gangguan elektrolit english 2011

8/11/2019 Gangguan Elektrolit English 2011

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KIDNEY

HOMEOSTATIS

volume,

Electrolyte concentration, acid-base balance of body fluids;

detoxify and eliminate wastes;

regulate blood pressureregulating fluidvolume.


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skin and lungs

The also play a role in fluid and electrolyte

balance. Sweating results in loss of sodiumand water

every breath contains water vapor.


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Mineral functions

Source of life

Basic component

enzyme and hormone functions

cells, tissues, bones, blood and body fluidscomponent

Help every life aspects: hormone and energyproduction, dygestion, nerve transmition and musclecontraction

Adjust pH, metabolism, cholesterol and bloodglucose.

Vitamins and enzyme activators


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FLUIDS COMPARTMENS

INTRA CELLULER

EXTRA CELLULERPLASMA

INTERSTITIAL

IN PATHOLOGIC

CONDITIONS:

THIRD ROUNDorgans:

INTRAPERITONEAL

THORAX

OTHERS


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FLUID EXCHANGE

BETWEEN BLOOD PLASMA AND INTERSTITIAL FLUID

OBJECTIVE: FLUID, ELEKTROLYTES AND PROTEIN

CONCENTRATION BALANCE

TWO PAIRS FORCES INFLUENCE:

THE FORCE THAT MOVE LUID FROM BLOOD VESSELS TO THEINTERSTITIAL

PLASMA HYDROSTATIC PRESSURE

TISSUE OSMOTIC PRESSURE

THE FORCE THAT MOVE FLUID INTO BLOOD VESSELS

PLASMA PROTEIN ONCOTIC PRESSURE

INTERSTITIAL FLUID HIDROSTATIC PRESSURE


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pH of body fluid

pH = 7.0pH = 7.35

pH = 7.35pH = 7.45


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Sistem Buffer

sistem carbonic acidbicarbonate (the most

important, work in lung)

haemoglobineoxyhaemoglobine system(work in red blood cells) haemoglobine

bind to free H+, the blood flow through lung

and the H+ combined with CO2.

Protein Buffer (in ECF and ICF)

Phosphat system (especially in ICF)


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BUFFERING

1. Bicarbonate:

HCl + NaHCO3H2O + NaCl

NaOH + H2CO3NaHCO3 + H2O

2. Hb

ProteinProteinate- + H+

N+ + ProteinateNa-Proteinate

(extracell)

K+ + ProteinateK-Proteinate

(intracell)


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BUFFERING

3. phosphate

Na2HPO4 +HClNaCl + NaH2PO4


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Keseimbangan Asam-Basa

7.8 Dangerous to life


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pH influence on enzyme actions


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ANION GAP CONSEPT

Total kations (Na+, K+, Ca++, Mg++ etc.) ar

always comparable with total anion (Cl-,

HCO3-, PO4-, SO4=, proteinate= etc.)

Routine measured: Na+, K+, Cl- and HCO3-)

Anion concentration always < kation

This difference called anion gape


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ANION GAP

Anion gap = [Na+ + K+]-[Cl- + HCO3-]

Ex: for normal electrolytes levels

Anion gap = [140+4][100 + 28] = 16 mEq/L

K+ is seldom measured in clinical practice

anion gap = [Na+][Cl- + HCO3-] = 12 4mEq/L

What happent to anion gape in too acid or too

basic conditions?


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pH = pK + log HCO3-

pCO2

PH = pK + log HCO3-

pCO2

Anion gap >>


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Pathophysiologic Consept of Acid-

Base

Acidemia:

Acidosis (MA dan RA)

alkalemia,

Alkalosis (MA dan RA)

Compensation


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Acidemia

PH arteri , H+ Ion into ICF. To get

extracellular elektricity of neutral intracel

pHthe number of equivalent K+ leave the

cellrelatif hyperkalemia.


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Acidosis

> konsentrasi ion H+ sistemik. Bila paru gagal mengeliminasi CO2 atau bila

produk asam-asam volatile (asam karbonat)

atau nonvolatile (asam laktat) hasil

metabolisme terakumulasi, konsentrasi ion H+

naik.

Acidosis dapat juga terjadi pada diare berat

hilang anion basa bikarbonat atau

ginjal gagal mensekresikan H+ atau

mereabsorbsi bikarbonat


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Alkalosis

H+ level < in the body

Causes:

Lost of CO 2 during hyperventilation,

Lost of nonvolatile acids during vomit, or

more basic intakehidrogen ion consentration >


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Alkalemia

Arterial blood pH > 7.45,relatively more

base in blood.

More H+ in ICF insist the to flow into ECF. For

ICF electrical homeostatis (neutralisation) K+

moves from ECF into ICF,relative

hypokalemia.


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COMPENSATION

LUNG AND KIDNEY, AND CHEMICAL BUFFER

OF INTRACELLULAR AND INTRACELLULAR

COMPARTMENTS WORK TOGETHER TOMAINTAIN PLASMA PH AT THE RANGE OF

7.35 to 7.45


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ACID/BASE BALANCE


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ACID/BASE DISTURBANCES AND

COMPENSATION


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Metabolic acidosis/ alkalosis


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Respiratory alkalosis


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Ketoasidosis


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Patofisiologi

Pengaturan konsentrasi elektrolit intraseluler

dan extraseluler tergantung pada:

Keseimbangan intake elektrolit dan output nya di

urin, feses, dan keringat

transport cairan dan elektrolit antara cairan

ekstraseluler dan intraseluler


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1. Pengertian imbalance ECF

Gangguan Volume :

air berlebih (Overhydration)ECF

air kurang (Dehydration)

Hipervolemia : kelebihan air dan elektrolit

Hipovolemia : kekurangan air dan elektrolit


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2. PENYEBAB OVERHYDRATION?

Kelebihan Na

Kelebihan infus, terutama yang hipertonis

Gangguan pengaturan homeostatik air dan Na: Chronic renal failure

Congestive heart failure

Kelebihan terapi corticosteroid

Sindroma kekurngan ADH (SIADH)


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3. PENYEBAB DEHYDRATION?

Kekurangan intake air dan elektrolit: Gangguan mekanisme haus

Tak mampu menelan cairan

Kehilangan cairan melalui sekresi atau ekskresi: Terapi diuretik kuat

Diabetes insipidus

Kehilangan cairan dari saluran GI Keringat berlebihan


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Tanda dan Gejala?

1. OVERHIDRASI:

Peningkatan berat badan tiba-tiba

Edema perifer

Nafas pendek dan paru-paru berbunyi

Perubahan perilaku : bingung, lemah

Pembuluh vena melebar

Pulsa meningkat (>)

BP meningkat

Pengosongan vena lambat


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TANDA DEHIDRASI

Berat badan turun tiba-tiba Turgor kulit menurun

Kekeringan membran mukosa

Kulit kasar

lidah kering

Perubahan perilaku: agitasi(terangsang), capek,lemah

Vena leher datar pada posisi tidur

Pulsa lemah

Hipotensi Orthostatic

Pengisian vena perifer lambat


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Ketidak seimbangan Elektrolit

Setiap mineral berpengaruh pada mineral lain

dalam tubuh Bila satu mineral tidak seimbang

mempengaruhi keseimbangan mineral-mineral

lain melalui serangkaian reaksi berantai


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Misalnya: Bila anda makan 1 tablet Fe

1. Na . Karena perangksangan kelenjar adrenal

2. Magnesium . Karena Na menurunkan Mg

3. Calcium . Karena bila Mg, Ca juga untukmempertahankan rasio calcium/ magnesium

4. K . Calcium dan potassium pindah ke arahberlawananBila calcium , potassium .


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Ex. If you take Iron tablet

5. Nitrogen . Karena oksiidasi cepat,kannibalisasiproteins. (proteolisis)

6. Cu . Karena peningkatan laju pernafasanCudiperlukan dan digunakan. Bila ratio zinc thd Cu >

Cu availability akan sangat


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A. SODIUM (Na+)

1. normal:

Serum Na 135-145 MEq/L

Serum Na+ Menentukan osmolalitas darah

2. Ketidakseimbangan

Hypernatremia B Serum Na+ > 145 mEq/L

Serum osmolality > 295 mOsm/kg

Hyponatremia Serum Na


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Functions

Maintenance of Membrane Potential Nutrient Absorption and Transport

Maintenance of Blood Volume and Blood

Pressure


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Pengaturan oleh Ginjal

Perubahan GFR atau hemodinamik ginjal

Aldosteron

Atrial natriuretic peptide (ANP)


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PENYEBAB HYPERNATREMIA?

Kehilangan air:

Diabetes insipidus

Gangguan pemekatan Ginjal

diarrhea

Menurun intake air meningkat intakeNa+ : Ketidakmampuan merespon mechanism haus

Susah menelan cairan

Makanan hipertonis kurang minum

Kelebihan penggunaan larutan NaCl atau NaHCO3hipertonis

Hiperfungsi AdrenalHyperaldosteronism


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PENYEBAB HIPONATREMIA

Peningkatan ambilan air

Enema air

Perangantsangan anti diuretic hormone (ADH)

Psychogenic polydipsia Kehilangan Na+:

Penggunaan diuretil loop gol thiazide

Kehilangan Na karena penyakit ginjal

Penggantian air tapi bukan elektrolit pad kasus terbakar,muntah atau diare

Adrenal insufficiency


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signs and symptoms Hypernatremia

Perubahan perilaku :

cemas stupor, coma

Haus berlebihan

Lemah otot Membran mukosa kering dan lengket


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sign and symptoms Hyponatremia

Perubahan perilaku:

Cemas

Convulsions dan coma

Lemah otot

Mual dan cramp perut

Hypotension Postural


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B. Potassium (K+)

1. normal:

Serum K+ 3.5 - 5.0 mEq/l

K+ is primarily intracellular (98%)

2. imbalance:

HyperkalemiaSerum K+ > 5.0 mEq/L HypokalemiaSerum K+ < 3.5 mEq/L


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Functions

Maintenance of Membrane Potential

Cofactor for Enzymes (K/Na ATPase, pyruvate

kinase)


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Causes hyperkalemia

Increased K+ intake:

Rapid IV administration of K+

Administration of aged blood

Increased oral intake causes hyperkalemia only if

accompanied by decreased K+ excretion Excessive use of salt substitutes (K+ClB)

Decreased renal excretion of K+:

Acute and chronic renal failure

Kerusakan sel (terbakar dll)K+ keluar dari sel Asidosis (H+ banyak dalam selK+ keluar)


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Causes hyperkalemia

Decreased production of Aldosterone

Adrenal insufficiency (Addison=s disease)

Excessive use of K+ conserving diuretics: Spironolactone(Aldactone) and Amiloride (Moduretic)

Movement of K+ into ECF: Tissue injury (burns, major surgery, or crush injury)

Acidosis B decreased pH with excess H+ in ECF (compensationcauses K+ to shift from cells to ECF)

Insulin deficiency


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Causes hypokalemia

Decreased K+ intake:

Anorexia nervosa

Gastrointestinal K+ loss:

Vomiting, gastric suction

Diarrhea, laxative abuse, recent ileostomy

Large sweat loss without K+ replacement Increased renal excretion of K+:


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Hypokalemia (cont)

Use of K+ losing diuretics without K+

replacement Ex.: Furosemide (Lasix),

Bumetanide (Bumex), and HCTZ

Hyperaldosteronism

Entry of K+ into cells:

Alkalosis : increased pH with decreased H+ in ECF

(compensation causes K+ to shift from ECF tocells)


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signs and symptoms hyperkalemia

Mental confusion

GI hyperactivity (abdominal cramping anddiarrhea)

Cardiotoxicity EKG changes (K+ > 6 mEq/L:

Cardiac arrhythmiasbradycardia and heart

block Cardiac arrest


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Sign and symptoms hypokalemia

Muscle weakness/paralysis, flaccid muscles(lack tone)

Decreased bowel motility (intestinal ileus,

nausea and vomiting) Polyuria

EKG changes (serum K+ < 3 mEq/L):

Cardiac arrhythmias Respiratory failureK+


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C. Calcium (Ca++)

1. normal?

Serum Ca++ 8.5-11 mg/dL

Serum Ca++ and serum phosphate vary inversely

2. imbalance?

HypercalcemiaSerum Ca++ > 11 mg/dL

HypocalcemiaSerum Ca++ < 8.5 mg/dL


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Physiological functions:

blood to clot,

bones hold up.

nerves fire,

for your brain to function, for your muscles to contract.

heart beating

Calcium maintains the organization of tissues Cofactor for Enzymes and Proteins

secretion of hormones (insuline)


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causes hypercalcemia?

Ca++ release from bone:

Hyperparathyroidism

Metastatic carcinoma

Multiple myeloma

Thyrotoxicosis

Prolonged immobilization

Increase GI absorption of Ca++ Excessive ingestion of Vitamin D


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Causes hypocalcemia:

Decreased intake or decreased GI absorption of Ca++: Vitamin D deficiency

Chronic insufficient dietary intake of Ca++

Acute pancreatitis

Overuse of antacids

Malabsorption Syndromes

Decrease in physiologically available Ca++:

Hypoparathyroidism

Overuse of phosphate-containing laxatives and enemas (Ex.:

Fleet Phospho-soda) Increased urinary excretion of Ca++:

Chronic renal failure

signs and symptoms?


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signs and symptoms?

hypercalcemmia

Nausea and vomiting

Constipation

Muscle weakness/flaccidity

Depressed deep tendon reflexes Confusion, lethargy, CNS depression (coma)

Polyuria

Pathological fractures (chronic)

Renal calculi EKG changes: Shortened QT interval, Cardiac arrest

brittle arteries


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Sign and symptoms hypocalcemia

Muscle cramps Confusion, anxiety

Tetany

Neuromuscular irritability:

Positive Chvostek= s signmuscle spasm at cheek and

corner of mouth in response to tap over facial nerve in frontof ear.

Positive Trousseau= s signcarpal spasms after occlusion ofblood flow to hand with BP cuff for three minutes.

Hyperactive deep tendon reflexes

Convulsions

EKG changes: Prolonged QT interval

Cardiac arrest


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D. Magnesium (Mg++)

1. normal?

Serum Mg++ 1.5-2.5 mEq/L

Mg++ is absorbed primarily through the small intestine

2. imbalance:

Hypermagnesemia B Serum Mg++ >2.5 mEq/L

Hypomagnesemia B Serum Mg++ < 1.5 mEq/L


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Functions:

structure and the function of the human body

Cell Signaling (involved in more than 300essential metabolic reactions )

Energy Production Synthesis of Essential Molecules

Ion Transport Across Cell Membranes

Cell Migration


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causes hypermagnesemia

Excessive intake or absorption of Mg++:

Overuse of antacids containing Mg++ (Maalox,Gelusil, Riopan)

Overuse of laxatives containing Mg++ (Milk ofMagnesia)

Impaired Mg++ excretion:Advanced renal

failure Adrenal insufficiency (Addison=s disease)


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causes hypomagnesemia

Decreased Mg++ intake or absorption:Chronicdiarrhea

Chronic malnutrition

Malabsorption syndrome B Steatorrhea

Small bowel resectionChronic alcoholism Prolonged IV administration without Mg++

supplementation

Gastrointestinal Mg++ loss:Prolonged diarrhea or

nasogastric suction Intestinal fistulas

Increased urinary excretion of Mg++:Prolongedexcessive diuretic therapy


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signs and symptoms hypermagnesemia

Hypoactive deep tendon reflexes

Drowsiness, lethargy

Mild hypotension

Nausea and vomiting

Respiratory depression (serum Mg++ > 15 mEq/L)

dan paralisis otot

Cardiac arrhythmias (bradycardia, heart block) Cardiac arrest (serum Mg++ > 25 mEq/L)

i & h i


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signs & symptoms hypomagnesemia

Hyperactive deep tendon reflexes

Coarse tremors

Tetany

Positive Chvosteks (FACE MUSCLE MOVING) andTrousseaus sign (MUSCLE CRAMP)

Intense confusion

Cardiac arrhythmias

Convulsions

Coma

ALL DUE TO NERVEMUSCLE ALTERATION


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TH NK YOU

gangguan elektrolit english 2011

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