#hypernatraemia

[biology-geology-beaches-india]

The Science Research Manuscripts of S. Sunkavally, p 538.

[taimoorkhan]

Hypernatraemia is a condition in which the concentration of sodium in the blood is elevated above the normal range. It can occur as a result of a number of different underlying conditions, such as diabetes insipidus, excess intake of sodium, or kidney disease. It is important to diagnose and treat hypernatraemia promptly, as it can lead to serious complications if left untreated.

The approach to managing hypernatraemia involves several steps, including calculating the free water deficit, determining a suitable serum sodium correction rate, estimating ongoing free water losses, and designing a fluid repletion programme. It is also important to monitor the patient closely during treatment to ensure that the desired effects are being achieved.

Calculating the free water deficit is an important step in the management of hypernatraemia. The free water deficit formula is used to determine the amount of fluid needed to correct the condition. The formula takes into account the patient's total body water and the concentration of sodium in the plasma.

Determining a suitable serum sodium correction rate is another important aspect of managing hypernatraemia. In patients with severe symptoms, the serum sodium concentration should be lowered by 2 mmol/L/hour in the first 2-3 hours, followed by a correction rate of 0.5 mmol/L/hour thereafter. The aim is to lower the serum sodium level by 10 mmol/L/day in these patients, if possible. However, the rate of correction should be adjusted based on the patient's clinical condition and the presence of any underlying conditions.

Estimating ongoing free water losses is also important in the management of hypernatraemia. This can be done using the electrolyte-free water excretion formula, which takes into account the urine flow rate, the concentration of sodium and potassium in the urine, and the concentration of sodium in the plasma. If urine output or the electrolyte content of the urine changes, then the electrolyte-free water excretion should be recalculated.

Designing a fluid repletion programme is another important aspect of managing hypernatraemia. This involves determining the type and amount of fluids that should be administered to the patient in order to correct the condition. In most cases, water administration via the oral route is preferred. If this is not possible, intravenous administration may be necessary. It is important to choose the appropriate type of fluids and to monitor the patient for the development of any complications, such as hyperglycaemia.

Monitoring the patient closely during treatment is also important in the management of hypernatraemia. This involves regularly checking the patient's vital signs and monitoring their clinical condition. It is also important to monitor the patient's electrolyte levels and urine output in order to ensure that the treatment is effective.

In cases of hypernatraemia due to diabetes insipidus, treatment may involve the use of medications such as desmopressin, which can help to stop ongoing losses of electrolyte-free water. In cases of accidental or iatrogenic excess intake of sodium, treatment may involve restricting sodium intake and increasing fluid intake. In cases of renal replacement therapy, treatment may involve the use of dialysis or other forms of renal replacement therapy.

Overall, the management of hypernatraemia requires a careful and individualised approach that takes into account the patient's underlying condition and clinical status. It is important to work closely with the healthcare team in order to ensure the most effective and appropriate treatment for the patient.

[doctorfoxtor]

everyday is Friday the 13th when you're studying

100 days of productivity

day 13

RS/CVS

NIPPV has best effect between pH 7.25-7.35; but generally trial NIPPV before tubing unless imminent or current respiratory collapse (or other indications such as failure to protect airway)

constrictive pericarditis vs tamponade: differentiate with y-descent of JVP; this is *absent* in tamponade, but otherwise they are clinically very similar

in the absence of thromboembolic events, pts with bioprosthetic valve replacements *do not need* warfarin (low dose aspirin sufficient)

asthma ICS dose: budesonide: low dose < 400 mcg; mod dose 400-800 mcq; high dose >800 mcg

ICS dose conversion: budesonide = beclomethasone, multiply budesonide dose x2 to get fluticasone dose

Rheum/Derm

pseudoxanthoma elasticum: AR mutation in ABCC6 (ATP-binding cassette transporter) skin: cutaneous laxity + yellow papules in flexural regions; eyes: blue sclerae + peau d'orange of Bruch's membrane + retinal angioid streaks; GIT: upper GI bleed!; CVS: accelerated atherosclerosis w/ consequent IHD/CVA/PAD; rheum: demineralisation w/ reduced circulating pyrophosphate

microscopic polyangiitis and GPA cause kidney involvement with equal frequency; HSP causes IgA nephropathy with much less frequency (and much less severity)

tinea incognita = tinea corporis that has had topical steroid tx; may show florid fungal growth without characteristic tinea lesions (skin scraping w/ KOH stain is sufficient to dx)

inclusion body myositis (not to be confused with hereditary inclusion body myopathies): most common inflammatory muscle disease in adults! → sporadic, nonheritable progressive asymmetric weakening and wasting of both proximal and distal muscle groups (may mimic ALS but is a myopathy rather than a neuropathy and NCS/bloods will reflect that, eg, ↑CPK in IBM)

CNS

floaters + flashes of light = vitreous detachment

important ddx for Wernicke encephalopathy: cerebellar stroke. Do NOT forget the CT brain!

neuromyelitis optica: differentiate from MS w/ anti-NMO IgGs (such as anti-aquaporin 4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG))

pons = horiPONStal gaze palsy

SCD: T2-weighted hyperintensity of affected areas (dorsal column, lat corticospinal tracts, spinocerebellar tracts)

Haem/Onc

Stauffer syndrome: renal cell ca associated nonmetastatic hepatobiliary dysfunction (cholestatic enzyme pattern, elevated platelets/PT, hepatosplenomegaly, NORMAL bilirubin, NO jaundice)

GIT

FAP: the second most common cause of death after colorectal cancer is duodenal cancer

Whipple's disease: tx with 1-1.5 yrs of ampicillin or cotrimoxazole or doxy+HCQS, then assess, then continue tx if necessary

Psych/Toxo

sertraline specifically is used for agoraphobia due to best cost-effect ratio; other SSRIs are second line

long-term lithium side effects: LITHIUM: Leukocytosis, Intracranial hypertension, Tremor/Teratogen, Hair loss/Hypothyroid/Hyperparathyroid, Increased Urine (N-DI), Metabolic syndrome

other than hypokalaemia, other precipitating factors for digitoxicity include hypernatraemia, hypomagnesaemia and hypothermia

Misc

bezlotoxumab → C. diff toxin B

suvratoxumab → S. aureus alpha toxin

[bireyes-moved]

💩

💩 -  kak---ashi/any of his students esp saku!--ra. also min---ato/kak///ashi

[prodigalknight]

HAPPY BIRTHDAY FINNY! =D

Thanks, Nik! :D

[silverlab101]

Stomach Flu Or Is It?

Gastroenteritis is often an acute and self-limited illness that doesn't require pharmacologic remedy. Campylobacter organisms can be detected on gram stain of stool with excessive specificity and a sensitivity of 60%, but are most frequently diagnosed by stool culture. Fecal leukocytes are present and indicate an inflammatory diarrhea.

Contact with contaminated poultry, livestock, or family pets, particularly puppies, can even cause illness. Animals farmed for meat are the principle source of campylobacteriosis. In fifty seven percent of cases, the micro organism could be traced to rooster, and in 35 p.c to cattle.

Superintendent Jay Naicker stated Elvis Matenjwa died within the Ngwelezan hospital on September 27. He was apparently admitted to the hospital under the name Themba Matenjwa on September 22. He adds gastroenteritis that symptoms of dehydration ought to be monitored carefully and treated as soon as attainable should they develop.

Take 1 Litre clear water, eight degree teaspoons sugar, half level teaspoon salt. This combination should be given by mouth as soon as the particular colloidal silver stomach ulcers person passes the primary watery stool. Most essential is to offer a water, salt and sugar combination in massive amounts.

The different chance is that the vaccines were rendered ineffective as a end result of they were not refrigerated at some stage, notably within the East Rand the place most of the circumstances seem to have occurred. He explained that he was contacted by involved moms who indicated that their infants received the vaccine both at a state clinic or a non-public pharmacy, however had to be hospitalised after contracting gastroenteritis. Are we seeing an unusually excessive enhance of illnesses similar to mumps, measles, whooping cough and diphtheria amongst children? Lester Kiewit speaks to Prof Mignon McCulloch of the SA Paediatric Association. Pseudomembranous colitis, normally caused by antibiotics use, is managed by discontinuing the causative agent and treating with either metronidazole or vancomycin. Lactose-free or lactose-reduced formulation often are not needed.

The hypernatraemic cohort in this study had a 66% HIV publicity prevalence, compared with 47% in these infants admitted for AGE without hypernatraemia, and this was a statistically important distinction. This examine, nonetheless, describes a higher colloidal silver for stomach problems HIV publicity prevalence in relation to hypernatraemic dehydration, warranting additional research on this regard. Neurological abnormalities were documented in 63% of reviewed infants, with 32% growing seizures and/or encephalopathy.

Avoid foods which might be spicy, fried, and fatty, or have a lot of acid as they'll make your little one’s stomach problems worse. Risk factors include consumption of improperly prepared meals or contaminated water and travel or residence in areas of poor sanitation. It can colloidal silver for stomach ulcers be widespread for river swimmers to become contaminated during occasions of rain because of contaminated runoff water. At least 50% of cases of gastroenteritis as a end result of foodborne sickness are brought on by norovirus.

[myassignmentonline]

Oral Candidiasis

  88 year old female referred by GP to Emergency Department for general decline from past 2 weeks. She has decreased oral intake. She has completed course of oral Cephalexin as per her General practitioner.   Diagnosis– Cellulitis Hypernatraemia Oral Candidiasis Dehydration   Allergies–  Penicillin   Past Medical History– Dementia Hypertension Diverticulitis Asthma UTIs GORD Bowel Cancer Chronia…

[assignmenttutoronline]

Oral Candidiasis

  88 year old female referred by GP to Emergency Department for general decline from past 2 weeks. She has decreased oral intake. She has completed course of oral Cephalexin as per her General practitioner.   Diagnosis– Cellulitis Hypernatraemia Oral Candidiasis Dehydration   Allergies–  Penicillin   Past Medical History– Dementia Hypertension Diverticulitis Asthma UTIs GORD Bowel Cancer Chronia…

[assignmentfreelancers]

Oral Candidiasis

  88 year old female referred by GP to Emergency Department for general decline from past 2 weeks. She has decreased oral intake. She has completed course of oral Cephalexin as per her General practitioner.   Diagnosis– Cellulitis Hypernatraemia Oral Candidiasis Dehydration   Allergies–  Penicillin   Past Medical History– Dementia Hypertension Diverticulitis Asthma UTIs GORD Bowel Cancer Chronia…

[assignmenttutorsforyou]

Oral Candidiasis

  88 year old female referred by GP to Emergency Department for general decline from past 2 weeks. She has decreased oral intake. She has completed course of oral Cephalexin as per her General practitioner.   Diagnosis– Cellulitis Hypernatraemia Oral Candidiasis Dehydration   Allergies–  Penicillin   Past Medical History– Dementia Hypertension Diverticulitis Asthma UTIs GORD Bowel Cancer Chronia…

[biology-geology-beaches-india]

TSRNOSS, p 516.

[antibod-y-blog]

Hi (not sure if i asked this before) im taking mls too and our major subjects start next sem (parasitlgy, bacte, clinchem etc). Do you have any tips on what to read or specific topics i should memorize in advance?

Hey! It’s so rare to find someone else in this course. I never really did any pre-reading before semesters, because often they only cover a small portion of what’s actually other there. I’ve done/am doing those subjects now, for parasitology look at your helminths (nematodes/roundworms) & platyhelminths (trematodes & cestodes). As for bacteria; gram positive cocci (strept, staph), rods (listeria, bacillus, clostridium, mycobacterium, corynebacterium) & gram negative rods (class = enterobacetriaceae, psuedomonaceae, burkholderiaceae, moraxellaceae, vibrionaceae) cocci/coccobacilli (pastuerellaceae, nesseriaceae). These are your most common classes/species of bacteria. Clinical Chem, I’m still trying to get a grasp of. I’m finding it super boring. But the topics I’ve covered so far are Acid-Base Balance (acidosis/alkalosis), Electrolyte Balance and Disturbances (hypo/hypernatraemia & hypo/hyperkalaemia) & Renal dysfunctions, Urinalysis. 

So, maybe don’t memorise. But have a read over them & then when you’re actually taught them it’ll further cement your understanding! Good luck, if you have any other questions let me know x

[thewaltzy]

Drug Profile - Lithium

Indication (What it’s used for):

Lithium Carbonate

Treatment and prophylaxis of Mania

Treatment and prophylaxis of Bipolar Disorder

Treatment and prophylaxis of recurrent Depression

Treatment and prophylaxis of aggressive or self-harming behaviour

Lithium Citrate

Treatment and prophylaxis of Mania

Treatment and prophylaxis of Bipolar Disorder

Treatment and prophylaxis of recurrent Depression

Treatment and prophylaxis of aggressive or self-harming behaviour

Contraindication (When you can’t use it):

Addison’s Disease

Heart Failure

Dehydration

Family or personal history of Brugada Syndrome

Low sodium diets

Rhythm disorder

Untreated Hypothyroidism

Cautions (When you need to be careful using it):

Cardiac Disease

Electroconvulsive Therapy

Diuretic treatment

Elderly

Epilepsy

Myasthenia Gravis

Psoriasis

QT Interval Prolongation

Mechanism of Action (How it works):

Lithium affects neurotransmitter release and binding, but exactly how it does so is unknown

Side Effects:

Rare or Very Dare

Nephropathy

Frequency Not Known

Abdominal Discomfort

Alopecia

Decreased appetite

Arrhythymias

AV Block

Delirium

Electrolyte Imbalance

Encephalopathy

Goitre

Hyperglycaemia

Hyperparathyroidism

Muscle Weakness

Nausea and Vomiting

Peripheral Odema

QT Interval Prolongation

Renal Impairment

Seizure

Sexual Dysfunction

Weight Gain

Signs of Toxicity/Overdose:

Increasing GI Disturbances

Visual Disturbances

Polyuria

Muscle Weakness

Increasing Tremor

CNS Disturbances

Abnormal Reflexes

Myoclonus

Incontinence

Hypernatraemia

Cardiac Arrhythmias

Circulatory Failure

Renal Failure

Interactions:

ACE Inhibitors (e.g. Ramipril, Perindopril, Captopril) can increase serum Lithium concentration

Aldosterone Antagonists (e.g. Eplerenone, Spironolactone) can increase serum Lithium concentration

Antiepileptics (e.g. Carbamazepine, Oxcarbazepine) may increase risk of neurotoxicity

Calcium Channel Blockers (e.g. Diltiazem, Verapamil) may increase risk of neurotoxicity

Diuretics (e.g. Indapamide, Furosemide) can increase serum Lithium concentration

NSAIDs (e.g. Ibuprofen, Naproxen) can increase serum Lithium concentration

Monitoring:

Monitor serum Lithium concentration

Take blood 12 hrs after dose to achieve a  serum Lithium concentration of 0.4 mmol/L to 1 mmol/L

Weekly after initiation and after dose changes until stable, then every 3 month thereafter

Monitor renal function

Monitor Urea and Electrolytes - especially Sodium

Monitor BMI and/or body weight

Monitor thyroid function

Monitor cardiac function

Points of Particular Interest:

Each brand has a different bioavailability so exact dose depends on brand and serum lithium concentration

Target serum Lithium concentration of 0.8 mmol/L to 1 mmol/L for acute episodes of Mania

Lithium should not be stopped abruptly. Cessation should occur with a gradual dose reduction over 1 month to 3 months

Sources:

BNF 78

[apartamentdeinchiriat-blog]

N1 hypernatraemia, 20 mg cialis surveillance, high-frequency along evolving presbyopia. http://ift.tt/2peKCV4

[casadevanzare-blog]

Atlanto-axial hypernatraemia, clot test-bed guide-wires, cialis guide treatments; returning. http://ift.tt/2oXnvun

[lindwurmkai]

Makes sense! And I mean … okay, my memory is failing me again but didn't Luke have a pretty normal childhood? Anakin, on the other hand, was given plenty of reasons to develop BPD. I'm not sure about Kylo. Like, he had awesome parents but I dimly recall having seen a post once about Snoke starting to influence him really early, I just have no idea if it was canon or speculation? (You know these things. Educate me, o wise one. :P)

I love them all. ;-;