Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
APPROACH TO AKI IN CHILDREN
ACUTE KIDNEY INJURY
It is defined as abrupt loss of kidney function leading to rapid decline in GFR , accumulation of waste products BUN and creatinine and dysregulation of extracellular volume and electrolyte homeostasis.
AKI can ranges from small increase in creatinine to complete anuric renal failure .
INCIDENCE
2-5 % of all hospitalization.
>25% in critically ill children .
CLASSIFICATION OF AKI
CAUSES
CLINICAL MANIFESTATION
DIAGNOSTIC TEST
HISTORY AND PHYSICAL
EXAMINATION
IDENTIFICATION OF PRECIPTATING CAUSE
COMPLICATION
MANAGEMENT
MANAGEMENT
There is no definitive therapy for AKI, supportive care is mainstay of management regardless of aetiology.
Goal of treatment is :
Minimize degree of insult.
Reduce extrarenal complication.
Restoration of AKI.
Optimize the systemic and renal hemodynamic(fluid resuscitation or use of vasopressor).
Avoid the nephrotoxic drugs (e.g aminoglycoside, NSAIDs, ACE inhibitor, ARB blocker, acyclovir) or adjust the dose .
Catheterize the patient in case of obstruction like PUV, UPJ obstruction
POST-RENAL AKI
Prompt relieve of urinary tract obstruction.
Relief of obstruction is usually followed by an appropriate diuresis and may require continue administration of iv fluids and electrolyte.
RENAL REPLACEMENT THERAPY
The purpose of RRT is to prevent morbidity.
It may be necessary for days or upto 12 weeks.
Mostly require dialysis support for 1-3 weeks.
Indication Of RRT :
A= ACIDOSIS, ANURIA
E= ELECTROLYTE DISTURBANCE (hypokalemia)
I= INTOXICATION
O= OVERLOAD(hypertension, pulmonary edema)
U= UREMIA
PROGNOSIS
Pre-renal and post-renal have better prognosis.
In case of post-infectious glomerulonephritis is 1%
In case of multi organ failure >50%.
Kidney may recover even after dialysis .
10% cases requiring dialysis develop CKD.
CARRY HOME MESSAGE
Diagnose early- biomarkers have great potential.
Look for aetiology.
Prevent rather than treat.
No role of low dose dopamine prevention and treatment .
Initiate RRT when indicated.
Hyperphosphatemia in CKD patients; The Magnitude of The Problem - Prof. Alaa ...MNDU net
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This is a presentation by Dada Robert in a Your Skill Boost masterclass organised by the Excellence Foundation for South Sudan (EFSS) on Saturday, the 25th and Sunday, the 26th of May 2024.
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2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
15. Ca2+-Sensing
Receptor
(CaSR)
In the kidney, activation of CaSR in the thick ascending limb
of Henle’s loop inhibits paracellular transport of Ca2+,
resulting in hypercalciuria.
In the inner medullary collecting duct, CaSR is localized in
the endosomes that contain vasopressin-regulated water
channel, aquaporin
Activation of CaSR causes: reduction in vasopressin-
stimulated water absorption, resulting in defective uri- nary
concentration. This results in polyuria, particularly in
conditions of hypercalcemia due to which the development
of nephrocalcinosis and nephrolithiasis is prevented.
20. Renal handling of Ca
• No calcium reabsorption is taking place in this segment, which
totally depends on the calcium load delivered by the CNT. Apical
CaSR-like proteins sense urine calcium concentration. This leads to
inhibition of water reabsorption and stimulates urine acidification,
decreasing the risk of stone formation
38. Treatment of
Acute
Hypocalcemia
IV preparation :
Intravenous calcium gluconate (1 g available
as 10% in a 10 mL ampule) is the treatment
of choice for symptomatic hypocalcemia.
One gram of calcium chloride (10%) contains
273 mg of elemental Ca2+; however, it is not
always preferred because of its unbearable
irritation to veins..
39. Treatment Acute Hypocalcemia
• Initially, one to two ampules of calcium gluconate in 50 mL of
5% dextrose should be given over a period of 10–20 min,
• followed by 0.3–1 mg of elemental Ca2+/kg/h, if necessary.
Once symptoms improve, the patient can be started on oral
Ca2+ tablets
• In order to increase total serum Ca2+ by 2–3 mg/dL, a 70 kg
patient requires 1 g of elemental Ca2+ (approximately ten
ampules of calcium gluconate).
40. precautions
Solution may be diluted in NS, D5W (mix in up to 1000 mL),
Do not mix in same bag or line with carbonates, and Ringer, to avoid precipitation
For intermittent IV infusion, maximum rate is 200 mg/min (2 mL/min)
May administer IV push at rate of 50-100 mg/min (0.5-1 mL/min); rapid IV
administration may produce arrhythmias, hypotension, myocardial infarction, or
vasodilation
Central line
If hypomagnesemia is the underlying cause for hypocalcemia, IV magnesium
sulfate (8 mEq) should be given.
42. Treatment chronic Hypocalcemia
• Treatment is aimed at correcting the cause, if possible.
• Oral calcium supplementation (500–1,500 mg elemental Ca2+)
• calcitriol 0.5–1 μg/day are generally used for patients with hypoparathyroidism or PTH
resistance, chronic kidney disease, and osteomalacia.
• A few patients with hypoparathyroidism may benefit from thiazide diuretics.
• For patients with nutritional vitamin D deficiency, either cholecalciferol
• (effective dose 400–1,000 U/day) or ergocalciferol (effective dose 25,000–
• 50,000 U three times/week) can be used. For many patients,
43. Empirical Ca administration prior to
dialysis in ESRD patient , first discovered ,
presented with emergency in need for
urgent dialysis?????
44.
45. Hypercalcemia
•serum [Ca2+] >10.2 mg/dL in an individual with normal
serum albumin concentration.
•severe hypercalcemia is considered when
serum [Ca2+] is above 14 mg/dL.
54. Treatment of acute hypercalcemia
• 1. Hydration with normal saline and then administration of
furosemide for volume overload. Note that furosemide-
induced volume depletion may increase reabsorption of Ca2+
by the proximal tubule
• 2. Inhibition of bone resorption of Ca2+.
• 3. Decrease intestinal absorption of Ca2+.
• 4. Removal of Ca2+ by hemodialysis using a dialysate bath
containing low Ca2+.
57. Treatment of
chronic
hypercalcemia
1. Correction of the underlying cause:
parathyroidectomy and chemotherapy. Use cinacalcet
(30–120 mg/day) for secondary hyperparathyroidism
2. Maintenance of euvolemia: prescribe adequate
amount of water that should be equal or slightly more
than urine output and insensible loss.
3. Decrease the production of 1,25(OH)2D3: low-
calcium diet, avoid vitamin D intake, steroids,
chloroquine (250 mg/day) and ketoconazole (100–200
mg/day).
4. Decrease intestinal absorption of Ca2+: low-calcium
diet, steroids, and avoidance of vitamin D
preparations.
58. Treatment of
chronic
hypercalcemia
5. Decrease bone resorption: steroids, lower
PTH levels, avoid vitamin D use,
bisphosphonates, and receptor activator of
nuclear factor-kB ligand (RANKL) inhibitor,
and denosumab.
6. Bisphosphonates are used to treat
hypercalcemia in patients with
malignancy.they inhibit osteoclast-induced
bone resorption.
7. Denosumab is a humanized monoclonal
antibody that inhibits osteoclastic activity
and thereby bone resorption.