assessment of Serum potassium levels. Description of pseudohyperkalemia and reverse pseudohyperkalemia. Causes of hyperkalemia. Clinical manifestation of hypokalemia and hyperkalemia.
Metabolism of potassium and its clinical significancerohini sane
A comprehensive presentation on Metabolism of Potassium and its clinical significance for MBBS, BDS, B Pharm & Biotechnology students to facilitate self- study.
Metabolism of potassium and its clinical significancerohini sane
A comprehensive presentation on Metabolism of Potassium and its clinical significance for MBBS, BDS, B Pharm & Biotechnology students to facilitate self- study.
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.
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.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
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.
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.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
Body Fluid and Compartments | DR RAI M. AMMAR | ALL MEDICAL DATA
by DR RAI M. AMMAR
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
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Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
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Esta publicação só está disponível em inglês até o momento.
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This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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3. Why serum has higher potassium content than plasma?
Best container for serum potassium?
Sample of choice for potassium?
Preservative used for urinary potassium?
Important Facts About Potassium
4. ★ Is little affected by alteration of water balance
★ A poor guide of total body K+ content
★ Doesn’t change unless there is 10% alteration of body K+ content
Role in body
● Maintains Oncotic Pressure & intracellular volume
● Resting Membrane, Acting membrane Potential & neuromuscular function → Tissue
excitability
● Cardiac impulse
● Acid base balance
● Helps in NA/protein synthesis
● Facilitates cell growth
Important Facts About Potassium
6. Hypokalemia
Rule out Pre analytical error
● Sample dilution (all parameters will be low)
● Electrolytes exclusion effect (electrolytes will be low with indirect ISE)
Causes of Hypokalemia
1. Decrease dietary potassium (chronic starvation)
2. Redistribution of potassium in body compartments
3. True potassium deficit
7. Insulin therapy
Insulin → express GLUT-4 channels on cells (muscles/adipose tissue/RBCs)
→GLUT-4 channel Cotransport Glucose/K+ into the cells →shift of serum
potassium into cells → Hypokalemia
Alkalosis
↓ H+ in plasma → to compensation H+ comes out of cells (mainly RBCs) into
plasma →K+ moves inside cells to keep electrochemical gradient constant →
hypokalemia
↓ H+ in plasma → DCT (kidney) conserve H+ by decreasing its excretion →to
keep electrochemical gradient K+ is secretion into lumen → ↑K+ excretion
→hypokalemia
Redistribution of potassium in body compartments
8. ↑ Catecholamine activity
Beta 2 receptor stimulation → dose dependent activation of Na/K ATPase pump
Hypothermia
Increase activity of Na/K ATPase pump in induction phase
Refeeding syndrome
Hypokalemia (weakness), hypophosphatemia (hypotension, fits) and
hypomagnesemia (hypocalcemia, GI symptoms) after initiation of feeding in
malnourished patients is called refeeding syndrome
Already deficiency of nutrients → Refeeding → ↑glucose in blood → release of
insulin → movement of K+, Mg+2 and PO-3 into cells along with glucose
Redistribution of potassium in body compartments
9. Periodic hypokalemic paralysis
Familial hypokalemic periodic paralysis
Gene mutation →mutated Kir 2.6 potassium channel in skeletal muscles
→increase K+ influx → altered muscle membrane excitability →paralysis
Thyrotoxic hypokalemic periodic paralysis
Kir 2.2 transcription is regulated by thyroid hormone →increase thyroid hormone
→ increase K+ influx → altered muscle membrane excitability →paralysis
Redistribution of potassium in body compartments
10. Loss of potassium from body →↓ Total body Potassium
K+ loss through kidneys
K+ loss through extra renal source
24 Hours Urinary K+ < 25 mmol/day → Extrarenal loss of K+
True Potassium Deficit
Through Gut Through Skin
Diarrhoea Excessive sweating
Fistula (involving gut) Burns
Ileostomy
11. 24 Hours Urinary K+ > 25 mmol/day → Renal loss of K+
True Potassium Deficit
Defective renal
tubules
Drugs ↑ Mineralocorticoid effect Compensatory
RTA (Type I/II) Thiazide Primary hyperaldosteronism Metabolic Alkalosis
ATN (Diuretic phase) Loop diuretics Secondary hyperaldosteronism NG suction Vomiting
Amphotericicn B Excess of Glucocorticoids Hypomagnessemia
Penicillin AME
12. 24 hrs urinary K+
Renal >25 mmol/L Extra renal <25 mmol/L
ABGs
Metabolic Alkalosis
Metabolic Acidosis
Normal
RTA Type I/II 24 hrs urinary Cl-
>10 mmol/L < 10 mmol/L
↑Aldosterone
↑Glucocorticoid
Vomiting
NG suction
Diuretics
Penicillin
ATN
Amphoterici
n B
13. Hyperkalemia →5.1 mmol/L
Severe hyperkalemia → > 7.0 mmol/L
Fatal hyperkalemia → > 10 mmol/L
Rule out Pre analytical error
Pseudohyperkalemia
● Traumatic venipuncture
● Prolonged tourniquet
● K+ - EDTA contamination
● Hemolytic sample
● Vigorous shake during transport
● Prolonged handling time
● Improper storage
Hyperkalemia
14. Reverse pseudohyperkalemia Leukemia (>100000/uL)
In vitro phenomenon in which plasma potassium concentration rises higher than
serum potassium concentration, usually due to extreme leukocytosis
Increase iron stores
Leukemic leukocytes are more fragile than normal leukocytes, leading to in vitro
lysis during centrifugation of plasma specimens and elevating potassium
concentrations. In serum specimens, the formation of a fibrin clot is hypothesized
to entrap and stabilize tumor cells during centrifugation. Whole blood can be used
as an alternative specimen in cases of reverse pseudohyperkalemia
Leukocytosis has higher energy consumption leading impaired Na/K ATPase
pump
Increase sensitivity to heparin induced membrane damage in haematological
malignancies
Hyperkalemia
15. Hyperkalemia
Pseudohyperkalemia →False ↑ in serum K+ in comparison to the normal plasma
levels
Pseudohyperkalemia →False ↑ in plasma K+ in comparison to the normal serum
levels
What is the difference between pseudohyperkalemia and reverse
pseudohyperkalemia?
Aldosterone escape phenomenon and lack of edema: Potassium-wasting
effect of excess aldosterone is counterbalanced by the potassium-retaining
effect of hypokalemia itself
16. Causes of Hyperkalemia
1. Redistribution
a. Acidosis (compensatory)
b. Drugs
i. Beta blocker
ii. Digoxin
c. ↓ Insulin (type 1 DM with severe insulin deficiency)
d. Release from ICF
i. Hemolytic anemia
ii. Tissue hypoxia
iii. Rhabdomyolysis
iv. Heavy exercise
v. Status epilepticus
vi. Severe burn
17. Causes of Hyperkalemia
2. True potassium gain
Normal kidneys are able to handle potassium load. When kidneys are able to
excrete out extra K+ look for underlying renal disease
A. Increase potassium intake (supplementation with compromised renal
function)
B. Massive transfusion
C. Hemolytic transfusion reaction
18. Causes of Hyperkalemia
2. True potassium gain
A. Decreased potassium excretion
a. Primary renal defect
b. Mineralocorticoid deficiency
i. Hypoaldosteronism
ii. Hyporeninemic Hypoaldosteronism
iii. Addison's disease
c. Drugs inhibiting Aldosterone
i. ACE inhibitors
ii. ARB II
iii. NSAIDs
B. Potassium sparing diuretics
a. Spironolactone
b. Amiloride