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PLENARY DISCUSSION
ASIHS PATIENT
GROUP 2
ANATHARAO A/L SUBRAMANIAM
DIAN PRATIWI BURNAMA FAJAR SATRIA PRATAMA
KHALIDAH
KEVIN MAULANDA
MEIVITA WULANDARI
SONYA VIESKA TIARA RAHMA ZAIN
VEGGY PRATAMA ANANDA PUTRA
WIDYATUL AINA
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Scenario 3 ;Asihs Patient
Asih is a medical school student who are undergoing their
clinical pediatrics section. One day, he gets a patient, a boy
aged 5 years who were admitted to hospital because of a
loss of consciousness. Typical symptoms in children are
kussmaul respiratory and growth retardation. Blood gas
analysis showed a significant decrease in the levels of
bicarbonate and anion gap within normal limits. laboratory
results of urine showed the pH of the urines is alkaline.
Doctors suspect the child is suffering kidney disease. basedon this, Asih try to analyze what happened to the child.
How do you explain what happened to the child?
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Learning objective1. Regulation of acid-base balance
2. Factors affecting the acid-base balance as well as water
and electrolyte
3. Buffer mechanism in maintaining acid-base balance
4. Regulation of fluid-electrolyte
5. Acid-base balance disorders as well as water andelectrolytes
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1. BODY REGULATION OF ACID-BASE BALANCE
Refers to precise regulation of free H+ concentration in bodyfluids
Acids
Group of H+ containing substances that dissociate in
solution to release free H
+
and anions(H2CO3)Bases
Substance that can combine with free H+ and remove it fromsolution(HCO3)
pH
Designation used to express the concentration of H+ pH 7 neutral
pH less than 7 acidic
pH greater than 7 basic
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BUFFER SYSTEM
The fastest performer, works in seconds
Bicarbonate ions combine with excess hydrogenions to form carbonic acid in a dynamic
relationship HCO3 + H+ H2CO3
For every molecule of carbonic acid, there are 20molecules of bicarbonate
Any change in the this 20:1 ratio is immediatelycorrected to maintain pH
An increase H+ causes an increase in H2CO3
A decrease in H+ causes a decrease in H2CO3
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BUFFER SYSTEM
Carbonic acid is a weak, volatile acid which must be eliminated The enzyme carbonic anhydrase causes the carbonic acid to
convert to carbon dioxide and water
The CO2 and the H2O are easily eliminated by the lungs andkidneys
Buffers system in the bodyBicarbonate: most important ECF buffer
Phosphate: important ICF and renal tubular buffer
HPO4-- + H+ H2PO4
-
Ammonia: important renal tubular bufferNH3 + H
+ NH4+
Proteins: important ICF and ECF buffers
Largest buffer store in the body
Albumins and globulins, such as Hb
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The respiratory system can activate changes in pHwithin 1 to 3 minutes and can eliminate or conserve Co2. As
discussed, when a strong acid is present in the body, thebicarbonate, carbonic acid buffer pair is activated to buffer theacid. This results in a net increase of carbonic acid, whichdissociates into Co2 and H2O. Carbon dioxide is theneliminated by the lungs. An increase in H+ concentration inthe blood stimulates the breathing center in the medulla to
increase the respiratory rate, which facilitates CO2elimination. If, on the other hand, pH is elevated secondary toan increase in HCO3-, the respiratory center is inhibited, andthe respiratory rate decreases.
This results in CO2 retention, which then becomesavailable to form carbonic acid, which buffers the excess
bicarbonate. The respiratory system is thus able tocompensate for changes in pH related to metabolic disordersby regulating Pc02, which alters the bicarbonatecarbonic acidratio. The respiratory system cannot, however, produce anyloss or gain of hydrogen ions. Respiratory compensation isactivated within minutes and is usually fully functional within I
to 2 days.
Respiratory System
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9
RENAL SYSTEM
Can take hours to days to workKidneys can retain bicarbonate ion, causing
a decrease in H+ and an increase in pH
Kidneys can excrete bicarbonate ion,
causing an increase in H+ and a decreasein pH
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Renal compensation is a slower process, requiring Ito 2 days for complete activation. The kidneys react tochanges in pH by regulating the excretion orconservation of HC03-
A low pH stimulates excretion of H+ into the urine.
As H+ enters the urine, it displaces another positive ion,usually Na+. At the same time, HC03- is reabsorbed inexchange for the H+. The Na+ is then reabsorbed intothe tubule cell, where it combines with HC03- to formNaHC03 which is then available to buffer other H+ in theblood. The rale of H+ excretion, and therefore the rate ofHC03- reabsorption, is proportionate to arterial Pc02.This reaction is reversed for increases in pH.
Renal System
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The transport of H+ in the renal tubules is facilitated by thebuffer's phosphate and ammonia, which is classified as a base.
Most ammonia is converted to urea by the liver and is eliminatedfrom the body in urine. The remaining ammonia combines with H+to form the ammonium ion (NH4+) in the renal tubules. NH4+ alsodisplaces Na+ and is eliminated in the urine. The Na+ is thenreabsorbed into the tubule cells, where it combines with HC03- toform NaHC03, which is absorbed into the blood to buffer excessH+.
The amount of H+ excreted in the urine can be measuredby determining the amount of alkali required to neutralize theurine and is called titratable acidity. As a result of H+ and NH4+excretion, urine usually has an acidic pH of 6. In the clinicalsetting, checking urine pH can be a useful indicator of the
degree of renal compensation when assessing acid-basestatus. For example, a low or acidic blood pH will beaccompanied a few days later by a low or acidic urine pH whenrenal compensatory mechanisms are active. The reverse is truein alkalotic states.
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2. FACTORS THAT AFFECT THEEQUILIBRIUM LIQUID ELECTROLYTE
AND ACID BASE
1.age
fluid composition in adult women in about 50% of the body weight
fluid composition in adult men 60% of body weight
on children's body fluid composition 75% of body weight
in the elderly komposis 40-50% of body fluid loss dsri Berst2. Climate
the colder the climate, the less caitan that ekskresikan by the body,and vice versa.
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3.diet
diet affect fluid and electrolyte intake, when nutrient intake is not strong,
the body will burn fat prtotein and, thus serum albumin and protein
reserves will decline.
4.stress
stress will lead to increased cell metabolism, thereby increasing the
levels of sodium and water retention in the body
5. ill
sunburnthis will lead to a lot of liquid which is excreted in the body surface.
cardiovascular-renal disease
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FACTORS THAT AFFECT ACID-BASE BALANCE
1. Hydrogen ion concentration in the body
2.konsentrasi bicarbonate ions in the body3.Partial pressure carbon dioxide in the body
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1. Bicarbonate Buffer SystemConsist of a weak acid H2CO3 and bicarbonate salt NaHCO3.
When a strong acid such as HCl is added to a solution of
bicarbonate buffer, an increase in H ions released by the HCl will
be supported by HCO3.
H + HCO3 H2CO3 CO2 + H2O
When strong bases such as NaOH is added to a solution of
bicarbonate buffer, ion OH from NaOH joined H2CO3 to form
HCO3 extra.
NaOH + H2CO3 NaHCO3 + H2O
3. Buffer System on Acid-Base Balance
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Henderson-Hasselbalch equation
Increasing the concentration of bicarbonate ions causes the pH to
rise, shifting the acid-base balance toward alkalosis.Increasing the concentration of H2CO3 cause decreased pH, acid-
base balance shifts toward acidosis.
pH= pKa + log [HCO3] / [H2CO3]
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2. Phosphate buffer system
Plays an important role in supporting the renal tubular fluid andintracellular fluid. The main elements of phosphate buffer system is
H2PO4 and HPO4.
When a strong acid such as HCl is added to the phosphate buffersolution, hydrogen accepted by HPO4 converted to H2PO4.
When strong bases such as NaOH is added to the phosphate
buffer system, OH supported by H2PO4 to form a number of
additions HPO4 + H2O
HCl + Na2HPO4 NaH2PO4 + NaCl
NaOH + NaH2PO4 Na2HPO4 + H2O
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3. Protein
Is an important intracellular buffer.
Diffusion elements of bicarbonate buffer system causing pH in
intracellular fluid change when there is a change of extracellularfluid pH.
60-70% of total chemical buffering fluid inside the cells and
mostly produced by the intracellular protein.
The slow movement of hydrogen ions and bicarbonate ions
through the cell membrane often slow intracellular protein
maximum capacity up to several hours to buffer acid-base
disturbances.
4. The Ammonia Buffer System
This ammonia buffer system occurs in 3 steps:1) synthesis ofNH4
+ from glutamine, an amino acid in the proximal tubule,
thick ascending loop of Henle & distal tubules
2) recycling & reabsorption ofNH3 in the kidneys medulla, &
3) buffering of H+ ions by NH3 in the collecting tubules
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4. Fluid Electrolyte Balance
Distribution of Body FluidsIntracellular = inside the cell; 42% of body weight
Extracellular = outside the cell, 17% of body weight Interstitial = contains lymph; fluid between cells and outside blood
vessels
Intravascular = blood plasma found inside blood vessels
Transcellular = fluid that is separated by cellular barrier,
Body fluids contain ElectrolytesAnions negative charge
Cl, HCO3, SO4
Cations positive charge
Na, K, Ca Electrolytes are measured in mEq
Minerals are ingested as compounds and are constituents ofall body tissues and fluids
Minerals act as catalysts
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Electrolytes in Body Fluids
Normal Values Sodium (Na+) 35 145 mEq/L
Potassium (K+) 3.5 5.0 mEq/L
Ionized Calcium (Ca++) 4.5 5.5 mg/dL
Calcium (Ca++) 8.5 10.5 mg/dL
Bicarbonate (HCO3) 24 30 mEq/L
Chloride (Cl--) 95 105 mEq/L
Magnesium (Mg++) 1.5 2.5 mEq/L
Phosphate (PO4---
) 2.8 4.5 mg/dL
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Regulation of Body Fluids
Homeostasis is maintained through Fluid intake Hormonal regulation
Fluid output regulation
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Fluid Intake Thirst control center located in the hypothalamus
Osmoreceptors monitor the serum osmotic pressureWhen osmolarity increases (blood becomes more
concentrated), the hypothalamus is stimulated resulting inthirst sensation Salt increases serum osmolarity
Hypovolemia occurs when excess fluid is lostAverage adult intake 2200 2700 mL per day Oral intake accounts for 1100 1400 mL per day
Solid foods about 800 1000 mL per day
Oxidative metabolism 300 mL per day
Those unable to respond to the thirst mechanism areat risk for dehydration Infants, patients with neuro or psych problems, and older
adults
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Hormonal Regulation
ADH (Antidiuretic hormone)Stored in the posterior pituitary and released in response to
serum osmolarity
Pain, stress, circulating blood volume effect the release ofADH Increase in ADH = Decrease in urine output = Body saves water
Makes renal tubules and ducts more permeable to water
Renin-angiotensin-aldosterone mechanismChanges in renal perfusion initiates this mechanismRenin responds to decrease in renal perfusion secondary to
decrease in extracellular volumeRenin acts to produce angiotensin I which converts to
angiotensin II which causes vasoconstriction, increasingrenal perfusionAngiotensin II stimulates the release of aldosterone when
sodium concentration is low
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Hormonal Regulation
AldosteroneReleased in response to increased plasma potassium levels
or as part of the renin-angiotensin-aldosterone mechanism tocounteract hypovolemia
Acts on the distal portion of the renal tubules to increase the
reabsorption of sodium and the secretion and excretion ofpotassium and hydrogen
Water is retained because sodium is retained
Volume regulator resulting in restoration of blood volume
Atrial Natriuretic Peptide (ANP) ANP is a hormone secreted from atrial cells of the heart in response to atrial
stretching and an increase in circulating blood volume
ANP acts like a diuretic that causes sodium loss and inhibits the thirstmechanism
Monitored in CHF
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Fluid Output Regulation
Organs of water loss Kidneys Lungs
Skin
GI tract
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Fluid Output RegulationKidneys are major regulatory organ of fluid balance Receive about 180 liters of plasma to filter daily
1200 1500 mL of urine produced daily
Urine volume changes related to variation in the amount and typeof fluid ingested
Skin Insensible Water Loss
Continuous and occurs through the skin and lungs
Can significantly increase with fever or burns
Sensible Water Loss occurs through excess perspiration
Can be sensible or insensible via diffusion or perspiration
500 600 mL of insensible and sensible fluid lost through skineach day
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Fluid Output RegulationLungs
Expire approx 500 mL of water daily
Insensible water loss increases in response to changes in
resp rate and depth and oxygen administration
GI Tract
3 6 liters of isotonic fluid moves into the GI tract and thenreturns to the ECF
200 mL of fluid is lost in the feces each day Diarrhea can increase this loss significantly
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Regulation of Electrolytes Major Cations in body fluids
Sodium (Na+)
Potassium (K+)
Calcium (Ca++)
Magnesium (Mg++)
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Sodium RegulationMost abundant cation in the extracellular fluid
Major contributor to maintaining water balance Nerve transmission Regulation of acid-base balance
Contributes to cellular chemical reactions
Sodium is taken in via food and balance is
maintained through aldosterone
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Potassium Regulation
Major electrolyte and principle cation in the
extracellular fluid
Regulates metabolic activities
Required for glycogen deposits in the liver andskeletal muscle
Required for transmission of nerve impulses, normal
cardiac conduction and normal smooth and skeletal
muscle contractionRegulated by dietary intake and renal excretion
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Calcium Regulation Stored in the bone, plasma and body cells
99% of calcium is in the bones and teeth
1% is in ECF
50% of calcium in the ECF is bound to protein (albumin) 40% is free ionized calcium
Is necessary for Bone and teeth formation
Blood clotting
Hormone secretion
Cell membrane integrity
Cardiac conduction
Transmission of nerve impulses
Muscle contraction
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Magnesium RegulationEssential for enzyme activities
Neurochemical activities
Cardiac and skeletal muscle excitability
RegulationDietary
Renal mechanisms
Parathyroid hormone action
50 60% of magnesium contained in bones 1% in ECF
Minimal amount in cell
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5. Acid-base balance disorders as well as water
and electrolytes
Acid-Base Imbalance
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PaCO2 & pHA primary disorder where the first change is an elevation ofPaCO2,resulting in decreased pH.
Compensation (bringing pH back up toward normal) is a secondary
retention ofHCO3 by the kidneys; this elevation of HCO3- is notmetabolic alkalosis since it is not a primary process.
Primary Event Compensatory Event
HCO3- HCO3- pH ~ --------- pH ~ ---------
PaCO2 PaCO2
RESPIRATORY ACIDOSIS
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A primary acid-base disorder where the first change isa lowering ofHCO3-, resulting in decreased pH.
Compensation (bringing pH back up toward normal) isa secondary hyperventilation; this lowering ofPaCO2,
Renal excretion of hydrogen ions & K+ exchangesPrimary Event Compensatory Event
HCO3- HCO3-
pH ~ ------------ pH ~ ------------PaCO2 PaCO2
Metabolic acidosis
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Metabolic Alkalosis
A primary acid-base disorder where the first change is anelevation ofHCO3-, resulting in increased pH.
Compensation is a secondary hypoventilation (increasedPaCO2), Compensation for metabolic alkalosis is less predictablethan for the other three acid-base disorders.
Primary Event Compensatory Event
HCO3- HCO3- pH ~ ------------ pH ~ ---------
PaCO2 PaCO2
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Respiratory Alkalosis
A primary disorder where the first change is a lowering ofPaCO2, resulting in an elevated pH.
Compensation is a secondary lowering(excreting)HCO3 by
the kidneys.
Primary Event Compensatory Event
HCO3- HCO3- pH ~ ------- pH ~ --------
PaCO2 PaCO2
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Water Electrolyte Disorders
Hipovolemia is a diminution of the circulating volume of Blooddue to multiple factors like Hemorrhage, dehydration, burns,
among others.
Dehydrationis the loss of water and salts essential for normal bodyfunction. Dehydration occurs when the body loses more fluid than
it takes in.
Hyponatremiais a medical term which refers to a dangerously lowlevel of sodium in the body.
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Edemais swelling that is caused by fluid trapped inyour bodys tissues. Edema happens most often in the
feet, ankles, and legs, but can affect other parts of the
body, such as the face, hands, and abdomen. It can
also involve the entire body.
Hyperkalemia is defined as a condition in which the
serum potassium level is greater than 5.3 mEq/L. Any
of 3 pathogenetic mechanisms can cause
hyperkalemia: excessive intake, decreased excretion,
d hif f i ll l ll l
Water Electrolyte Disorders