5 tutor guide arf

7/28/2019 5 Tutor Guide ARF

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TUTORIAL GUIDE

BLOCK TITLE : GENITO-URINARY SYSTEMWEEK TITLE : RENAL FAILUREWEEK SCHEDULLE : THIRD WEEKWEEK THEME : ACUTE RENAL FAILURE

INTRODUCTION:

Welcome to tutoring in the genitourinary block. The case ofMr Arifrepresents the thirdweek of the genito-urinary block. It is designed for students to learn issues around renalfailure. The primary focus of this case is normal and abnormal volume production of theurine, introduction to acute renal failure with its definition, etiology, classification,complications and clinical presentation of ARF, The associated aspects of electrolytehomeostasis (especially potassium homeostasis) and acid base imbalance disorders.

CASE SYNOPSIS:

Mr Arif has acute renal failure prior to massive watery diarrhea and vomiting suspectedof food poisoning, leading to oliguria, hypovolemic syok, metabolic acidosis andhyperkalemia. The case shall only focus on the genito-urinary aspects of renalfailure rather than the infection in the intestines or food poisoning aspects of this case.

CASE OBJECTIVES:

After completing the Mr. Arif case, students should be able to:1. Define the normal volume of urine production.2. Define oliguria, polyuria and anuria and the etiology of both of them.3. Define, classify, describe stages of ARF and each clinical manifestation

4. Recognize the physical examination, laboratory findings of ARF5. Describe the pathogenesis of high concentration of urea and creatinine in ARF

(explain the mechanism of urea excretion)6. Describe normal, abnormal potassium homeostasis and factors that cause

hyperkalemia, sign and symptoms of hyperkalemia7. Describe the electro-cardiographic changes in hyperkalemia8. Explain acid base and electrolyte homeostasis (describe major processes that can

result metabolic acidosis)9. Describe the treatment of ARF: rehydration with fluid, pharmacological properties of

diuretics and dopamine, treatment of metabolic acidosis and hyperkalemia and renalreplacement therapy : hemodialysis and acute peritoneal dialysis)


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CASE :

When you are at the ER (Emergency Room) at the Hasan Sadikin Hospital working as adoctor assistant, a 25 years old man Mr Arifwas admitted to the hospital complains ofsmall producing urine. Before this, his urine was normal. This complains occurred prior

to massive diarrhoeas and vomiting .It all started three days before admitted to thehospital

He also complained of shortness of breath, weakness, and fatigue and according to hisfamily sometimes he looked delirious. It occurred one day before he was admitted to thehospital

His physical examination revealed a male who is delirious. Blood pressure of 90/60mmHg, a small pulse 120x/mnt, a deep and rapid respiration of 34x/mnt and atemperature of 37.5 C. he is not anaemic, no sign of pulmonary rales, no enlargement ofthe heart with a regular tachycardia heart rate. His belly is flat and smooth with areduced elasticity skin together with reduced elasticity skin of both legs.

Laboratory findings:Haemoglobin level: 15,6 gr./dl, Hematocrit: 50%, White blood cell: 10.000/ mm3, serumurea level of 180 mg/dl, serum creatinine level of 5,3 mg/dl, serum potassium level of 7meq/L, serum sodium level of 145 meq/L,Blood gas analysis : ph 7.245, pO2 94 cmH2O, HCO3 -: 7 meq/L.His urine analysis has no sediments or cast and no proteinuria.Stool analysis showed no erythrocytes, parasites but viewed only a few leukocytes

EKG : tall and peak T wave and widening QRS complex

After the diagnose was established as Acute Renal Failure because of volume depletion,this patient was given intravenous crystalloid fluid to restore his renal function andcorrection of hyperkalemia and metabolic acidosis

Epilog :Good rehydration treatment with crystalloid fluid, management of metabolic acidosis, andhyperkalemia save Mr Arif renal function and he doesn't have to be dialysed


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Page 1

When you are at the ER (Emergency Room) at the Hasan Sadikin Hospital working as a

doctor assistant, a 25 years old man Mr Arifwas admitted to the hospital complains ofsmall producing urine. Before this, his urine was normal. This complains occurred priorto massive diarrhoeas and vomiting .It all started three days before admitted to thehospital

1. Identify Mr. Arifs problem !The problem of Mr. Arif is : a small producing urine volume

2. What is your hypothesis list and provide your rationale1. Oliguria2. Anuria

3. What further information do you need?

Guiding questions for student :1. What is the definition of normal volume of urine production ?2. What is the definition of oliguria, polyuria and anuria and the etiology of both

of them ?

Answer :

1. Definition of normal volume of urine production:

Daily intake of water to the body has to main sources: (1) It is ingested in the form ofliquids or water in the food, which together normally add about 2100 ml/day to the bodyfluids, and (2) it is synthesized in the body as a result of oxidation of carbohydrates,adding about 200 ml/day. This provides a total water intake of about 2300 ml/day. Intakeof water is highly variable among different people and even within the same person ondifferent days, depending on climate, habits, and level of physical activity.Daily loss of body water could happen by insensible water loss (evaporation from therespiratory tract and diffusion through the skin), fluid loss in sweat, water loss in feces.The remaining water loss from the body occurs in the urine excreted by thekidneys. There is multiple mechanism that controls the rate of urine excretion. In fact themost important means by which the body maintains balance between water intake andoutput as well as a balance between intake and output of most electrolytes in the body isby controlling the rates at which the kidneys excrete this substances. For example, urinevolume can be as low as 0,5 L/day in a dehydrated person or as high as 20 L/day in aperson who has been drinking tremendous amounts of water.


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Table 1 Daily intake and output of water (in ml/day)________________________________________________________

Normal Prolonged HeavyExercise

________________________________________________________

IntakeFluid ingested 2100 ?From metabolism 200 200Total intake 2300 ?

OutputInsensible-skin 350 350Insensible-lungs 350 650Sweat 100 5000Feces 100 100Urine 1400 500Total output 2300 6600

________________________________________________________

In health, the volume of urine passed is primarily determined by diet and fluid intake. Intemperate climates it lies within the range 800-2500 mL/24 hours. The minimumamount passed to stay in fluid balance is determined by the amount of solute- mainlyurea and electrolytes, being excreted and the maximum concentrating power of thekidneys. On a normal diet, some 800 mOsm of solute are passed daily. Since themaximum urine concentration is approximately 1200 mOsm/kg, the minimum volume ofurine obligated by excretion of 800 mOsm of solute would thus be approximately 650 mL(table 2). Fluid intake is generally greater than this, so a larger volume of more diluteurine is passed. A diet rich of carbohydrates, fat and low in protein and salt results in alower solute excretion and as little as 300 mL of urine per day may be required.Conversely, a high salt, high protein intake obligates a larger urine flow and via the thirst

mechanism, a higher fluid intake. The appropriateness of given daily urine output musttherefore be related to factors such as diet, body size and fluid intake.

In disease, impairment of concentrating ability requires increased volumes ofurine to be passed, given the same daily solute output. An increased solute output, suchas in glycosuria or increased protein catabolism following surgery or associated withsepsis, also demands increased urine volumes.

The maximum urine output depends on the ability to produce a dilute urine.Intakes of 10 or even 20 L daily can be tolerated by normal humans but, given dailysolute output of 800 mOsm require the ability to dilute 80 and 40 mOsm/kg, respectively.Where diluting ability is impaired, the ability to excrete large volumes of ingested water isalso impaired.

Table 2 Relationship between Diet, Kidney Function and Urine Volume


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________________________________________________________Diet Approximate solute Minimum urine volume required to excrete

Output (mOsm/24hr) solute load (mL/24hr)

With normal urine In disease (impairedConcentration (max urine concentration

1200 mOsm/kg) (max 300 mOsm/kg)_______________________________________________________________________________Normal 800 667 2667High prot/salt 1200 1000 4000Low prot/salt 360 300 1200

_______________________________________________________________________________

2. Definition and etiology of Oliguria, Polyuria and Anuria :

Oliguria and Anuria:Define as the excretion of less than 300 mL of urine per day, may be `physiological` asin patient with hypotension and hypovolemia , where urine is maximally concentrated inan attempt to conserve water. More often, it is due to intrinsic renal disease orobstructive nephropathy.

Anuria (no urine) suggest urinary tract obstruction until it proved otherwise; bladderoutflow obstruction must always be considered first.

Polyuria:Polyuria is a persistent, large increase in urine output, usually associated with nocturia. It

must be distinguished from frequency of micturition with the passage of small volumes ofurine. Documentation of fluid intake and output may be necessary. Polyuria is the resultof an excessive (hysterical) intake of water, an increased excretion of solute (as inhyperglycemia and glycosuria), or a defective renal concentrating ability or failure ofproduction of ADH.

Bibliography

Kumar P, Clark M. Renal Disease In: Clinical Medicine, 5 th ed. W.B Saunders, 2001,pp: 593-4

The Body Fluid Compartments: Extracellular and Intracellular fluids;interstitial Fluidand edema pp: 264-5


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page 2

He also complained of shortness of breath, weakness, and fatigue and according to his

family sometimes he looked delirious. It occurred one day before he was admitted to thehospital

His physical examination revealed a male who is delirious. Blood pressure of 90/60mmHg, a small pulse 120x/mnt, a deep and rapid respiration of 34x/mnt and atemperature of 37.5 C. he is not anaemic, no sign of pulmonary rales, no enlargement ofthe heart with a regular tachycardia heart rate. His belly is flat and smooth with areduced elasticity skin together with reduced elasticity skin of both legs.

1. What are the further problems of this patient? Short of breath with rapid and deep respiration rate

Weakness, fatigue, delirious

Low blood pressure

Rapid and weak/small pulse rate

Reduced elasticity of the skin

2. Confirm your hypothesis !

Dyspnea (Kussmaul Breathing)

Hypotension

Rapid and weak/small arterial pulse

Pathogenesis of hypovolemic shock and dehydration

3. What further information do you need? Justify your rationale

Guiding questions for student :

1. Define Short of breath (Dyspnea) and types of respiration

2. Define Hypotension

3. Define rapid and small or weak arterial pulse

4. Define Shock and describe the classification of shock based on cause5. Describe the pathogenesis of hypovolemic shock


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Answer :

1. Define Short of breath (Dyspnea) and types of respiration:

Dyspnea:Dyspnea is the patient's subjective awareness of discomfort associated with ventilatoryeffort. Dyspnea refers to a non-painful but uncomfortable awareness of breathing that isinappropriate to the circumstances. Only the patient can report dyspnea. An observermay notice abnormally rapid or deep breathing, but this cannot be equated withthe subjective sensation. Dyspnea commonly results from cardiac orbronchopulmonory disease but also frequently accompanies anxiety. Many lungdiseases result in increased respiratory effort per unit volume air. The sensation of

dyspnea is particularly likely when mechanical impairment to respiratory movements orstiffening of the lung is present (decreased compliance). Decreased oxygen supply tothe body tissues is due to diffusion impairment or ventilatory-perfussion imbalance,accumulation of carbon dioxide, or acid shifts of blood pH cause minute ventilation toincrease, producing dyspnea. Striking increases in rate and depth of respiration,however, may occur without the patients complaining of dyspnea, as in metabolicacidosis.The normal respiratory rate is about 14-20 per minute in normal adults and up to 44 perminute in infants.

Abnormality in rate and rhythm of breathing:

rapid shallow breathing Rapid deep breathing (hyperpnoe, hyperventilation): rapid and deep breathing

also has a number of causes, including exercise, anxiety, and metabolicacidosis. In the comatose patient, infarction, hypoxia, or hypoglycemiaaffecting the midbrain or pons should be considered. Kussmaul Breathing isdeep breathing associated with metabolic acidosis. It may be fast, normal inrate, or slow

slow breathing

Cheyne-Stokes breathing

Ataxic breathing (Biot`s breathing)

Sighing respiration

Obstructive breathing

Bibliography:

Barbara Bates, An approach of symptoms and Abnormalities in rate and rhythm ofbreathing In: A Guide To Physical Examination and History Taking 5th ed.J.BLippincott Company. 1991 pp: 74, 256

Delp, Manning Examination of the chest In: Major`s Physical Diagnosis Anintroduction to the Clinical Process 9 th ed. W.B Saunders Company Philadelphia,1981 PP: 191.


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2. Define Hypotension:

Hypotension or low blood pressure results from either a decrease in cardiac output or adecrease in peripheral resistance. A decreased in cardiac output occurs in Addison`sdisease, myocarditis, myocardial infarction, and pericarditis with effusion; it may alsofollow hemorrhage, depletion of blood volume. A sudden decrease in peripheral

resistance (vasomotor collapse) may occur in pneumonia, septicemia, acute adrenalinsufficiency (Waterhouse-Fredrichsen syndrome), and drug intoxication. The fall inblood pressure on standing may be sufficient magnitude to produce cerebral ischemiaand syncope. This orthostatic hypotension is common in severely anemic persons and inthe elderly patients with severe atherosclerosis who are unable to respond quickly to asudden change in body position. It may be a sign of disordered autonomic regulation inthe Shy-Drager syndrome

3. Define rapid and small or weak arterial pulse:

The arterial pulse may be describe most clearly in terms of the following characteristics:

a. Rate : rapid or slowb. Size : large or smallc. Type of wave : quick or prolongedd. Rhythm : regular or irregulare. Tension : hard or soft.

The average pulse rate in normal adults is 60-90 beats per minute, in chlidren 90-140,and in aged 70-80 beats per minute.

Small and Weak arterial pulse: The pulse pressure is diminished, and pulse feels weakand small. The upstoke may feel slowed, the peak prolonged. Causes include: (1)decreased stroked volume as in heart failure, hypovolemia and severe aortic stenosis,(2) increased peripheral resistance, as in exposure to cold or severe congestive heartfailure.

Bibliography:

Barbara Bates, An approach in abnormalities of arterial pulse In: A Guide ToPhysical Examination and History Taking 5th ed.J.B Lippincott Company. 1991 pp:308-9

Delp, Cardiovascular system In: Major`s Physical Diagnosis An introduction to theClinical Process 9th ed. W.B Saunders Company Philadelphia, 1981 PP: 237-245


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4. Define Shock and describe the classification of shock based on cause:

Definition of shock:Shock may be define as the state in which profound and widespread reduction in theeffective delivery of oxygen and other nutrients to tissue leads first to reversible and

then, if prolonged, to irreversible cellular injury

Classification of shock based on cause:

Oligemic or hypovolemic shock

Cardiogenic shock

Extracardiac obstructive shock

Distributive shock

(See figure 34-1 Joseph.E P Shock, The pathogenesis of shock in human. In :Harrison`s Principles of Internal Medicine, Isselbacher, Braunwald , Wilson et al editors,13th ed. McGraw-Hill, Inc New York .1994 pp: 187-192)

5. Describe the pathogenesis of hypovolemic shock:

Hemorrhage or large loss of fluid secondary to vomiting, diarrhea, burns ordehydration leads to inadequate ventricular filling i.e., to severely decreased preload,reflected in decreased left and right ventricular end-diastolic volumes and pressures.This changes leads to shock by causing an inadequate stroke volume and inadequatecardiac output.

Loss of fluid from all fluid compartments of the body is called dehydration; thistoo can reduce blood volume and cause hypovolemic shock similar to that resulting from

hemorrhage. Some of the causes of this type of shock are (1) excessive sweating, (2)fluid loss in vomiting and diarrhea, (3) excess loss of fluid by nephrotic kidneys, (4)inadequate intake of fluid and electrolytes, and (5) destruction of the adrenal cortices,with consequent failure of the kidneys to reabsorb sodium chloride, and water, whichoccur in the absence of the adrenocortical hormone aldosterone.

Bibliography:

Joseph.E P Shock, The pathogenesis of shock in human. In: Harrison`s Principles ofInternal Medicine, Isselbacher, Braunwald, Wilson et al editors, 13 th ed. McGraw-Hill,Inc New York .1994 pp: 187-192)


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Laboratory findings:Haemoglobin level: 15,6 gr./dl, Hematocrit: 50%, White blood cell: 10.000/ mm3, serumurea level of 180 mg/dl, serum creatinine level of 5,3 mg/dl, serum potassium level of 7meq/L, serum sodium level of 145 meq/L,Blood gas analysis : ph 7.245, pO2 94 cmH2O, HCO3 -: 7 meq/L.His urine analysis has no sediments or cast and no proteinuria.Stool analysis showed no erythrocytes, parasites but viewed only a few leukocytes

EKG : tall and peak T wave and widening QRS complex

1. What is the significance of this laboratory test according to the clinical andphysical examination of this patient?

High range of hematocrit

High level of serum ureum and creatinine concentration

High level of serum potassium

Low bicarbonate level

2. What is the diagnosis of this patient?

Acute Renal Failure or prerenal azotemia because of volume depletion

Hyperkalemia

Metabolic acidosis

3. Are there other modalities or test to diagnose the patient?

Radionuclide scan : to assess abnormal renal perfusion

4. What is the management plan for this patient?


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Guiding questions for student :1. Define Acute Renal failure2. Define the phases of ARF and each clinical manifestation3. What are the causes of ARF4. Describe the normal potassium homeostasis5. Describe factors can cause hyperkalemia by shifting potassium out of cells

6. Describe electrocardiographic changes occur in patient with hyperkalemia7. Describe some signs and symptoms of hyperkalemia8. Desribe the physiological Aspects of Acid Base Balance9. Define the meaning of pH and how can I translate pH to free H+

10. How can you adapt the Henderson Hasselbach equation foe clinical practice11. Describe three major processes that can result in a metabolic acidosis12. Describe the guidelines for treatment of prerenal azotemia (ARF)

Answer :

1. Define Acute Renal failure:

Acute renal failure (ARF) means abrupt deterioration in parenchymal renal functionwhich is usually, but not invariably, reversible over a period of days and weeks. In clinicalpractice, such deterioration in renal function is sufficiently severe to result in uremia.Oliguria is usually but not invariably a feature. ARF may cause sudden, life threateningbiochemical disturbances and is a medical emergency. Renal failure results in reducedexcretion of nitrogen waste products of which urea is the commonly measured.

2. Define the phases of ARF and each clinical manifestation

Oliguria Phase:Occurs within hours or days after the circulatory failure or nephro-toxicity. The

duration will maintain for 1-2 weeks, if it is prolonged for more than 4 weeks , it shouldalways consider to diagnose acute tubular necrosis. The volume urine production isabout 150 mL/day and total anuria seldom exist

Biochemical changes during oliguria state: increased serum urea and creatinine,hyponatremia because of vomiting and nausea, thirsty (dilutional hyponatremia), severehyponaterima can cause peripheral edema, brain edema, and acute pulmonary edema.Brain edema causes uremic convulsion and cardiac arrhythmia

Hyperkalemia is more prominent in this phase and can caused cardiac arrest orventricular fibrillation.

Acidosis occurs because of fixed acid generation from 50-100 mEq/day and

causes kussmaul breathing (rapid and deep).

Diuretic Phase:During this early diuretic phase, the renal function is still impaired, the blood urea

and creatinine is increased although the urine volume production is raised 1-3 L/day.This phase maintain for 5-10 days. This phase will be follow by the late diuretic phase,with 6 L/day of urine volume production. At this stage the urine osmolarity will equals


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plasma osmolarity (280-295 mOsm/L) and it is called isostenuria. The urine spesificgravity will reach 1.010.

Convalescence Phase:

The renal function improvement will last for about 3-12 months depend to the

patient`s age. In the older patients this phase will persist for years and the ability toconcentrate and acidification of the urine is still impaired because of tubular celldysfunction.

3. What are the causes of ARF:

Prerenal Causes: Prerenal ARF is rapidly reversible if the underlying cause is corrected.In the outpatient setting, vomiting, diarrhea, poor fluid intake, fever, use of diuretics andheart failure are all common causes

Postrenal Causes: ARF occurs when boyh urinary outflow tracts are obtructed or whenone tract is obstructed in a patient with a single functional kidney. Obstruction iscommonly due to prostatic hypertrophy, cancer of the prostat or cervix or retroperitonealdisorders. It could also be intraluminal, such as bilateral renal calculi, papillary necrosis,coagulated blood, bladder carcinoma.

Intrinsic Causes: Intrinsic renal diseases that result in ARF are categorized according tothe primary site of injury: tubules, interstitium, vessels or glomerulus. Injury to the tubulesis most often ischemic or toxin in origin (drugs)


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DIAGNOSTIC EVALUATION OF THE PATIENT WITH ARF


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4. Describe the normal potassium homeostasis:

Total body potassium stores range between 3000 mmol and 4000 mmol. Approximately98% of total body potassium are intracellular. Primarily the gastrointestinal tract and thekidneys regulate potassium absorption and excretion respectively. Extracellularpotassium concentration also depends critically on shifts of the cation between the intra-

and extracellualr pool. As a corollary, hypokalemia or hyperkalemia do not necessarilyreflect total body potassium stores.

5. Describe factors can cause hyperkalemia by shifting potassium out of cells:

Insulin deficiency (hyperglycemia)

Beta Blockade

Metabolic acidosis

Hypertonicity

Muscle depolarizing agents such as succinylcholine

Exercise

6. Describe electrocardiographic changes occur in patient with hyperkalemia:

Initially peaked narrow T waves

Subsequently prolonged p wave, PR prolongation, QRS widening, and ST segmentelevation or depression

Eventually cardiac standstill

Electrocardiogram in severe hyperkalemia. Note the widening of the QRS complex andthe high peaked T waves compared to the normal tracing. The plasma potassium in thispatient was 7.6 mmol/L

7. Describe some signs and symptoms of hyperkalemia:


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Paresthesias

Muscle weakness

Cardiac arrest

8. Physiological Aspects of Acid Base BalanceSource: Guyton and Hall, Textbook of Medical Physiology, 10 th Ed., 2000, pp 346-363

Precise hydrogen ion regulation is essential because the activities of almost all enzymesystems in the body are influenced by hydrogen ion concentration. Therefore, changesin hydrogen concentration alter virtually all cell and body functions.

Regulation of hydrogen ion balance is similar in some ways to the regulation of otherions in the body. However, precise control of extracellular fluid hydrogen ionconcentration involves much more than simple elimination of hydrogen ions by thekidneys. There are three primary systems that regulate the hydrogen ion concentration

in the body fluids to prevent acidosis or alkalosis, i.e. 1) the chemical acid-base buffersystems of the body fluids, which immediately combine with acid or base to preventexcessive changes in hydrogen ion concentration; 2) the respiratory center, whichregulates the removal of CO2 (and, therefore H2CO3) from the extracellular fluid; and 3)the kidneys, which can excrete either acid or alkaline urine, thereby readjusting theextracellular fluid hydrogen ion concentration toward normal during acidosis or alkalosis.

When there is a change in hydrogen ion concentration, the buffer systems of the bodyfluids react within a fraction of a second to minimize these changes. Buffer systems donot eliminate hydrogen ions from the body or add them to the body but only keep themtied up until balance can be re-established. The second line of defense, the respiratorysystem, also acts within a few minutes to eliminate CO2 and, therefore, H2CO3 from the

body. These first two lines of defense keep the hydrogen ion concentration fromchanging too much until the more slowly responding third line of defense, the kidneys,can eliminate the excess acid or base from the body. Although the kidneys are relativelyslow to respond, compared with the other defenses, they are over a period of hours toseveral days by far the most powerful of the acid-base regulatory systems.

Buffer SystemsThere are at least three kinds of buffer system which play a role in acid-base balance,i.e. the bicarbonate buffer system, the phosphate buffer system and protein, animportant intracellular buffer.

The bicarbonate buffer systemThe bicarbonate buffer system consists of a water solution that contains two ingredients:1) a weak acid, H2CO3 and 2) bicarbonate salt, such as NaHCO3. For the bicarbonatesystem, the pK is 6.1, and it is known the Henderson-Hesselbach equation to calculatethe pH of a solution if the molar concentration of bicarbonate ion and the PCO2 areknown, as follow: pH = 6.1 + log HCO3

-0.03XPCO2

The bicarbonate buffer system can not be expected to be the most powerful for tworeasons: First, the pH of the extracellular fluid is about 7.4, whereas the pK of the


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bicarbonate buffer system is 6.1. This means that there is about 20 times as much of thebicarbonate buffer system in the form of HCO3

- as in the form of dissolved CO2. For thisreason, this system operates on the portion of the buffering curve where the slope is lowand the buffering power is poor. Second, the concentrations of the two elements of thebicarbonate system, CO2 and HCO3

-, are not great.

Despite these characteristics, the bicarbonate buffer system is the most powerfulextracellular buffer in the body. This apparent paradox is due maintly to the fact that thetwo elements of the buffer system, HCO3

- and CO2, are regulated, respectively, by thekidneys and the lungs. As a result of this regulation, the pH of the extracellular fluid canbe precisely controlled by the relative rate of removal and addition of HCO3

- by thekidneys and the rates of removal of CO2 by the lungs.

The phosphate buffer systemAlthough the phosphate buffer system is not important as an extracellular fluid buffer, itplays a major role in buffering renal tubular fluid and intracellular fluids. The mainelements of the phosphate buffer system are H2PO4

- and HPO4--. The phosphate buffer

system has a pKa of 6.8, which is not far from the normal pH of 7.4 in the body fluids;

this allows the system to operate near its maximum buffering power. However, itsconcentration in the extracellular fluid is low, only about 8 per cent of the concentrationof the bicarbonate buffer. Therefore, the total buffering power of the phosphate systemin the extracellular fluid is much less than that of the bicarbonate buffering system.

In contrast to its rather insignificant role as an extracellular buffer, the phosphate bufferis especially important in the tubular fluids of the kidneys for two reasons: 1) phosphateusually becomes greatly concentrated in the tubules, thereby increasing buffer power ofthe phosphate system, and 2) the tubular fluid usually has a considerably lower pH thanextracellular fluid, bringing the operating range of the buffer closer to the pK (6.9) of thesystem.

The phosphate buffer system is also important in buffering intracellular fluids becausethe concentration of phosphate in these fluids is many times that in the extracellularfluids. Also, the pH of intracellular fluid is lower than that of extracellular fluid andtherefore usually closer to the pK of the phosphate buffer system, compared with theextracellular fluid.

ProteinsProteins are among the most plentiful buffers in the body because of their highconcentration, especially within the cells. Approximately 60-70 per cent of the totalchemical buffering of the body fluids is inside the cells, and most of this results from theintracellular proteins. However, except for the red blood cells, the slowness ofmovement of hydrogen ions and bicarbonate ions through the cell membranes often

delays for several hours the maximum ability of the intracellular proteins to bufferextracellular acid-base abnormalities.

Another factor besides the high concentration of protein in the cells that contributes totheir buffering power is the fact that the pKs of many of these protein systems are fairlyclose to 7.4.

Respiratory role in acid-base balance


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The second line of defense against acid-base disturbances is control of extracellular fluidCO2 concentrations in the lungs. An increase in ventilation eliminates CO2 fromextracellular fluid, which, by mass action, reduces the hydrogen ion concentration.Conversely, decreased ventilation increases CO2, thus also increasing hydrogen ionconcentration in the extracellular fluid.

In general, the overall buffering power of the respiratory system is one to two times asgreat as the buffering power of all other chemical buffers in the extracellular fluidcombined. That is, one to two times as much acid or base can normally be buffered bythis mechanism as by the chemical buffers.

Renal control of acid-base balanceThe kidneys control acid-base balance by excreting either an acidic or a basic urine.Excreting an acidic urine reduces the amount of acid in extracellular fluid, whereasexcreting a basic urine removes base from the extracellular fluids.

The overall mechanism by which the kidneys excrete acidic or basic urine is as follows:Large numbers of bicarbonate ions are filtered continuously into the tubules, and if they

are excreted into the urine, this removes base from the blood. Large numbers ofhydrogen ions are also secreted into the tubular lumen by the tubular epithelial cells,thus removing acid from the blood. If more hydrogen ions are secreted than bicarbonateions are filtered, there will be a net loss of acid from the extracellular fluids. Conversely,if more bicarbonate ions are filtered than hydrogen ions are secreted, there will be a netloss of base.

The body produces each day about 80 milliequivalents of nonvolatile acids, mainly fromthe metabolism of proteins. These acids are called nonvolatile because they are notH2CO3 and, therefore, cannot be excreted by the lungs. The primary mechanism forremoval of these acids from the body is by renal excretion. The kidneys must alsoprevent the loss of bicarbonate in the urine, a task that is quantitatively more important

than the excretion of nonvolatile acids. Each day the kidneys filter about 4320milliequivalents of bicarbonate (180 L/day x 24 mEq/L), and under normal conditions,almost all of this is reabsorbed from the tubules, thereby conserving the primary buffersystem of the extracellular fluids.

Both the reabsorption of bicarbonate and the excretion of hydrogen ions areaccomplished through the process of hydrogen ion secretion by the tubule. Because thebicarbonate ion must react with a secreted hydrogen ion to from H2CO3 before it can bereabsorbed, 4320 mEq of hydrogen ions must be secreted each day just to reabsorbedthe filtered bicarbonate. Then an additional 80 mEq of hydrogen ions must be secretedto rid the body of the nonvolatile aids produced each day, for a total of 4400 mEq ofhydrogen ions secreted into the tubular fluid each day.

In addition to secretion of hydrogen ions and reabsorption of filtered bicarbonate ions,the kidneys have also capability in producing new bicarbonate ions to regulateextracellular hydrogen ion concentrations.

9. Define the meaning of pH and how can you translate pH tofree H+


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pH is the negative logarithm of the hydrogen ion concentration of a solution,expressed in equivalents per liter. The concentration of free hydrogen ion in bodyfluids is approximately 40 X 10 -9 Eq/L or 40 nEq/L. This corresponds to a pH ofapproximately 7.40. The number of free hydrogen ions per liter of body fluid can becalculated using the following approximation: A pH of 7.00 equals 100 nEq/L. Foeevery 0.10 increase in pH the corresponding H+ number is 80% of the preceding

value. For example at a pH 7.10, H+ = 80 nEq/L, at pH 7.20, H+ = 64 nEq/L

10. How can you adapt the Henderson Hasselbach equationfor clinical practice:

H+= 24 X pCO2 / HCO3

If one knows two of the three variables in the equation, the third can be calculated,allowing quick bedside assesment of acid base disorders

11. Describe three major processes that can result in ametabolic acidosis:

Acid production in excess of the kidneys ability to excrete th acid and regeneratebicarbonate

Decreased ability of a diseased kidney to excrete acid and generate bicarbonate

Loss of bicarbonate from extracellular fluid through either kidneys or thegastrointestinal tract.

12. Describe the guidelines for treatment of prerenal azotemia (ARF):

Restore the normal circulating blood volume. In the absence of heart failure,administration of fluids (usually normal saline) at the rate of 75-100 ml/hr isadequate.

The type of fluid administered and the rate at which replacement fluids are givenwill depend on the serum electrolytes (especially serum sodium, potassium, andthe acid base status of the patient) and the clinical status of the patient

Monitor the adequacy of fluid replacement by clinical examination of the patientand by serial determinations of serum creatinine concentrations, which reflectrenal function. Follow daily weight, fluid intake, and urine output, as well as urinesodium excretion and serial measurements of serum creatinine, urea, serum

electrolytes, and acid base parameters. Hemodynamic monitoring may benecessary if clinical assessment of cardiovascular function and fluid status isdifficult. Response to proper fluid replacement in prerenal azotemia is rapid, renalfunction usually returns to previous baseline within 3-4 days.


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After the diagnose was established as Acute Renal Failure because of volume depletion,this patient was given intravenous crystalloid fluid to restore his renal function andcorrection of hyperkalemia and metabolic acidosis

1. In case of treatment failure what are the other management possibilities ?

Renal replacement therapy : hemodialysis or acute peritoneal dialysis


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Epilog :

Good rehydration treatment with crystalloid fluid, management of metabolic acidosis, andhyperkalemia save Mr Arif renal function and he doesn't have to be dialysed.

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