approach to diagnosis of hypokalemia

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  • 7/26/2019 Approach to Diagnosis of Hypokalemia

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    Dr Chaitanya Vemuri

    Approach to Diagnosis of

    Hypokalemia

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    Most abundant cation in human body

    Regulates intracellular enzyme function and helps to determine

    neuromuscular & cardiovascular tissue excitability.

    9 !of total body "# $ %ntracellular

    predominantly in muscle '

    ( ! $ )xtracellular fluid

    * ( ! $ +lasma

    Introduction : Potassium

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    Ratioof extracellular "# to %ntracellular "# $ determines

    the membrane potential

    ,he acuity of changesin serum potassium concentration& membrane potential determines clinical symptoms and

    underlying signs

    +lasma concentration varies from -. to ./ mmol0l

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    1igh intracellular concentration of "# is maintained by

    several factors that govern "# upta2e & release from

    intracellular compartment

    "# upta2e into cells $ actively driven by 3a#"#4,+ase

    5ea2bac2 into )C6 $ opposed by electrical gradient

    Physiology Of PotassiumHomeostasis

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    4cid base status

    +ancreatic hormones $ insulin 7 glucagon

    Catecholamines

    4ldosterone

    +lasma 8smolality

    )xercise

    Cellular "# content

    Factors modifying transcellular K+distribution

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    4l2alemiapromotes "# upta2e by cells

    4cidemia diminishes "# upta2e by cells

    4cute respiratory al2alosis7 incontrast increase plasma "#

    by . mmol0l per .( p1 unit

    d0t increased adrenergic activity

    Acid ase !tatus

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    %nsulinstimulates cellular upta2e of "# by activating

    3a#"#4,+ase decreasing plasma "# '

    %nsulin affects "# transport independently of glucose

    upta2e

    :lucagon increase plasma "#independently of changes

    in plasma glucose 0 insulin

    Pancreatic Hormones

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    ;eta adrenergic activity < hypo2alemia

    4lpha adrenergic antagonists < hypo2alemia

    "atecholamines

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    %nvitro studies4ldosterone stimulates 3a#"#4,+ase and thereby

    activating 3a # influx

    Aldosterone

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    1yperosmolality Mannitol infusion 0 hyperglycemia in

    DM ' $ increase plasma "#

    )ach ( m8sm 0 "g rise in plasma osmolality7 increases

    plasma "# by ./ mmol0l

    Osmolality

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    Recurrent contraction increases "# egress from muscle

    Modest exercise $ high "# in )C6 in local environment

    produces vasodilatation & thereby increased regional blood

    flo=

    >evere exercise $ increase plasma "# modestly

    +hysical training increases 3a#"#4,+ase activity in s2eletal

    muscle =hich helps s2eletal muscle to ta2e up "# again

    #$ercise

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    %ntracellular "# affects intra to extracellular "#

    ?ith "# depletion 7

    "# loss from )C6 @ %C6 losscausing increased "i # 0 "e#

    "# depletion $ hyperpolarization

    "# retention $ depolarization

    "ellular K+ "ontent

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    "idney is dominant in sustaining "# balance

    @9 ! "# $ excreted in urine

    Remainder through feces

    Decrease in :6R7 "# excretion via feces increased

    :% 5oss $ "# secretion by proximal & distal colon

    K+ alance

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    %enal Handling of K+:lomerulus$ freely filtered

    +C,7 ,hic2 4s limb 581 $

    reabsorbed

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    "ortical "ollecting Duct

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    Defined as plasma concentration of "# * -.A m)B05

    Mild 1ypo2alemia $ -. < -.A m)B05 $ asymptomatic

    1ypo2alemia * -. m)B05 $ symptomatic

    Clinical manifestations of hypo2alemia vary greatly

    bet=een individual patients&

    their severitydepends on degree of hypo2alemia

    Hypokalemia

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    Clinical features

    %nvestigations

    Diagnosis

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    Mild hypo2alemia $ generally asymptomatic

    %ncreased ris2 of mortality for pts =ith cardiovascular disease < trigger ventricular

    tachycardia 0 ventricular fibrillation

    decrease "# $ d0t sympathetic stimulation'

    Digitalis induced arrhythmias < can occur =ith normal drug levels if hypo2alemia is

    present

    Diuretic induced hypo2alemia & hypomagnesemia must be avoided in pts on drugs

    that prolong , interval $ as it predisposes topolymorphic V, 0 ,orsade de pointes

    1ypo2alemia * - m)B05 $ >ymptomatic

    "linical Features

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    Digitalis %ntoxication $ ventricular extrasystoles

    ventricular tachycardia

    ventricular fibrillation

    partialcomplete 4V bloc2bradycardia

    atrial flutter

    atrial fibrillation

    Ventricular arrhythmias $ tachycardia 0 fibrillation

    "ardiac

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    6atigue

    Myalgia

    Muscular =ea2ness involving lo=er limbs

    >evere 1ypo2alemia $

    +aralysis extremities '

    ?ea2ness of respiratory muscles dyspnea '

    Rhabdomyolysis exercise induced'

    &euro'muscular

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    Constipation

    +aralytic ileus

    (astro'intestinal

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    Chronic interstitial nephritis

    d0t functional decrease in renal blood flo= , >egment

    development of prominent u =aves

    >evere hypo2alemia $ increased amplitude of p =ave

    increased R> duration

    >.+otassium

    asic In*estigations

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    In*estigations ) etiologyErinary "#

    ,,":

    Erinary Chloride

    C;C+eripheral >mear

    4;:

    )chocardiogram

    Cardiac )nzymes

    >erum aldosterone

    >erum renin

    E>: 4bdomen

    C, 0 MR% 4bdomen

    6;> 0 ++;> 0 Erine "etones

    ,>1 0 free ,- 0 free ,

    Colonoscopy 0 8:Dscopy

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    :rossly due to

    Decreased net inta2e

    >hift into cells

    %ncreased net loss

    Diagnosis ) #tiology

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    8ccurs in patients =ith extreme leu2ocytosis

    eg $ in myeloproliferative disorders

    %nvitro ?;C upta2e potassium =ithin the test tube

    3ot associated =ith any internal 0 external potassium

    balance

    !purious Hypokalemia

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    >tarvation

    Clay ingestion binds to dietary "# & %ron '

    Decreased Intake

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    4cid < ;ase >tatus $Metabolic 4l2alosis

    1ormonal $ %ncreased %nsulin

    %ncreased ;eta 4drenergic activity

    Drugs $ ;eta agonists

    ,heophylline

    ;arium %ntoxicationChloroBuine

    Calcium Channel ;loc2ers

    ranscellular shifts

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    Catecholamine release associated =ith $

    4sthma

    C8+D < exacerbations

    1eart failure

    Myocardial infarction 0 angina

    Drug =ithdra=al syndrome < alcohol 0 narcotics 0 barbiturates

    ranscellular shift

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    %nsulin administration < for treatment of D"4

    Refeeding >yndrome

    1ypo2alemic +eriodic +aralysis

    ,hyrotoxic +eriodic +aralysis

    ,reatment of anemia $ Vit ;( 0 6olic acid deficiency

    Ese of :M < C>6 in patients =ith 3eutropenia

    ranscellular shift

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    Decreased total body "#Decreased inta2eRenal loss of "#)xtra renal loss of "#

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    Erinary "#$ @ m)B05< Renal loss

    Erinary " # $ * m)B05< )xtrarenal loss

    ,,": $ ,ranstubular +otassium :radient

    Erine "# 0 +lasma "# '

    Erine 8sm 0 +lasma 8sm '

    ,,": $ Renal loss $ @

    )xtra renal loss $ *

    %enal ,s #$tra renal loss

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    #$tra %enal -ossErinary "# * Metabolic 4cidosisMetabolic 4l2alosis

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    Erinary loss "# @ Metabolic 4cidosisErinary chloride levelErinary chloride levelMetabolic 4l2alosisErinary chloride level

    %enal -oss

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    4mphotericin ; $ tubular damage

    increased excretion of "#

    4minoglycosides $ renal =asting of "#

    ,hiazides7 6urosemide7 4cetazolamide $ renal loss "#

    Cisplatin

    1F+8M4:3)>)M%4 $ >ignificant renal "# =asting

    %enal loss ' Drugs

    %enal -oss + .etabolic

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    Erinary Chloride

    %enal -oss + .etabolicAlkalosis

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    1igh $ ;artter71igh $ ;artter71,3 7 %ncreased )C61igh $ ;artter71igh $ ;artter7

    %enal loss +/rine "l 0 12 m#34-

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    RENIN HIGHALD HIGH

    RENIN LOWALD HIGH

    LOW RENINLOW ALD

    R4> +rimary 1yperaldosteronism 38RM45 C8R,%>85 $

    Malignant 1,3 :lucorticoid remediable 1,3 )xogenous mineralocorticoid

    Renin >ecreting ,umor 5iddles syndrome

    58? C8R,%>85 $

    4drenogenital syndrome

    1%:1 C8R,%>85 $

    6amilial :lucocorticoidResistance

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    HA&K 5O/