Re: Diabetes and Potassium?

On Feb 7, 2:07 pm, "kumar" <lordshiva5...@xxxxxxxxxxxxxx> wrote:
On Feb 7, 12:28 am, "Andrew B. Chung, MD/PhD"





<ach...@xxxxxxxxxxxxxxxxxxx> wrote:
convicted neighbor Kumar wrote:
Andrew, in the Holy Spirit, boldly wrote:
convicted neighbor Kumar wrote:
Andrew, in the Holy Spirit, boldly wrote:
convicted neighbor Kumar wrote:
snip> > > > > The tendency for cations to diffuse from an area of higher
concentration to an area of lower concentration.

Can such diffusion of K just be effected by hypertonicity of ECF,
supoose if glucose is higher in ECF?

No.

By variations in pH of ICF or ECF?

No.

pH and K are related.

Still does not affect diffusion of potassium cations down its
concentration gradient.

Probably, a low level in ICF got maintained persistenty on
hyperglycemia to maintain normal blood levels of K and Mg?

Actually, potassium levels are higher in the ICF than the ECF.

How much low levels og K and Mg can be maintained to below cell's
death levels?

A serum potassium level of less than 3.5 mg/dL can start triggering
cardiac dysrhythmias.

Do many cells keep on dying prematured due insulin resistance?

Cells dying prematurely would be as a direct conseqence of
inflammatory cytokines rather than from insulin resistance.

"Potassium is also affected by acid/base
balance because potassium exchanges with hydrogen, to some extent,
across cell membranes.
http://www.nlm.nih.gov/medlineplus/ency/article/003600.htm";

See above.

How K level can be effected by disturbance of acid/base balance in ECF
and vice versa?

It is not an issue for folks outside of an intensive care unit who are
not in critical condition (i.e. the type-2 diabetic reading this).

Sorry, how body system compensate used substances or possible
defficiencies?

It does not.

Will it not by stimulating hunger and encouraging ingestions?

No.

On excesses, whether body mechanism can stimulate to get just
sensation (cephalic phase effect) of that substances which are in
excesses WHEREAS on defficiencies sensation+ingestions?

No.

Whether cephalic phase effect is just a sensation effect?

Simply a sign of a working gastrointestinal system.

Whether all sensations creates somewhat cephalic phase type effect?

No.

How sensation of food etc. promote proper metabolism of that food?

Serves to reward the person for his/her efforts to chew the food
properly.

Suppose we just sense or taste food/sugar but not ingest it, will it
benefit in controlling hyperglycemia due to cephalic phase effect?

No.

Can getting occasional craving fo food be meant for this purpose..to
get cephalic phase effect?

No.

For this reason, it is wise to eat a varied diet in order to avoid
deficiencies while eating the optimal amount. Your hunger will inform
you that you have avoided deficiencies.

"Hunger is good." -- Holy Spirit

Amen.

I am just thinking, if K (Mg also alongwith) is trying to become
defficient than optimal amount, can hunger of it encourage its eating?

There is no craving for either potassium or magnesium.

Most of foods can have sufficient K?

Potassium is plentiful.

Yes, but can't body demand more food to fullfil requirements of these?

Not clinically seen.

Are glycogen abnormilities(store and breakdown) common in diabetics2?

Not in those folks on a regular diabetic diet.

On glycogen abnormilities, can body system opt to maintain
hyperglycemia to compensate it?

Type-2 diabetics do not have glycogen abnormalities.

Thanks.

Thanks be to GOD.

Whether vasoconstrictions can cause one to excrete more urine
via kindney and less sweating, vasodilation opposite?

This would have nothing to do with either glycogen abnormalities or
diabetes.

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com-Hide quoted text -

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Followings are quite interesting discussions, hich may indicate
possibilty of hyperkalemia and decreased K in ICF due to persisting
hyperglycemia;

"Discussion

Acid-base and potassium disturbances are common in patients with
uncontrolled diabetes mellitus [1,2]. This was an interesting case of
DKA presenting as an emergency, with neurological symptoms and
electrocardiographic changes associated with hyperkalaemia.
Decompensated metabolic acidosis (as manifested by hypercapnia) and
ECG abnormalities indicate the need for rapid intervention and a
meticulous approach to management [1,2].

The development of metabolic acidosis causes a compensatory
hyperventilatory response owing to stimulation of both the central and
peripheral chemoreceptors. This increase in alveolar ventilation
results in a drop in pCO2, which tends to raise pH towards normal. In
contrast to other causes of acidaemia, in cases of DKA it is the
carotid body chemoreceptors that provide the major stimulus for
respiration driven by a reduced pH. This means that hyperventilation
is taking place earlier in DKA. However, in this case, pCO2 was
raised, suggesting inadequate respiratory compensation, which may have
been related to profound hyperkalaemia. Potassium excess (>8 mmol/l)
is associated with muscle weakness. The lower extremities are affected
initially, the trunk and upper extremities being affected later [2].
Respiratory muscle involvement is rare and presents a life-threatening
complication. In this case, respiratory muscle weakness was related to
high plasma potassium levels adversely affecting the respiratory
compensatory mechanisms. On the other hand, acidosis was aggravated by
hyperkalaemia, which is known to induce a mild metabolic acidosis by
impairing NH+ production and excretion [2].

Mild to moderate increases in serum potassium occur frequently with
DKA [2,3]. However, severe hyperkalaemia is uncommon and is likely to
be a consequence of acidosis, insulin deficiency, hyperosmolality,
severe dehydration and renal potassium retention [2,3].

It is well documented that the buffering of excess hydrogen ions in
cells leads to potassium movement into the extracellular fluid in
order to maintain electoneutrality. This is true in metabolic acidosis
caused by accumulation of mineral acids (normal-anion gap,
hyperchloraemic acidosis), but is less likely to occur in the organic
acidoses, such as DKA [2]. Thus, the acidaemia could not explain the
severe hyperkalaemia noted in this patient. In DKA, the combination of
insulin deficiency and the hyperglycaemia-induced hyperosmolality
frequently leads to hyperkalaemia, even though the patient may be
markedly potassium-depleted owing to potassium losses in the urine
secondary to osmotic diuresis [1,2]. Insulin promotes potassium entry
into cells. When circulating insulin is lacking, as in DKA, potassium
moves out of cells, thus raising plasma potassium levels even in the
presence of total body potassium deficiency [2,3]. Furthermore, an
elevation in plasma osmolality causes osmotic water movement from the
cells into the extracellular fluid, which is paralleled by potassium
movement out of the cells.

Most of urinary potassium is derived from potassium secretion in the
distal nephron, particularly by the principal cells in the cortical
collecting tubule. This process is mainly influenced by two factors:
aldosterone and the distal delivery of sodium and water [2]. In cases
of severe volume depletion, the ability to handle a potassium load is
impaired due to decreased distal fluid delivery, which can diminish
potassium secretion despite the hypovolaemia-induced secondary
hyperaldosteronism [2]. Notably, in our patient the administration of
an angiotensin-converting enzyme inhibitor (namely quinapril) can
limit the aldosterone release, thus aggravating the hyperkalaemia.
These drugs can reduce the concentrations of circulating angiotensin
II and diminish the intra-adrenal angiotensin II, which can mediate
part or most of the stimulating effect of hyperkalaemia [2,4].
Hyporeninaemic hypoaldosteronism (presenting as asymptomatic
hyperkalaemia in patients with long-standing diabetes mellitus) could
result in a further increase in potassium levels. However, this was
not true in the present case, as the patient's plasma creatinine,
urea, potassium, chloride and bicarbonate levels restored to normal
upon discharge [2,3].

Pre-renal azotaemia in patients with DKA is primarily due to volume
depletion and/or relative hypotension leading to reduced glomerular
perfusion and impairment of renal function [1,2]. However, creatinine
levels may not always securely predict the status of hydration and the
target towards fluid resuscitation. Elevated serum creatinine levels
in patients with uncontrolled diabetes mellitus should be evaluated in
the light of baseline values. Methodological problems must be
considered because certain substances may interfere with the assay
(especially colorimetric assays), thereby artefactually increasing
serum creatinine levels. Enzymatic assays, which lack this
interference, may be more advantageous on these occasions.http://ndt.oxfordjournals.org/cgi/content/full/18/1/198";

As such hyperkalemia, decreased levels of K in cells and may be
hypokalemia in chronic/persisting condition(due to prolonged efflux of
K from ICF to ECF>Blood>urine) can be feared. More movement water or
other ECF substances to ICF and ICF substances to ECF due to above
hypertonic/acidosis effect can be feared in diabetics2?- Hide quoted text -

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More;

Inverse distribution of serum sodium and potassium in uncontrolled
inpatients with diabetes mellitus.Saito T, Ishikawa S, Higashiyama M,
Nakamura T, Rokkaku K, Hayashi H, Kusaka I, Nagasaka S, Saito T.
Division of Endocrinology and Metabolism, Department of Medicine,
Jichi Medical School, Tochigi, Japan.

"It has been reported that there is an inverse relationship between
serum sodium (Na) and potassium (K) levels in patients with diabetic
coma. The present study was undertaken to determine whether such an
inverse relation depends upon plasma glucose levels in diabetic
patients for their glycemic control. We examined two hundred and fifty-
two patients with diabetes mellitus admitted to our hospital during
the one-year period to control their plasma glucose levels, except for
those having nephropathy or liver dysfunction. Serum Na and K, plasma
glucose, and serum and urinary C-peptide levels were determined. There
was a negative correlation between serum Na levels and fasting plasma
glucose (FPG), and, conversely, a positive correlation between serum K
levels and FPG. The changes were more evident in the patients with
insulin-dependent diabetes mellitus than those with non-insulin-
dependent diabetes mellitus. There was an inverse relation between
serum Na and K levels and it was profoundly dependent upon plasma
glucose levels in all the diabetic patients before tight control of
their glycemic levels. The disorder may be based on the movement of
electrolytes between intra- and extracellular spaces, dependent on the
impaired insulin action as well as hyperosmolality.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10426570&dopt=Abstract
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I thing subsstances which attract and retain water or which can effect
osmolalty AND pH are relavent tothis aspect?



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