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33 Cards in this Set

  • Front
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Total electrolyte distribution in PLASMA

Total cations=Total anions=150mmol/l


The total cation is cation in both plasma (Na+,K+,Ca2+,Mg2+)


Total anions (Cl-,HCO3-,proteins,phosphates,organic acids,sulphates)

Reference range for HCO3-

18-31mmol/l

Osmolarity of plasma in mmol/kg

285mmol/kg=285mOsm/kg


Since the same value you know

Anion gap

Anion gap is the difference between the measured primary cations( Na+, K+)and the measured primary anions ( Cl- , HC03 -) . It should be between range of 6-20mmol/ lCation -anion = 6-20mmol/l.


IT IS CALLED ANION GAP BECAUSE IT'S THE ANION THAT'S LAGGING

Osmolarity is the same(285mmol/kg) in all body organs except

KIDNEY (where it can go as high as 1200mmol/kg in medulla)

ADH is also known as

Arginine Vasopressin (AVP)

Total sodium level in a 7okg man is

Total sodium level = 3700mmol75% is Exchangeable( found majorly in ECF); E in Exchangeable for Ecf25% is NOT exchangeable (because it is incorporated in the bones)

Sodium daily intake

100-300mmol/day



2 major hormones regulate Sodium Excretion

Aldosterone


Atrial Natriuretic Peptide (ANP)


ANP is produced by cells of "RIGHT ATRIUM"

3 means of sodium excretion

Sodium is excreted by 3 means:(a) kidney ( majority of sodium is excreted by kidney)(b) Sweat(c) Faeces Sweat & Faeces account for 5mmol/l loss

ANP Is produced by which atrium

RIGHT ATRIUM

Nephrotic syndrome

It is a condition that causes the body to excrete TOO MUCH PROTEINS IN URINE. Nephrotic Syndrome= HYPERPROTEINURIA, HYPOPROTEINEMIA


•The proteins lost are:


a) Albumin (causing decreaied oncotic pressure & edema)


b) Immunoglobulin ( lncreasing chance of infection)


c) Anti thrombin III(increasing chance of hypercoagulability)



Causes of hyponatremia

•Hypovolemic causes : Diarrhoea, Vomiting, Diuresis , Dehydration, Drains (fistula)


•Euvolemic causes : SIADH


• Hypervolemic causes : Congestive Heart failure (CHF) , Liver cirrhosis, Nephrotic syndrome, renal failure (Cells can't produce renin to retain sodium)


Hypovolemic & Euvolemic are NON-EDEMATOUS. Only Hypervolemic causes are EDEMATOUS



Aldosterone antagonists

Triamterine


●Spironolactone

Tests to determine Kidney function

G.F.R Test


●Creatinine Level test


●Urea test

Features of Hyponatremia due to water overload

• Non-edematous• Absence of kidney disease (Normal GFR, Urea, Creatinine)• Absence of heart failure (normal B.P.)


Treated by Fluid restriction

Causes of hypernatremia

a) Loss of free water ( eg sweat, diarrhoea, Vomiting , Insensible loss)b) Decreased intake of free waterc) Sodium overload ( due to Conn Syndrome ,Cushing syndrome , Sodium bicarbonate infusion for acidosis, etc)

Management for hypernatremia

1) Give oral fluid (to balance Na distribution)


2) Administer 5% dextrose(isotonic)


Both serve as hypotonic fluid effectively

Clinical features of hypokalemia

a) Cardiac arrhythmia


b) Muscle weakness ( decreased muscle strength)


c) Hyporeflexia

Digoxine act by inhibiting

ATPases (Sodium-potassium, Calcium)It increases force of contraction of muscle(by inviting Ca ATPase, hence Ca inside the cell is not transported out)


ATPases (Sodium-potassium, Calcium)It increases force of contraction of muscle(by inviting Ca ATPase, hence Ca inside the cell is not transported out)●It is used to slow down heart rhythm thereby correcting arrhythmias.

£CG presentation of Hypokalemia

Hypokalemia =Incomplete Repolarization


Therefore you observe:


• Flattened T wave ( due to incomplete repolarization of ventricle)


• Elevated subsequent U wave [ 1 flat, 1 elevated]

Digoxin binds to where in Na K ATPase

It binds to the site that K+ usually bind to ( thus inhibiting the action of ATPase). Its binding inactivate the ATPase preventing it from working at all (so it can't even transport sodium)

Common cause of reduction of any kind of electrolyte

GIT loss ( vomiting, diarrhoea, drains/fistula)


GI losses causes reduction in any kind of electrolyte- Na(causing hyponatremia), K (causing hypokalemia) GI LOSSES ALWAYS CAUSE REDUCTION IN ELECTROLYTE

Thiazide Diuretics

Blocks Na+-K+-Cl transporter causing increased excretion of Na+,K+,Cl-,Mg2+,Ca2+.


So the diuretic cause both Hyponatremia and Hypokalemia

Total potassium pool in body

3600mmol

Distribution of potassium intracellularly and extracellularly

98% intracellularly


2% extracellularly

Causes of hypokalemia

GIT losses (vomiting, diarrhoea, fistula)


●Renal loss (increased aldosterone, renal disease that prevent PCT reabsorption)


●Drugs(thiazide diuretics, corticosteroids)


●Alkalosis( via H+K+ ATPase)

The most common and emergency case of electrolyte imbalance

HYPERKALEMIA (because it causes cardiac arrest)

Cardiac arrest occurs when serum potassium is above

7mmol/l

ECG presentation of hyperkalemia

Peaked T wave (because of fast and continuous repolarization that progressed to hyperpolarization)


Widened QRS Complex(because it will take longer time to depolarization cell due to hyperpolarization so Na influx last for a long time, to first eliminate hyperpolarization then depolarize)

Dialysis

Aka Renal Replacement Therapy


In dialysis, artificial means are used to remove EXCESSIVE fluids, electrolytes (like sodium, potassium), wastes, etc. It acts like KIDNEY, hence renal replacement. It is often used when the kidney is not properly functioning

Treatment of hyperkalemia

a) Insulin and glucose administration(to increase uptake of potassium)


b) Calcium gluconate administration( to counter ventricular fibrillation especially, by causing forceful contraction that still produces normal Cardiac Output)


c) Dialysis( to remove excess potassium)


d) Cation exchange resin (resonium A)

Examples of intravenous fluid

1.26% sodium bicarbonate (for acidotic patients)