PARALYSIS IN

HYPOKALEMIA
Bima Yuswanti
Hendy Million
 Hypokalemia defined as a plasma K+
concentration < 3.5 mmol/L, may result from
one (or more) of the following : decreased net
intake, shift into cells, or increased net loss.

Singer G. Brenner B. Fluid and Electrolyte Disturbance. In :

Harrisons Principles of Internal Medicine 18ed 2012
 Etiology
1. Decreased intake
a.
 Clinical Features
Severity depends on the degree of hypokalemia
Symptoms usually occur when the plasma K+
concentration is below 3mmol/L
Common complaints : fatigue, myalgia, and
muscular weakness of the lower extremities
Severe hypokalemia : progressive weakness,
hypoventilation, and eventually complete
paralysis
May also cause rhabdomyolisis, paralytic ileus,
ventricular arrhytmias
Muscle contraction flow chart
Contraction phase
Resting state

Motor nerve action potential arrives at motor end plate

Action potential reached when the cells have high depolarization

so they trigger the Na+ gate opening Na+ enter the cell.
Sudden influx of calcium ions causes changes in the cell so that
the charge becomes more positive, reaching about +30 mV at a
nerve cell
When the cell becomes positive, Na+ gate began to close. K+ are also
affected by changes in membrane potential is open and allows
potassium ions stormed out of the cell. This causes the negatively
charged cell back on the inside opened calcium gate.

Corwin E J. buku saku patofiologi. 2001.

 Acetylcholine released, sarcolemma and membranes
depolarized (Na + flux into fiber)
Action potential transmitted via T-tubules to SR
Ca++ released from SR terminal cisternae into sarcoplasm
Ca++ bound by troponin
Myosin ATPase activated and ATP hydrolized
Tropomyosin shift actin binding site
Action-myosin crossbbridge formation
Repeated formation and breaking of crossbridges
resulting in sliding of filaments and sarcomere
shortening
Aberle, Elton D, Forrest, John C, Gerrard, David E, Mills, Edward W. In :
Principles of Meat Science 4ed 2013
Relaxation phase
Cholinesterase released and acetylcholine

breakdown
Sarcolemma and T-tubules repolarized

SR Ca++ pump activated and Ca++ returned to

SR terminal cisternae
Actin-myosin crossbridge formation

terminated
Return of tropomyosin to actin binding site
 Mg++ complex formed with ATP
Passive sliding of filaments
Sarcomers return to resting state
Hypokalemic Periodic Paralysis
The history of the disease is difficult to trace,
but the first unmistakable account was
probably that of Hartwig in 1874
The usual pattern of inheritance is autosomal
dominant with reduced penetrance in women
(male-to-female ratio of 3 or 4 :1).
Fontaine and coworkes localized the mutation
to a region containing the gene that encodes
alpha subunit of the calcium channel of skeletal
muscle and the gene has now been determined
 Mutation in genes and coding three ion
channels [CACNA1S (1q32), SCN4A (17q23.1-
q25.3), and KCNJ2 (17q23.1-q24.2)] account for
most cases.
Hypokalemic periodic paralysis has been
related to mutation in the CACNL1A3, SCN4A,
or KCNE3 (11q13-q14) gene and its
characterized by attacks that tend to occur on
awakening after exercise or after a heavy meal
and may last for several days.
Venance SL. et al. The primary periodic paralysis: diagnosis, pathogenesis, and treatment. Brain. 2006 Jan; 129(Pt
1):8-17. [PMID: 16195244]
Hypokalemic Periodic Paralysis
Paralysis from severe hypokalemia can also
occur in some clinical settings, including
chronic diarrhea, renal tubular acidosis,
primary aldosteronism, and alcoholism.
Certain drug and substance, intoxications, from
licorice, cola, and clay for example, can also
trigger this phenomenon

Up to date
 Pathogenesis
How precisely the reduced calcium channel
function relates to hypokalemia-induced
attacks of muscle weakness is not fully known

Ropper, Allan H, Samuels, Martin A. In : Adams and Victor's

Principles of Neurology 9ed 2009
Treatment Brown, Robert H,
Amato, Anthony A,
Mendell, Jerry R. In :
Harrisons Neurology
in Clinical Medicine
2ed 2010
TERIMA KASIH