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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