 72)Prolactin? A. Facilitates B. Prevents ovulation in lactating women C. In responsible for formation of corpus luteum D. Is responsible for progesterone secretion Ans:B 73)Herpes zoster involves? A. Otic ganglion B. Gasserian ganlion C. Geniculate D. Celiac ganglion Ans:B 74)In wolf- parkinson white syndrome, there exist a connection between atria and? A. Bundle of His B. Ventricles C. A-V node D. Purknje fibres Ans:B 75)Polyhydramnios is seen in all the following except: A. Diabetes B. Renal agenesis C. Esophageal atresia D. Hydronephrosis Ans:B 76)Following is the adjuvant for the treatment of nephrotic syndrome? A. levamisole as immunomodulant B. B.complex C. cyclosporin D. steroid Ans:D 77)Subarachnoid Haemorrhage is diagnosed by? A. Lumbar puncture B. CT scan C. MRI D. X-ray skull Ans:A 78)Disturbances of affect include all except? A. Panic B. Apathy C. Phobia D. Obsession Ans:D 79)Deep transverse arrest is seen in? A. Occipito-posterior position B. Occipito-anterior position C. Breech delivery D. Face presentation Ans:A 80)Kallu, a 25 yr male pt.presented with a red eye and complains of pain, photophobia ,watering and blurred vision. He gives a history of trauma to his eye with a vegetable matter. Corneal examination shows a dendritic ulcer. A corneal scraping was taken and A. Herpes simplex B. Acanthambea C. Candida D. Aeno virus Ans:B 81)Glass vessels and syringes are best sterilised by A. Hot air oven B. Autoclaving C. Irradiation D. Ethylene oxide Ans: A 82)Management of extradural hemorrhage is: A. Immediate evacuation B. Evacuation after 24 hrs C. Antibiotics D. Observation Ans:A 83)A Post- Thyroidectomy patient develops signs and symptoms of Tetany. The management is? A. I.v.Calcium gluconate B. Bicarbonate C. Calcitonin D. Vitamin D Ans:A 84)The most effective treatment in the early stages of trachoma is? A. Penicillin locally B. Choromycetin systemically C. Sulphonamides systemically D. Soframycin locally Ans:C 85)Ideal treatment of Tinosporidiosis is: A. Rifamipicin B. Excision with cautery at base C. Dapsone D. Laser Ans:B 86)Epithelium of cornea is? A. Pseudostratified B. Transitional C. Stratified squamous keratinized D. Stratified squamous non-keratinised Ans:D 87)Bagasosis can be prevented by spraying Bagasse with? A. 10% acetic acid B. 5% acetic acid C. 1% propionic acid D. 2% propionic acid Ans:D 88)Mc Ardles disease is due to the deficiency of? A. Glu 1 phosphatase B. Gluc1, 6 diphosphatase C. Gluc 6 phosphatase D. Myophosphorylase Ans:D 89) Satiety center in hypothalamus is regulated by? A. Gastric dilatation B. Blood glucose levels C. Blood insulin levels D. All of the above Ans:B 90)Coagulative necrosis is seen in all except? A. Myocardial infarction B. Burns C. Tuberculosis D. Zenker's degeneration Ans:D 91)The relationship between incidence and prevalence can be expressed as the? A. Product of incidence and mean duration of disease B. Divident of incidence and mean duration of disease C. Sum of incidence and mean duration of disease D. Difference of incidence and mean duration of disease Ans:A 92)In twin pregnancy, treatment of choice when first baby is in transverse lie is: A. Home delivery B. Cesarean section C. High forceps D. Low forceps after external rotation Ans:B 93)Coose among the following the most important lab finding in nephrotic syndrome? A. B-J protine B. hyperkalemia C. hypoalbuminemia D. hypertension Ans:C 94)Which statement is not true regarding Cryptic military Tuberculosis? A. X-ray diagnsis is possible B. It is seen in PEM Children C. Mntoux test is negative D. Leucocytosis is seen Ans:B 95)Commonest histology of carcinoma of endometrium is? A. Squamous cell B. Clear cell C. Adeno carcinoma D. Anaplastic carcinoma Ans:C 96)True regarding Felty's syndrome is all EXCEPT A. Splenomegaly B. Rheumatoid arthritis C. Neutropenia D. Nephropathy Ans:D 97)The true statement about Zenker's diverticulum is; A. It is outpouching of ant.pharyngeal wall above the cricopharyngeus muscle B. Barium swallow lateral view for diagnosis is the best investigation C. it is a true diverticulum D. it is congenital Ans: A 98)Which of the following statements about aging is true? A. Zoo animals have shorter lifespans than animals in their normal habitat B. All animal species have approximately the same lifespan C. Men are programmed to live longer than women. D. Identical twins have a natural lifespan of approximately similar duration Ans:D 99)Characteristic features of kwashiorkor include following EXEPT? A. Anorexia B. Flaky paint dematosis C. Hepatomegaly D. Splenomegaly Ans:D 100)Most common site of obstruction in gallstone ileus is? A. Colon B. Illeum C. Jejunum D. Duodenum Ans: B MEDICAL SCIENCE Questions and Answers pdf Download Read the full article

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mariebenz · 5 years

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Racial & Ethnic Differences in Pregnancy Rates Among Women on Dialysis

MedicalResearch.com Interview with:

Dr. Silvi Shah Silvi Shah, MD, MS, FACP, FASN| Assistant Professor Division of Nephrology, University of Cincinnati Cincinnati, OH-45267 MedicalResearch.com: What is the background for this study? Response: Our study uses data from the largest retrospective cohort of dialysis patients in the United States from the United States Renal Data System to determine pregnancy rates and factors associated with pregnancy in 47,555 women aged 15-44 years on dialysis. We identified 2,352 pregnancies with a rate of 17.8 pregnancies per 1000 person-years (PTPY) with the highest rate in women aged 20-24 years (40.9 PTPY). MedicalResearch.com: What are the main findings? Response: The present study shows racial/ethnic differences in the occurrence of pregnancy among women on dialysis. Native American, black and Hispanic women had a higher likelihood of pregnancy as compared to white women. Women with end-stage kidney disease (ESKD) due to glomerulonephritis, malignancy and hypertension had a higher likelihood of pregnancy than women with end-stage kidney disease due to diabetes, while women on peritoneal dialysis had a lower likelihood of pregnancy than women on hemodialysis. MedicalResearch.com: What should readers take away from your report? Response: Our study highlights higher pregnancy rates in women with end-stage kidney disease in the United States than the prior reports. Pregnancy therefore is not uncommon among women undergoing dialysis. Our report uses data from a national registry and did not have the limitation of the reporting bias from the surveys or voluntary registries. The study improves our understanding of various factors associated with pregnancy like race/ethnicity, ESKD cause and type of dialysis modality. This information is particularly important during pre-pregnancy counseling and shared decision making. MedicalResearch.com: What recommendations do you have for future research as a result of this work? Response: The real reasons for racial and ethnic differences in pregnancy rates among women on dialysis remain unknown and further study future research is therefore needed to better understand and reduce these differences. We were also not able to determine the differences in unintentional and intentional pregnancies and whether level of education was associated with the likelihood of pregnancy. MedicalResearch.com: Is there anything else you would like to add? Response: I would like to thank my entire team at the University of Cincinnati who participated in the project. The research was supported by intramural funds of Division of Nephrology, Kidney C.A.R.E (Clinical Advancement, Research and Education) Program, University of Cincinnati. The authors have no disclosures. Citation: Racial Differences and Factors Associated with Pregnancy in End Stage Kidney Disease Patients on Dialysis in the United States Silvi Shah, Annette L. Christianson, Karthikeyan Meganathan, Anthony C. Leonard, Daniel P. Schauer and Charuhas V. Thakar JASN September 2019, ASN.2019030234; DOI: https://doi.org/10.1681/ASN.2019030234 The information on MedicalResearch.com is provided for educational purposes only, and is in no way intended to diagnose, cure, or treat any medical or other condition. Always seek the advice of your physician or other qualified health and ask your doctor any questions you may have regarding a medical condition. In addition to all other limitations and disclaimers in this agreement, service provider and its third party providers disclaim any liability or loss in connection with the content provided on this website. Read the full article

#ASNKidney #ESRD #hemodialysis #kidneydisease #pregnancy #uc_health

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smarthelpers-blog · 5 years

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didanawisgi · 7 years

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Clinical Significance

Guidelines by the Center for Nutrition Policy and Promotion recommend a daily sodium intake to be less than 2300 mg/d in the general population and 1500 mg/d among people at greater risk of cardiovascular diseases (ie, individuals aged >50 years, African Americans, and those who have hypertension, type 2 diabetes mellitus, or chronic kidney disease).1 The American Heart Association has recently emphasized goals to achieve “Ideal Cardiovascular Health” by 2020, and one of the dietary metrics is daily sodium intake of less than 1500 mg/d.2

Evidence concerning a possible beneficial effect of dietary sodium restriction on cardiovascular events and cardiovascular and all-cause mortality is largely indirect. Most of the studies testing a “low sodium diet” use surrogate markers for detecting sodium intake, such as 24-hour dietary recall, food questionnaires, and urinary sodium excretion. Moreover, most trials testing a low sodium diet offer dietary advice to restrict sodium and do not randomize patients to the exact same diets, with the only difference being a reduction in the sodium intake.

On the outcomes side, most evidence for the effects of sodium on cardiovascular-related outcomes relates to blood pressure. Although there are reasonable data to support that sodium restriction lowers blood pressure, the effects may be transient and inconsistent, with some individuals even having paradoxical increases in blood pressure. The degree of blood pressure lowering on average might be clinically trivial, approximately 2 mm Hg in normotensive individuals and approximately 4 mm Hg in hypertensive individuals. Finally, sodium restriction also has the adverse effects of activating the renin-angiotensin-aldosterone system, increasing catecholamines, and adversely affecting insulin and lipids.3 Whether a reduction in any of the surrogate markers will lead to a decrease in morbidity and mortality of the population needs to be established independently of these surrogates, and such evidence is scarce.4

Reaching a definitive position is further complicated because a large portion of evidence supporting low sodium diets comes from observational studies and nonrandomized trials.5 Among the randomized studies, many evaluated a large decrease in the sodium intake for a short period of time or a small decrease in the sodium intake for a long period of time. Both of these study designs represent situations that may not be directly applicable to real-life situations.

This review critically analyzes the data for low sodium diets, starting with surrogate markers such as blood pressure and other risk factors such as type 2 diabetes mellitus, and then moving to clinical outcomes such as cardiovascular morbidity and events, and cardiovascular and overall mortality.

Surrogate Markers

Much of the support for the idea that a low sodium diet leads to a lower blood pressure comes from the Dietary Approaches to Stop Hypertension (DASH) study.6 This study enrolled 412 participants and randomly assigned them to receive the control diet or the DASH diet. In both groups, the participants were assigned randomly to a high sodium diet (150 mmol/d), normal sodium diet (100 mmol/d), or low sodium diet (50 mmol/d) for 30 consecutive days and were then crossed over within their assigned groups. When the participants were shifted from a high sodium diet to a normal sodium diet, the systolic blood pressure decreased by 2.1 mm Hg (P < .001) in the control group and by 1.3 mm Hg (P = .03) in the DASH group. When they were shifted from a normal sodium diet to a low sodium diet, there was a further reduction in systolic blood pressure of 4.6 mm Hg in the control group (P < .001) and 1.7 mm Hg in the DASH group (P < .01). When compared with the controls, the DASH diet led to a lower systolic blood pressure of 7.1 mm Hg in participants without hypertension and 11.5 mm Hg in participants with hypertension. However, the DASH diet was significantly different from the control diet in terms of more fruits, vegetables, low-fat dairy foods, whole grains, poultry, fish, nuts, potassium, calcium, magnesium, dietary fiber, and protein, and less red meat, sweets, sugar-containing beverages, total and saturated fat, and cholesterol. Although the group on the DASH diet had a lower urinary sodium excretion, this does not necessarily imply that the benefit was being solely delivered by a dietary sodium reduction. In addition, this study did not evaluate the long-term effects of the intervention and the clinically relevant variables, such as mortality or morbidity.

Salt and Type 2 Diabetes Mellitus

In patients with type 2 diabetes mellitus, a low sodium diet has been associated with increased cardiovascular and all-cause mortality.7 Even moderate salt reduction may lead to increased activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, and insulin resistance.

A cohort study7 enrolled 638 diabetic persons who were consistently followed for a period of 9.9 years. Their baseline urinary sodium excretion levels were 184 ± 73 mmol/24 hours, which remained constant throughout the study duration. Urinary sodium levels were inversely related to the all-cause mortality rate (P < .001) and cardiovascular mortality rate (sub-hazard ratio [HR], 0.65; confidence interval [CI], 0.44-0.95; P = .03). Each 100 mmol increase in the urinary sodium excretion led to a decrease in all-cause mortality of 28% (95% CI, 6-45; P = .02). This study implies a potential contraindication to a low sodium diet not only in those with type 2 diabetes mellitus but also by extension in the general population because of the widespread prevalence of type 2 diabetes mellitus. This leads to the question, are the current dietary guideline recommendations for a low sodium diet in the general population (including type 2 diabetes mellitus) appropriate? The limitation index of these data is that the results are based on a cohort study examining urinary sodium excretion levels versus a randomized controlled trial of patients receiving identical diets, with the only variation being the amount of sodium intake.

Patient-oriented Outcomes: Morbidity and Mortality

Congestive heart failure is characterized by various processes that lead to reduced renal perfusion and activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system.8 This leads to preferential retention of water compared with sodium and can cause hyponatremia. Restricted dietary sodium intake may further exacerbate these processes, therefore precipitating hyponatremia.

A study9 enrolled 410 patients with congestive heart failure and followed them for 6 months to compare the dietary sodium intake levels with doses of diuretics in these patients. These patients were divided into 8 groups: group A received 1000 mL/d of fluid intake, 120 mmol/d, and 250 mg furosemide twice daily; group B received 1000 mL/d of fluid intake, 120 mmol/d, and 125 mg furosemide twice daily; group C received 1000 mL/d fluid intake, 80 mmol/d, and 250 mg furosemide twice daily; group D received 1000 mL/d fluid intake, 80 mmol/d, and 125 mg furosemide twice daily; group E received 2000 mL/d fluid intake, 120 mmol/d, and 250 mg furosemide twice daily; group F received 2000 mL/d fluid intake, 120 mmol/d, and 125 mg furosemide twice daily; group G received 2000 mL/d fluid intake, 80 mmol/d, and 250 mg furosemide twice daily; and group H received 2000 mL/d fluid intake, 80 mmol/d, and 125 mg furosemide twice daily for 30 days or more after discharge and for 180 days afterward. Group A showed the greatest statistically significant reduction in readmissions, brain natriuretic peptide, aldosterone, and plasma renin activity compared with the other groups (P < .001). Therefore, a normal sodium diet (2.8 g/d) and a higher dose of a diuretic (250 mg twice daily) yielded the best results as opposed to a low sodium diet (1.8 g/d) and a lower diuretic dose (125 mg twice daily).

The low sodium diet caused increased mortality and heart failure hospitalizations versus a normal sodium diet in patients with systolic heart failure. These results have been verified across multiple randomized controlled trials in patients with systolic heart failure.10,11,12,13 These findings can be explained partially on the basis of studies conducted in mice.14 It has been shown that the renin-angiotensin-aldosterone system has a central role in atherogenesis and that dietary salt intake plays a significant role in controlling this system. A study in rats has shown a 4-fold increase in plaque formation with a low sodium diet compared with a normal sodium diet, and this effect can be blocked by the use of angiotensin-converting enzyme inhibition, which suggests that it is mediated by the renin-angiotensin-aldosterone system. Effects observed with a high sodium diet include reduced vascular inflammation and atherogenesis and a modest increase in systolic blood pressure (5 ± 1 mm Hg). These data, although generated from mice, may explain the inverse relationship between dietary sodium intake and mortality rate.

The majority of data relating dietary sodium to cardiovascular health are based on its effects on blood pressure. Data from the 3 epidemiologic studies National Health And Nutrition Examination Survey (NHANES) I to III have been analyzed to assess the relationship between dietary sodium intake and cardiovascular mortality rates.15,16,17 NHANES I acquired information from 20,729 participants via interview and examination, and followed them using interview, tracking, and vital events registry. An inverse association was seen between dietary salt intake and all-cause mortality (lowest to highest salt intake quartile 23.18 to 19.01, P < .0001) and cardiovascular mortality (sodium 11.80 to 9.60, P < .0019; calories 12.80 to 8.94, P < .0002; sodium/calorie ratio 9.73 to 11.35, P = .017).15 Moreover, sodium intake was inversely associated with all-cause (P = .0069) and cardiovascular mortality (P = .086). NHANES II followed a similar population of 7154 participants for 13.7 years and yielded similar results. The sodium adjusted for calories and sodium/calorie ratio were both independently and inversely associated with cardiovascular mortality (P = .03 and P = .008, respectively; adjusted HR of cardiovascular mortality for sodium <2300 mg, 1.37; CI, 1.03-1.81; P = .033) and all-cause mortality (HR, 1.28; CI, 1.10-1.50; P = .003).16 However, these results did not hold true for participants aged more than 55 years, obese participants, and non-white participants. NHANES III was a cohort study based on 8699 participants who were followed using national vital entries registries for the outcomes of all-cause and cardiovascular mortality.17An inverse association between dietary sodium intake and cardiovascular mortality was shown (HR, 1.80; CI, 1.05-3.08; P = .03). Moreover, an inverse association of continuous sodium (per 1000 mg) intake with cardiovascular and all-cause mortality was observed with a 99% CI of 0.73 to 1.06 (P = .07) and 0.86 to 1.04 (P = .11), respectively. These findings question any potential survival advantage with a low sodium diet and indicate caution for population-wide sodium restriction.

Conversely, some studies have suggested a lower and higher mortality rate with a high sodium diet depending on the New York Heart Association (NYHA) functional class status. An observational study18 in 302 patients showed that patients with a daily urinary sodium excretion level >3 g had a reduced risk for a cardiovascular events (HR, 0.44; CI, 0.20-0.97) for NYHA functional class I/II congestive heart failure, but an increased risk (HR, 2.54; CI, 1.10-5.84) for NYHA III/IV congestive heart failure compared with a urinary sodium excretion level <3 g. This study was an observational study, in contrast to the randomized controlled trials indicating benefits of a normal sodium diet, and used urinary sodium levels as a measure of dietary sodium intake, which may be a reasonable surrogate marker for normal individuals but not for patients with congestive heart failure, who have severe renal excretory disturbances.

A large observational analysis of 2 cohorts,19 including 28,880 patients (from the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial [ONTARGET] and Telmisartan Randomized Assessment Study in ACE-intolerant Subjects With Cardiovascular Disease [TRANSCEND] trials), was conducted to investigate the effects of sodium and potassium intakes on the incidence of cardiovascular disease. The primary composite outcome measure was death related to cardiovascular causes, myocardial infarction, stroke, and hospitalization for congestive heart failure. The mean estimated baseline 24-hour urinary sodium excretion and standard deviation were 4.77 g (1.61) and 4 to 5.99 g, respectively, in the reference group. The patients were followed for an average of 56 months, during which the primary outcome was observed in 4729 patients (16.4%), with 2057 cardiovascular deaths, 1412 patients with myocardial infarction, 1282 patients with stroke, and 1213 patients hospitalized for congestive heart failure. In the control group, there was an incidence of 6.3% cardiovascular death, 4.6% myocardial infarction, 4.2% stroke, and 3.8% hospitalizations with congestive heart failure. In the cohort, a higher and lower urinary sodium excretion was associated with increased cardiovascular mortality. A higher baseline urinary sodium excretion had a statistically significant association with cardiovascular death (9.7% for 7-8 g/d; HR, 1.53; 95% CI, 1.26-1.86; and 11.2% for >8 g/d; HR, 1.66; 95% CI, 1.31-2.10), myocardial infarction (6.8%; HR, 1.48; 95% CI, 1.11-1.98 for >8 g/d), stroke (6.6%; HR, 1.48; 95% CI, 1.09-2.01 for >8 g/d), and hospitalization for congestive heart failure (6.5%; HR, 1.51; 1.12-2.05 for >8 g/d). Likewise, a lower urinary sodium excretion also had a statistically significant correlation with an increased risk of cardiovascular death (8.6%; HR, 1.19; 95% CI, 1.02-1.39 for 2-2.99 g/d; 10.6%; HR, 1.37; 95% CI, 1.09-1.73 for <2 g/d) and hospitalization for congestive heart failure (5.2%; HR, 1.23; 95% CI, 1.01-1.49 for 2-2.99 g/d). This cohort study suggests a J-shaped relationship between dietary sodium intake and cardiovascular risk factor; therefore, a higher and lower dietary sodium intake may be related to adverse cardiovascular outcomes. Moreover, the lowest cardiovascular event rates occurred in the moderate sodium excretion (4-5.99 g/d) and high potassium excretion (>3 g/d) groups. Thus, it seems that a normal sodium diet (4-6 g/d) in addition to a high potassium intake may be best for the general population.

Trials of Hypertension Prevention (TOHP) phases I and II were 2 large randomized controlled trials enrolling 2182 and 2382 patients, respectively. In TOHP I,20 the patients were randomized to 3 interventions, one of which was a low sodium diet; however, the low sodium diet and control groups were not given the exact same diets. Although a lowered dietary sodium intake, as measured by a urinary sodium excretion of 44 mmol/24 hours, was able to reduce the diastolic blood pressure by 0.9 mm Hg (P < .05) and systolic blood pressure by 1.7 mm Hg (P < .01), it may have been due to the diet that lowers urinary sodium and not necessarily the lower sodium content. In TOHP II,21 counseling was used to reduce the dietary sodium intake in the test group. During the study period, the urinary sodium excretion decreased 50 and 40 mmol/d at 6 and 36 months, respectively. This decrease in urinary sodium excretion was associated with a 2.9/1.6 mm Hg decrease in the intervention group (all groups, P < .001). However, this study treated the intervention group differently from the control group. The groups were not given the same diets, and the intervention group was counseled to reduce sodium in their diet. Moreover, the intervention group also was counseled to increase spices, which alone may have cardiovascular benefits. Thus, a lower urinary sodium does not necessarily indicate that the results are due to a lowered sodium intake.

Other Unintended Consequences Relevant to Cardiovascular Health

A Cochrane review based on 167 studies showed that a low sodium diet in normotensive whites leads to a small reduction in systolic blood pressure (−1.27 mm Hg; CI, −1.88 to −0.66; P = .0001), without significantly reducing diastolic blood pressure (−0.05 mm Hg; CI, −0.51 to 0.42; P = .85).22 However, a low sodium diet caused an increase in renin (P < .00001), aldosterone (P < .00001), noradrenaline (P < .00001), adrenaline (P < .0002), cholesterol (P < .001), and triglycerides (P < .0008). This meta-analysis included studies that were only 2 weeks long and did not use good screening measures for quality. Inclusion of trials with an acute reduction in dietary sodium intake may not fully elucidate its long-term effects. Despite this fact, the potential harmful effects of sodium reduction may outweigh its benefits, especially in those individuals who generally did not have a significant reduction in blood pressure (normotensive whites and Asians).

With a lack of consistent efficacy of a low sodium diet, and potential harm, the cost-effectiveness of such a worldwide approach to a low sodium diet is questionable. A major source of dietary iodine is through salt. Therefore, a low sodium diet could lead to worsening of thyroid diseases. Salt also gives palatability to food and possesses numerous antimicrobial effects. It is possible, at least theoretically, that food-borne infections could increase if we were to decrease the amount of salt in foods.

A low sodium diet may even be counterproductive from a public health perspective. In addition to possibly exacerbating, it may distract efforts from other, more worthwhile programs that have a stronger foundation in evidence.23 Here again, the possibility that a low sodium diet may lead to worsened cardiovascular survival rates is a concern. The potential population-level effects of such an extreme intervention, with the American Heart Association recommending a sodium intake of <1.5 g/d for all Americans,2 can be expected to lead to potentially negative results on morbidity and mortality.

Even if a low sodium diet was advisable, is it physiologically possible? Although a low sodium diet may have benefit, there is still evidence that states it is not possible to modify human sodium intake levels because of complex neurohumoral homeostatic mechanisms.24 This makes public health programs focusing on salt reduction in the general population potentially counterproductive. Whether or not dietary salt intake is physiologically determined is still not known.25 If it is physiologically determined, with an optimal dietary range, then any modification to the dietary intake may be risky.

Conclusions

There is no conclusive evidence that a low sodium diet reduces cardiovascular events in normotensive and pre-hypertensive or hypertensive individuals. On the contrary, there is sound evidence that a low sodium diet leads to a worse cardiovascular prognosis in patients with systolic congestive heart failure or type 2 diabetes mellitus. Worldwide sodium restriction, through its adverse effects on insulin resistance, may lead to an increase in the rates of type 2 diabetes mellitus. By potentially moving the food industry to produce lower-sodium products could lead to greater consumption of processed foods and greater incidence of metabolic syndrome. Other adverse effects also are possible with attempted sodium restrictions, whereas low sodium diets themselves may not be possible because of inherent physiologic regulation. Advising low sodium diets seems misguided and potentially dangerous and illustrates the problem of guidelines based on flawed studies using surrogate measures.

References

Dietary Guidelines for Americans, 2010. Alexandria, VA: US Department of Agriculture, Center for Nutrition Policy and Promotion. Available at: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/Chapter3.pdf. Accessed December 18, 2012.

Whelton, P.K., Appel, L.J., Sacco, R.L. et al. Sodium, blood pressure, and cardiovascular disease: further evidence supporting the American heart association sodium reduction recommendations.Circulation. 2012; 126: 2880–2889

Alderman, M.H. Reducing dietary sodium: the case for caution. JAMA. 2010; 303: 448–449

Ciani, O., Buyse, M., Garside, R. et al. Comparison of treatment effect sizes associated with surrogate and final patient relevant outcomes in randomised controlled trials: meta-epidemiological study. (f457)BMJ. 2013; 346

Graudal, N.A., Galloe, A.M., and Garred, P. Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols and triglyceride. JAMA. 1998; 279: 1383–1391

Sacks, F.M., Svetkey, L.P., Vollmer, W.M...., and DASH-Sodium Collaborative Research Group. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med. 2001; 344: 3–10

Ekinci, E.I., Clarke, S., Thomas, M.C. et al. Dietary salt intake and mortality in patients with type 2 diabetes. Diabetes Care. 2011; 34: 703–709

Gupta, D., Georgiopoulou, V.V., Kalogeropoulos, A.P. et al. Dietary sodium intake in heart failure.Circulation. 2012; 126: 479–485

Paterna, S., Parrinello, G., Cannizzaro, S. et al. Medium term effects of different dosage of diuretic, sodium, and fluid administration on neurohormonal and clinical outcome in patients with recently compensated heart failure. Am J Cardiol. 2009; 103: 93–102

Licata, G., Di Pasquale, P., Parrinello, G. et al. Effects of high-dose furosemide and small-volume hypertonic saline solution infusion in comparison with a high dose of furosemide as bolus in refractory congestive heart failure: long-term effects. Am Heart J. 2003; 145: 459–466

Paterna, S., Di Pasquale, P., Parrinello, G. et al. Changes in brain natriuretic peptide levels and bioelectrical impedance measurements after treatment with high-dose furosemide and hypertonic saline solution versus high-dose furosemide Alone in refractory congestive heart failure. J Am Coll Cardiol. 2005; 45: 1997–2003

Paterna, S., Fasullo, S., Parrinello, G. et al. Short-term effects of hypertonic saline solution in acute heart failure and long-term effects of a moderate sodium restriction in patients with compensated heart failure with New York heart Association Class III (Class C) (SMAC-HF study). Am J Med Sci. 2011;342: 27–37

Paterna, S., Gaspare, P., Fasullo, S. et al. Normal-sodium diet compared with low- sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?. Clin Sci (London). 2008; 114: 221–230

Tikellis, C., Pickering, R.J., Tsorotes, D. et al. Activation of the renin-angiotensin system mediates the effects of dietary salt intake on atherogenesis in the apolipoprotein E knockout mouse. Hypertension. 2012; 60: 98–105

Alderman, M.H., Cohen, H., and Madhavan, S. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet. 1998; 351: 781–785

Cohen, H.W., Hailpern, S.M., Fang, J., and Alderman, M.H. Sodium intake and mortality in the NHANES II: follow-up study. Am J Med. 2006; 119: e7–e14

Cohen, H.W., Hailpern, S.M., and Alderman, M.H. Sodium intake and mortality follow-up in the Third National Health and Nutrition Examination Survey (NHANES III). J Gen Intern Med. 2008; 23: 1297–1302

Lennie, T.A., Song, E.K., Wu, J.R. et al. Three gram sodium intake is associated with longer event-free survival only in patients with advanced heart failure. J Card Fail. 2011; 17: 325–330

O'Donnell, M.J., Yusuf, S., Mente, A. et al. Urinary sodium and potassium excretion and risk of cardiovascular events. J Am Med Assoc. 2011; 306: 2229–2238

TOHP group. The effects of nonpharmacologic interventions on blood pressure of persons with high normal levels. Results of the Trials of Hypertension Prevention, Phase I. JAMA. 1992; 267: 1213–1220

TOHP group. Effects of weight loss and sodium reduction intervention on blood pressure and hypertension incidence in overweight people with high-normal blood pressure. The Trials of Hypertension Prevention, phase II. The Trials of Hypertension Prevention Collaborative Research Group. Arch Intern Med. 1997; 157: 657–667

Graudal, N.A., Hubeck-Graudal, T., and Jurgens, G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Review).(CD004022)Cochrane Database Syst Rev. 2011; 11

Lucan, S.C. Attempting to reduce sodium intake might do harm and distract from a greater enemy.(e3)Am J Public Health. 2013; 103

McCarron, D.A., Drüeke, T.B., and Stricker, E.M. Science trumps politics: urinary sodium data challenge US dietary sodium guideline. Am J Clin Nutr. 2010; 92: 1005–1006

McCarron, D.A., Geerling, J.C., Kazaks, A.G., and Stern, J.S. Can dietary sodium intake be modified by public policy?. Clin J Am Soc Nephrol. 2009; 4: 1878–1882

#diet #low sodium diet #Nutrition #electrolytes #family medicine #best practices #controversy #cardiology #sodium #heart disease #Hypertension #internal medicine #Integrative Medicine

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caduet tablets Uses, Dosage, Side Effects, Precautions & Warnings

Drug Online

caduet Generic drug of the Therapeutic class: Cardiology and angiology Active ingredients: Amlodipine , Atorvastatin

what is caduet medication?

This medication is supplied as blue, oval-shaped, film-coated tablets debossed with “Pfizer” on one side and “CDT 101” on the other side.

Boxes of 7, 10, 14, 20, 28, 30, 50, 56, 60, 90, 100 or 200 tablets.

Not all presentations may be marketed.

what is caduet medication used for and indication?

CADUET is indicated for the prevention of cardiovascular events in hypertensive patients with 3 associated cardiovascular risk factors, with normal to moderately elevated cholesterol without established coronary artery disease, and in whom, according to current recommendations, the concomitant use of amlodipine and a low dose of atorvastatin is suitable .

CADUET should be used when the response to regimen and other non-pharmacological measures is inadequate.

caduet dosage

Oral route

The usual starting dose is 5 mg / 10 mg once daily.

If tighter blood pressure control is required, a dosage of 10 mg / 10 mg once daily may be administered.

The tablets can be taken at any time of the day, with or without food.

CADUET can be used alone or in combination with other antihypertensive drugs, but it must not be used in combination with other calcium channel blockers or another statin.

The combination of CADUET and fibrates should generally be avoided (see sections 4.4 and Interactions with other medicinal products and other forms of interaction ).

Patients with renal impairment : No dosage adjustment is necessary in patients with impaired renal function (see sections 4.4 and Pharmacokinetic properties ).

Patients with hepatic impairment : CADUET is contraindicated in patients with active hepatic disease.

Children / Adolescents : The safety and efficacy of CADUET have not been established in children / adolescents. Therefore, the use of CADUET is not recommended in this population.

Elderly : It does not appear necessary to adjust the dose in the elderly (see section Pharmacokinetic properties ).

Combination with other medicinal products : In combination with ciclosporin, the dose of atorvastatin should not exceed 10 mg (see section Interactions with other medicinal products and other forms of interaction ).

Contraindications

CADUET is contraindicated in patients:

Being hypersensitive to dihydropyridines *, to amlodipine, to atorvastatin or to any of the excipients of this medicine,

have active liver disease or a persistent and unexplained increase in serum transaminases exceeding 3 times the upper limit of normal,

In women who are pregnant, breastfeeding or of childbearing potential and not using reliable contraceptive methods (see section Pregnancy and breast-feeding ),

In combination with itraconazole, ketoconazole, telithromycin (see section Interactions with other medicinal products and other forms of interactions ),

having severe hypotension,

Having shock (including cardiogenic shock),

Having an obstruction of the efferent pathway to the left ventricle (for example severe aortic stenosis),

With haemodynamically unstable heart failure after acute myocardial infarction.

* amlodipine is a calcium channel blocker derived from dihydropyridine.

HOW TO TAKE CADUET?

Always take this medicine exactly as your doctor or pharmacist has told you. Check with your doctor or pharmacist if in doubt.

Adults

The recommended starting dose of CADUET is one 5 mg / 10 mg tablet per day. Your doctor may increase the dose if necessary to 1 tablet of CADUET 10 mg / 10 mg per day.

The tablets should be swallowed whole with a glass of water. They can be taken at any time of the day, with or without food. However, it is best to take them at the same time each day.

Continue to follow your doctor’s dietary advice, especially to eat a low fat diet, avoid tobacco, and exercise regularly.

If you have the impression that the effect of CADUET tablets is too strong or too weak, talk to your doctor or pharmacist.

Use in children and adolescents

This medication is not recommended for children and adolescents.

If you take more CADUET 10 mg / 10 mg film-coated tablets than you should

If you accidentally take too many CADUET tablets (more than your usual dose), ask your doctor or the nearest hospital for advice. Take any remaining tablets, the carton or the whole carton with you so that hospital staff can quickly identify which medicine you have taken.

If you forget to take CADUET 10 mg / 10 mg film-coated tablets

If you forget to take your dose of CADUET, take your next dose at the normal time.

Do not take a double dose to make up for the dose you forgot to take.

If you stop taking CADUET 10 mg / 10 mg film-coated tablets

Do not stop taking CADUET unless your doctor tells you to.

If you have any further questions on the use of this medicine or want to stop taking your treatment, ask your doctor or pharmacist for more information.

How To Store Caduet?

Keep this medication out of the sight and reach of children.

Do not use this medicine after the expiry date which is stated on the blister, the carton and the vial after “EXP”. The expiration date refers to the last day of that month.

Store at a temperature not exceeding 30 ° C.

Do not throw away any medicines via a wastewater treatment plant or with household waste. Ask your pharmacist how to throw away the medicines you no longer use. These measures will help protect the environment.

caduet side effects

The safety of CADUET has been evaluated in double-blind, placebo-controlled studies in 1092 patients treated for concomitant hypertension and dyslipidemia. During clinical trials with CADUET, no specific adverse events specific to this combination were observed.

Adverse events were limited to those previously reported for amlodipine and / or atorvastatin (see table of adverse events below).

In controlled clinical trials, discontinuation of treatment due to clinical adverse events or laboratory abnormalities was observed in 5.1% of patients treated with amlodipine and atorvastatin versus 4.0% of patients treated with amlodipine and atorvastatin. patients taking a placebo.

The adverse events below, listed according to MedDRA system organ classification and frequency order, relate to amlodipine and atorvastatin individually.

Very common: ³ 1/10, common: ³ 1/100 and <1/10, infrequent: ³ 1/1000 and <1/100, rare: ³ 1/10000 and <1/1000, very rare: < 1 / 10,000, frequency not known (cannot be estimated from the available data).

MedDRA

System organ classes

Side effects

Frequency

Amlodipine

Atorvastatin

Infections and infestations

Nasopharyngitis

–

Frequent

Blood and lymphatic system disorders

Leukopenia

Very rare

–

Thrombocytopenia

Very rare

Rare

Immune system disorders

hypersensitivity

Very rare

Frequent

Anaphylaxis

–

Very rare

Metabolism and nutrition disorders

Hyperglycemia *

Very rare

Frequent

Weight gain

Infrequent

Weightloss

Infrequent

–

Hypoglycemia

–

Infrequent

Anorexia

–

Infrequent

Psychiatric disorders

Insomnia

Infrequent

Mood disorders (including anxiety)

Infrequent

–

Nightmares

–

Infrequent

Depression

Infrequent

Frequency not known

Confusion

Rare

–

Disorders of the system nervous

Drowsiness

Frequent

–

Dizziness

Frequent

Infrequent

Headache (especially at the start of treatment)

Frequent

Tremors

Infrequent

–

Hypoesthesias, paresthesias

Infrequent

Syncope

Infrequent

Hypertonia

Very rare

–

Peripheral neuropathy

Very rare

Rare

Amnesia

–

Infrequent

Dysgeusia

Infrequent

Extrapyramidal syndrome

Frequency not known

–

Eye disorders

Blurred vision

–

Infrequent

Visual disturbances (including diplopia)

Infrequent

Rare

Ear and labyrinth disease

Tinnitus

Infrequent

Hearing loss

–

Very rare

Cardiac disorders

Palpitations

Frequent

–

Angina pectoris

Rare

–

Myocardial infarction

Very rare

–

Arrhythmia (including bradycardia, ventricular tachycardia and atrial fibrillation)

Very rare

–

Vascular disorders

Flushing

Frequent

–

Hypotension

Infrequent

–

Vasculitis

Very rare

–

Respiratory, thoracic and mediastinal disorders

Pharyngolaryngeal pain

–

Frequent

Epistaxis

–

Frequent

Dyspnea

Infrequent

–

Rhinitis

Infrequent

–

Cough

Very rare

–

Interstitial lung disease, especially during long-term treatment

Frequency not known

Gastrointestinal disorders

Gingival hyperplasia

Very rare

–

Nausea

Frequent

Upper and lower abdominal pain

Frequent

Infrequent

Vomiting

Infrequent

Dyspepsia

Infrequent

Frequent

Changes in intestinal transit (including diarrhea and constipation)

Infrequent

–

Dry mouth

Infrequent

–

Dysgeusia

Infrequent

–

Diarrhea, constipation, gas

–

Frequent

Gastritis

Very rare

–

Pancreatitis

Very rare

Infrequent

Eructation

–

Infrequent

Hepatobiliary disorders

Hepatitis

Very rare

Infrequent

Cholestasis

–

Rare

Jaundice

Very rare

–

Hepatic insufficiency

–

Very rare

Skin and subcutaneous tissue disorders

Bullous dermatosis including erythema multiforme

Very rare

Rare

Angioedema

Very rare

–

Erythema multiforme

Very rare

–

Alopecia

Infrequent

Purpura

Infrequent

–

Skin discoloration

Infrequent

–

Pruritus

Infrequent

Eruption

Infrequent

Hyperhidrosis

Infrequent

–

Exanthema

Infrequent

–

Urticaria

Very rare

Infrequent

Angioneurotic edema

Very rare

Rare

Exfoliative dermatitis

Very rare

–

Photosensitivity

Very rare

–

Stevens-Johnson syndrome

Very rare

Rare

Bullous erythroderma with epidermolysis

–

Rare

Musculoskeletal and connective tissue disorders

Swelling of the joints (including swelling of the ankles)

Frequent

Arthralgia, myalgia

(see section Warnings and precautions for use )

Infrequent

Frequent

Muscle cramps, muscle spasms

Infrequent

Frequent

Back pain

Infrequent

Frequent

Neck pain

–

Infrequent

Pain in extremity

–

Frequent

Muscle fatigue

–

Infrequent

Myositis (see section Warnings and precautions for use )

–

Rare

Rhabdomyolysis, myopathy

(see section Warnings and precautions for use )

–

Rare

Tendinopathies, in rare cases tendon rupture

–

Rare

Immune-mediated necrotizing myopathy

–

Frequency not known

Kidney and urinary tract disorders

Urination disorder, nocturia, pollakiuria

Infrequent

–

Reproductive system and breast disorders

Incapacity

Infrequent

Gynecomastia

Infrequent

Very rare

General disorders and administration site conditions

Edema

Frequent

Infrequent

Peripheral edema

–

Infrequent

Tired

Frequent

Infrequent

Chest pain

Infrequent

Asthenia

Infrequent

Pain

Infrequent

–

Discomfort

Infrequent

Fever

–

Infrequent

Investigations

Increased liver enzymes: alanine aminotransferase, aspartate aminotransferase (mainly related to cholestasis)

Very rare

Frequent

Blood CK increased (see section 4.4 )

–

Frequent

Leukocyturia

–

Infrequent

* Diabetes: The frequency depends on the presence or absence of risk factors (fasting blood sugar ³ 5.6 mmol / l, BMI> 30 kg / m², increased triglyceride levels, history of high blood pressure).

caduet Interactions

Taking other medications

Tell your doctor or pharmacist if you are taking or have recently taken any other medicines, including medicines obtained without a prescription. Some medicines may interact with CADUET 10 mg / 10 mg film-coated tablets. This interaction may cause one or both of the medicines to be less effective, or on the contrary, this interaction may increase the risk or severity of side effects, including major muscle disorders known as rhabdomyolysis and myopathy (see section 4). .

Some medicines may interact with CADUET 10 mg / 10 mg film-coated tablets:

certain antibiotics such as rifampicin or certain “macrolide” antibiotics such as erythromycin, clarithromycin, telithromycin, fusidic acid or certain drugs used to treat infections caused by fungi such as ketoconazole, itraconazole,

medicines used to regulate lipid levels: fibrates, such as gemfibrozil or colestipol,

medicines used to regulate your heart rhythm, such as amiodarone, diltiazem and verapamil,

medicines used to treat or prevent seizures such as carbamazepine, phenobarbital, phenytoin, fosphenytoin, primidone,

medicines used to change how your immune system works, such as cyclosporin

protease inhibitors such as ritonavir, indinavir, nelfinavir used in the treatment of HIV,

medicines used to treat depression, such as nefazodone and imipramine,

medicines used to treat mental disorders, such as neuroleptics,

medicines used to treat heart failure, such as beta blockers

medicines used to treat high blood pressure, such as angiotensin II inhibitors, converting enzyme inhibitors, verapamil and diuretics,

alpha blockers used to treat high blood pressure or prostate problems

other medicines known to interact with CADUET 10 mg / 10 mg film-coated tablets such as ezetimibe (which lowers cholesterol), warfarin (which decreases blood clotting), oral contraceptives, stiripentol (an anticonvulsant used for treatment of epilepsy), cimetidine (used for heartburn and stomach ulcers), phenazone (a pain reliever), antacids (containing aluminum or magnesium, used to relieve problems stomach), and amifostine (used to treat cancer),

sildenafil (used in the treatment of erectile dysfunction, impotence),

dantrolene and baclofen (muscle relaxants),

steroids,

over-the-counter St. John’s Wort products.

CADUET may lower your blood pressure further if you are already taking other medicines to treat your high blood pressure.

If you are taking or have recently taken any other medicines, including medicines obtained without a prescription, talk to your doctor or pharmacist.

INTERACTIONS OF CADUET 10 MG / 10 MG WITH FOOD AND DRINK

Food and drinks

CADUET 10 mg / 10 mg film-coated tablets can be taken at any time of the day, with or without food.

Grapefruit juice

Do not take more than one or two glasses of grapefruit juice per day as large amounts of grapefruit juice may affect the effects of CADUET 10 mg / 10 mg film-coated tablets.

Alcohol

Avoid drinking too much alcohol while taking CADUET 10 mg / 10 mg film-coated tablets. See also section 2 “Take special care with CADUET 10 mg / 10 mg film-coated tablets” for more details.

Drive and use machines

Do not drive or use machines if you feel dizzy after taking this medicine.

Warnings and Precautions

Heart failure

Liver function monitoring

Clinical signs of hepatic dysfunction

Increased transaminases

Heavy alcohol consumption

Hepatic insufficiency

History of liver disease

Predisposing factor to the occurrence of rhabdomyolysis

Subject over 70 years of age

Unexplained muscle pain

Muscle cramp

Muscular weakness

Increase in CPK

Rhabdomyolysis

History of hemorrhagic stroke

History of lacunar infarction

Interstitial lung disease

Risk of diabetes

Woman of childbearing age

Heart failure

Patients with heart failure should be treated with caution. In a long-term placebo-controlled study in patients with severe heart failure (NYHA class III and IV), the reported incidence of pulmonary edema was higher in the amlodipine group compared to the placebo group. (see section Pharmacodynamic properties). Calcium channel blockers including amlodipine should be used with caution in patients with congestive heart failure because they may increase the risk of cardiovascular events and mortality.

Liver effects

Liver function tests should be performed before the start of treatment and then regularly after initiation of treatment, as well as in the event of signs or symptoms suggestive of liver damage. In the event of elevation of the serum transaminase level, monitoring is necessary until normalization.

A persistent increase in ALT or AST exceeding 3 times the upper limit of normal (ULN), should lead to discontinuation of treatment.

The half-life of amlodipine is increased and its AUC (Area Under the Curve) is greater in patients with hepatic impairment; dosage recommendations have not been established.

Due to the presence of atorvastatin, CADUET should be used with caution in patients who consume large amounts of alcohol, in patients with hepatic impairment and / or a history of liver disease.

Muscle effects

Like other HMG-CoA reductase inhibitors, atorvastatin can affect skeletal muscles and lead to myalgia, myositis and myopathies. These muscle damage may rarely progress to rhabdomyolysis, characterized by high levels of creatine kinase (CK) (more than 10 times the ULN), myoglobinemia and myoglobinuria which can lead to kidney failure, and in some cases be fatal.

Regular testing of CK or other muscle enzymes is not recommended in asymptomatic patients treated with statins. However, dosing of CKs is recommended before initiating statin therapy in patients with predisposing factors to rhabdomyolysis as well as in those with muscle symptoms during statin therapy (see below).

Very rare cases of autoimmune-mediated necrotizing myopathies (IMNM) have been reported during or after treatment with certain statins. IMNM is clinically characterized by proximal muscle weakness and increased serum creatine kinase, which persist despite discontinuation of statin therapy.

Before initiation of treatment

CADUET should be prescribed with caution in patients with predisposing factors to rhabdomyolysis. Before starting treatment with a statin, creatine kinase (CK) levels should be checked in the following situations:

Renal failure.

Hypothyroidism.

Personal or family history of genetic muscle diseases.

Personal history of muscle toxicity during treatment with a statin or a fibrate.

History of liver disease and / or excessive alcohol consumption.

In elderly patients (> 70 years), the need for these measures should be assessed, depending on the presence of other factors predisposing to rhabdomyolysis.

Situations in which increased plasma concentrations may occur, due to interactions (see section 4.5) and use in special populations including genetic polymorphisms (see section 5.2). ).

In these situations, a regular reassessment of the benefit / risk of the treatment, as well as regular clinical monitoring is recommended.

If the initial CK level is significantly elevated (more than 5 times the ULN) treatment should not be started.

Creatine kinase measurement

Creatine kinase (CK) should not be measured after heavy exercise or in the presence of another possible cause of increased CK, as this will make interpretation of the results difficult. In the event of a significant elevation of CK (more than 5 times the ULN) before treatment, this should be systematically checked again within 5 to 7 days to confirm the results.

During treatment

It is recommended that patients be asked to promptly report any unexplained muscle pain, muscle cramps or weakness, particularly if accompanied by malaise or fever.

· If symptoms appear when a patient is under treatment with CADUET, a CK levels should be measured; if the CK level is significantly elevated (more than 5 times the ULN), treatment should be discontinued.

· If muscular symptoms are severe and cause daily discomfort, discontinuation of treatment should be considered, even if CK levels did not exceed 5 times the ULN.

· If symptoms resolve and CK levels return to normal, the reintroduction of CADUET may be considered at the lowest dose and under close supervision.

Treatment with CADUET should be discontinued in the event of a clinically significant increase in CK level (> 10 times the ULN) or if rhabdomyolysis is diagnosed or suspected.

Amlodipine has no effect on laboratory parameters.

Combinations with other drugs

As with other statins, the risk of rhabdomyolysis is increased when CADUET is administered in combination with certain drugs which may increase the plasma concentration of atorvastatin, such as strong inhibitors of CYP3A4 or protein transporters (eg, cyclosporin, telithromycin, clarithromycin, delavirdine, stiripentol, ketoconazole, voriconazole, itraconazole, posaconazole, determovir and HIV protease inhibitors including ritonavir, lopinavir, atazanavir, indinavir, darunavir, tipranavir, etc / ritonavir). The risk of myopathy may also be increased in combination with gemfibrozil and other fibrates, antivirals used in the treatment of hepatitis C (HCV) (boceprevir, telaprevir, elbasvir / grazoprevir), erythromycin, niacin, l ‘ ezetimibe or colchicine. Therapeutic alternatives (not exhibiting these interactions) should be considered as far as possible.

In the event that the combination of these medicinal products with CADUET is necessary, the benefit / risk of concomitant treatments should be carefully assessed and appropriate clinical monitoring is recommended (see section Interactions with other medicinal products and other forms of interactions).

CADUET should not be administered simultaneously with fusidic acid in systemic form, and for up to 7 days after stopping treatment with fusidic acid. In patients where the use of systemic fusidic acid is considered essential, statin therapy should be discontinued for the duration of fusidic acid therapy. Cases of rhabdomyolysis (some fatal) have been reported in patients receiving fusidic acid and a statin in combination (see section Interactions with other medicinal products and other forms of interactions). Patients should be informed of the need to seek immediate medical attention if they experience symptoms of muscle weakness, pain, or muscle tenderness.

Statin therapy can be restarted seven days after the last dose of fusidic acid.

In exceptional circumstances, when prolonged treatment with systemic fusidic acid is required, e.g. for the treatment of severe infections, the need for co-administration of CADUET and fusidic acid should only be considered in cases of per case and under close medical supervision.

Prevention of stroke by aggressively lowering cholesterol levels (SPARCL study)

In a posteriori analysis performed in subgroups of patients with recent stroke or transient ischemic attack (TIA) but without coronary artery disease, a higher frequency of hemorrhagic stroke was observed in treated patients. per 80 mg atorvastatin compared to patients on placebo.

This high risk is particularly observed in patients who have already had a hemorrhagic stroke or a lacunar infarction at the inclusion of the study.

In patients with a history of hemorrhagic stroke or lacunar infarction, the benefit / risk balance of atorvastatin 80 mg is uncertain. Therefore, the potential risk of occurrence of haemorrhagic stroke should be carefully assessed before any initiation of treatment (see section Pharmacodynamic properties).

Interstitial lung disease

Cases of interstitial lung disease have exceptionally been reported with certain statins, particularly during long-term therapy .

Symptoms may include dyspnea, a non-productive cough, and altered general condition (fatigue, weight loss, and fever). If interstitial lung disease is suspected in a patient, statin therapy should be discontinued.

Diabetes

There is some evidence that statins, as a pharmacological class, increase blood sugar. In some patients at high risk of developing diabetes, statins may cause hyperglycaemia requiring the initiation of diabetes treatment. This risk is nevertheless compensated by the reduction in the vascular risk under statins and therefore it should not be a reason for stopping statins. Patients at risk (fasting blood glucose between 5.6 and 6.9 mmol / l, BMI> 30 kg / m², increased triglyceride levels, arterial hypertension) should be monitored clinically and biologically in accordance with national recommendations.

PREGNANCY & BREAST-FEEDING & FERTILITY

Caduet is contraindicated during pregnancy and lactation.

Women of childbearing age

Women of childbearing potential should use reliable contraceptive measures during treatment ( see Contraindications ).

Pregnancy

The safety of atorvastatin has not been established in pregnant women. No controlled clinical trials have been performed in pregnant women treated with atorvastatin. Following intrauterine exposure to HMG-CoA reductase inhibitors, birth defects have rarely been reported. Studies in animals have shown reproductive toxicity ( see Preclinical safety ).

Treatment of the mother with atorvastatin may reduce the fetal level of mevalonate, which is a precursor of cholesterol biosynthesis. Atherosclerosis is a chronic process, and stopping a lipid-lowering drug during pregnancy should generally have little effect on the long-term risk associated with primary hypercholesterolemia.

For these reasons, Caduet should not be used during pregnancy, or in a woman planning to become pregnant or in whom pregnancy is suspected. Caduet treatment should be withheld during pregnancy or until it has been determined that the woman is not pregnant ( see Contraindications ).

If pregnancy is discovered during treatment, it should be stopped immediately.

Feeding with milk

Amlodipine is excreted in breast milk. The proportion of maternal dose received by the infant has been estimated at an interquartile range of 3-7%, with a maximum of 15%. The effect of amlodipine on infants is unknown. The excretion of atorvastatin or its metabolites in human milk is not known. In rats, the plasma concentrations of atorvastatin and its metabolites are similar to those found in milk ( see Preclinical safety ). Due to the possibility of serious side effects, women treated with Caduet should not breast-feed their infants ( see Contraindications ). Atorvastatin is contraindicated during breastfeeding ( see Contraindications ).

Fertility

No effect of atorvastatin on fertility has been demonstrated in studies conducted in male or female animals ( see Preclinical Safety ).

Reversible biochemical changes in the sperm head have been reported in some patients treated with calcium channel blockers. There is insufficient clinical data regarding the potential effect of amlodipine on fertility. In a study carried out in rats, adverse effects were detected on male fertility ( see Preclinical safety ).

What happens if I overdose from Caduet?

No information is available regarding overdose of Caduet in humans.

Amlodipine:

For amlodipine, experience with intentional overdose in humans is limited. Massive overdose could cause extensive peripheral vasodilation and possibly reflex tachycardia. Marked and possibly prolonged systemic hypotension up to and including shock with fatal outcome has been reported. Any hypotension resulting from acute intoxication requires monitoring in an intensive cardiological care unit. A vasoconstrictor can be used to restore vascular tone and blood pressure. Since amlodipine is highly protein bound, dialysis is unlikely to provide any benefit.

Atorvastatin:

There is no specific treatment for atorvastatin overdose. In the event of overdose, the patient should receive symptomatic treatment and supportive measures should be implemented as needed. Liver function and serum CK concentrations should be monitored. Due to the strong binding of the drug to plasma proteins, hemodialysis is not expected to significantly increase the clearance of atorvastatin.

What should I do if I miss a dose?

If you forget to take CADUET 5/ 10 mg -5/ 10 mg film-coated tablets:

If you forget to take your dose of CADUET, take your next dose at the normal time.

Do not take a double dose to make up for the dose you forgot to take.

What is Forms and Composition ?

SHAPES and PRESENTATIONS

5 mg / 10 mg film-coated tablet (oval, debossed with “Pfizer” on one side and “CDT 051” on the other side; white) and 10 mg / 10 mg (oval, debossed with “Pfizer “On one side and” CDT 101 “on the other side; blue): Boxes of 30 and 90, in blisters.

COMPOSITION

p cpAmlodipine (INN) as amlodipine besilate5 mgor10 mgAtorvastatin (INN) as atorvastatin calcium trihydrate10 mg

Excipients (common): Core: calcium carbonate, croscarmellose sodium, microcrystalline cellulose, pregelatinized corn starch, polysorbate 80, hydroxypropylcellulose, colloidal anhydrous silica, magnesium stearate. Film- coating : 5 mg / 10 mg tablet: Opadry II white 85F28751 (polyvinyl alcohol, titanium dioxide E171, macrogol 3000, talc). 10 mg / 10 mg tablet: Opadry II blue 85F10919 (polyvinyl alcohol, titanium dioxide E171, macrogol 3000, talc, indigo carmine aluminum lake E132).

NOT’s

Edrug-online contains comprehensive and detailed information about drugs available in the medical field, and is divided into four sections:

general information:

Includes a general description of the drug, its use, brand names, FAQs, and relevant news and articles

Additional information:

General explanation about dealing with the medicine: how to take the medicine, the doses and times of it, the start and duration of its effectiveness, the recommended diet during the period of taking the medicine, the method of storage and storage, recommendations in cases for forgetting the dose and instructions to stop taking the drug and take additional doses.

Special warnings:

For pregnant and breastfeeding women, the elderly, boys and drivers, and use before surgery.

Side effects:

It treats possible side effects and drug interactions that require attention and its effect on continuous use.

The information contained in this medicine is based on medical literature, but it is not a substitute for consulting a doctor.

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thesittingduck · 4 years