SBM 2024 CLINICAL BIOCHEMISTRY SEM II, 2011/2012

GROUP TUTORIAL

GROUP MEMBERS :

NOR AMIRA BT MOHD SHAFIE NOOR NABILAH BT TALIK SISIN HANISAH BT MOHD MOHADIS AQILAH NABIHAH BT OMAR ATHIRAH NUR BT AHMAD ROSLEE WAFDA BT ROHHIMI SITI NOR AINI BT HARUN NOOR IZZATI BT MASRI ANITH SYUHADA BT MOHD SHAFEIN YAUMIL HIKMAH BT FAISAL ANIS NAAZIRA BT ABDUL RAUF

0917304 1010914 1011968 1012988 1013060 1013342 1014058 1018808 1019514 1019840 1028108

DATE OF SUBMISSION : 10TH MAY 2012

Introduction Oxygen is essential for human to continue respire. As an exchange, the body cell will use up the oxygen and excrete carbon dioxide. The carbon dioxide will be transported through the blood stream to the lungs, to be excreted through exhalation. Exhalation is one of the mechanism of maintaining blood pH, that controlled by the respiratory centre in medulla oblongata and this mechanism is must be maintained. However, some reasons might cause the respiratory system disturbed to proceed with normal rate of respiration and can cause carbon dioxide cannot be excreted at optimum rate. Therefore, the concentration of carbon dioxide will build up in blood and causing the blood pH to decrease and body system become more acidic. The condition referring to previous statement is called respiratory acidosis.

Hyperventilation as Compensatory Response of Acidosis In the case of metabolic acidosis, the body uses hyperventilation as a compensatory the central mechanism to decrease in medulla acidity of the and blood. The hyperventilation mechanism starts with the detection of the low blood pH by chemoreceptors oblongata peripheral chemoreceptors in aortic and carotid arteries. The initial stimulation of the central chemoreceptors is due to small increases of hydrogen ions concentration in brain interstitial fluid. Then, this detection will stimulate the inspiratory area in medulla oblongata. As a result, the diaphragm and other respiratory muscles contract more forcefully and rapidly, so more CO2 is exhaled. As less H2CO3 forms and less H+ is present, blood pH increases. When the blood pH increases to normal range, the normal acid-base homeostasis will return.

The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilised across the blood brain barrier. The increase in ventilation usually starts within minutes and is usually well advanced at 2 hours of onset but maximal compensation may take 12 to 24 hours to develop. This is maximal compensation rather than full compensation as it does not return the extracellular pH to normal. In situations where a metabolic acidosis develops rapidly and is shortlived there is usually little time for much compensatory ventilatory response to occur. An example is the acute and sometimes severe lactic acidosis due to a prolonged generalised convulsion: this corrects due to rapid hepatic uptake and metabolism of the lactate following cessation of convulsive muscular activity, and hyperventilation due to the acidosis does not occur. Renal H+ ion Excretion The third compensatory response of respiratory acidosis is the renal H+ excretion. This response mainly occurs in the kidney at the proximal convoluted tubule (PCT) and the collecting duct. This process includes Na+/H+ antiporters in the PCT and proton pump in the collecting duct that secretes the H+ ion into the tubular fluid. For Na+/H+ antiporters in PCT, the reabsorption of Na+ into the capillaries is accompanied by the secretion of H+ into the tubular fluid. Meanwhile, proton pumps are located at the apical membrane (contact with the fluid in the kidney) of intercalated cells of the collecting duct. The H+ from the intercalated cells is secreted into tubular fluid against the concentration gradient, making the urine can be up to 1000 times more acidic than blood. However in some intercalated cells, the proton pumps are located at the basolateral membrane (contact with the interstitial fluid and capillaries). The kidneys not only secrete H+ ions but they also regenerate bicarbonate ions. The renal handle the electrolytes acid base balance. All aspects of renal involvement in acid base balance are interlinked.

The Carbonic Acid-Bicarbonate Buffer System The carbonic acid-bicarbonate buffer system is based on the bicarbonate ion (HCO-3), which can act as a weak base and carbonic acid (H2CO3), which can act as a weak acid. As we have already learned, HCO 3is a significant anion in both intracellular and extracellular fluid. It is because the kidneys also synthesis new HCO3- and reabsorbed filtered HCO3- , this important buffer is not lost in the urine. If there is an excess H+, the HCO3- can function as a weak base and remove the excess H+. Then, H2CO dissociate into water and carbon dioxide, and CO2 is exhaled from the lungs. The reaction is as follow: H+ (aq) + HCO3- (aq) (weak base) On the other hand, if there is a shortage of H+, the H2CO3 function as a weak acid and provide H+ as follows: H2CO3 Carbonic acid (weak acid) To be more clear, the two equilibrium reactions in the carbonic-acidbicarbonate buffer with the direct involvement of water, the equation is rewritten as below: H+ hydrogen ion + HCO3 bicarbonate ion <=> H2CO3 (aq) <=> CO2 (g) + H2O (l) hydrogen ion bicarbonate ion carbonic acid

When the normal blood pH of 7.4 is outside the optimal buffering range, the addition of protons to the blood due to strenuous exercise may be too great for the buffer alone to effectively control the pH of the blood. When this

happens, other organs must help control the amounts of CO2 and HCO3- in the blood such as lungs and kidneys.

Conclusion These compensatory responses may take several days to occur and need sufficient time to be steady, approximately 24 hours. Many organs need to cooperate to compensate this problem. While hyperventilation helps by increasing the exhalation of CO2, the kidneys instruct their renal tubules to secrete H+ into urine and reabsorb HCO3- and the buffer systems convert the strong acids and bases into weak acids and bases. However, not all the responses return the pH to normal.