S.t Lideta Lemaryam Health
Sciences And Business
College
Dep. Pharmacy
Sec. D Group-I
Physiology Assignment
ID 305/12
Submitted to-Mr. Bizuneh
Submitted date 5/08/2013
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Table of contents
Chapter-1 (Altitude can affect breathing)
Introduction ----------------------------------------------------------------------------------------------- 3
How high altitude can affect breathing ------------------------------------------------------------ 4
What relate circulatory and hemalologic
to Respiratory adaption -------------------------------------------------------------------------------6
Conclusion-- ---------------------------------------------------------------------------------------------- 7
Reference ------------------------------------------------------------------------------------------------- 8
Chapter-2 (GIT)
Introduction -------------------------------------------------------------------------------------------- 10
Gastrointestinal Disorders ------------------------------------------------------------------------ 11
Conclusion----------------------------------------------------------------------------------------------13
Reference------------------------------------------------------------------------------------------------14
Chapter-3 Fluid and Electrolyte Balance
Introduction---------------------------------------------------------------------------------------------16
Water balance----------------------------------------------------------------------------------------17
Regulation of Water intake----------------------------------------------------------------------17
Events in regulation of water output---------------------------------------------------------18
Excess water intake--------------------------------------------------------------------------------18
Electrolyte balance---------------------------------------------------------------------------------19
Regulation of electrolyte Intake & output---------------------------------------------------20
Electrolyte Balance --------------------------------------------------------------------------------20
Conclusion--------------------------------------------------------------------------------------------22
Reference----------------------------------------------------------------------------------------------23
Chapter-4( Acid Base Balance)
Introduction------------------------------------------------------------------------------------------ 25
Acid-base balance----------------------------------------------------------------------------------26
Conclusions------------------------------------------------------------------------------------------31
Reference--------------------------------------------------------------------------------------------- 32
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INTRODUCTION
Mountains are defined as landforms higher than 600 meters. As a
consequence of the increased altitude, the barometric pressure falls
and the environmental partial pressure of inspired oxygen decreases,
with consequent ambient hypoxia. This, in combination of low
temperature, low humidity, increased solar radiations and presence
of wind, in association with strong physical activities, imposes the
human body important physiological adaptations affecting primarily
the cardiovascular and respiratory systems.
PHYSIOLOGICAL ADAPTATIONS Oxygen is transported from the
environment to the cells by means of four linked mechanisms
ventilation, pulmonary diffusion, circulation, and tissue diffusion.
Upon ascent to, and during life at, altitude there are several
physiological adjustments of these mechanisms that compensate
for the decrease in availability of environmental oxygen. Although
all four mechanisms play important role, For this comparative
review, the physiological responses to altitude will be grouped into
respiratory, circulatory, and hematological adaptation.
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How high altitude can affectbreathing
Mountains are defined as landforms higher than 600 meters. As a
consequence of the increased altitude, the barometric pressure falls
and the environmental partial pressure of inspired oxygen decreases,
with consequent ambient hypoxia. This, in combination of low
temperature, low humidity, increased solar radiations and presence of
wind, in association with strong physical activities, imposes the human
body important physiological adaptations affecting primarily the
cardiovascular and respiratory systems.
Physical modifications begin to be significant over 2500 meters. In
normal subjects, the variability of this response may be very high and
generally it is well tolerated. On the contrary, these adjustments may
induce major problems in patients with preexisting cardiovascular
diseases in which the functional reserves are already limited.
The initial response to reduced partial pressure of oxygen is the
increase in depth and rate of breathing, which results in an increase in
alveolar ventilation. This is brought about by hypoxic stimulation of the
peripheral chemoreceptors, mainly the carotid bodies, which sense the
low PaO2 in the arterial blood. Hyperventilation reduces the alveolar
PCO2 (hypocapnia) with consequent respiratory alkalosis. The kidneys
correct the alkalinity of the blood over a few days by removing alkali
(in the form of bicarbonate ions, HCO3-) from the blood. As ventilation
increases, PaCO2 drops, pH increases and the central receptors
activity subsides. Nocturnal Cheyne-Stokes breathing is a common
experience when sleeping at high altitude. It results from the
fluctuations of PaO2 and PaCO2 that are exaggerated during sleep,
causing alternating periods of apnea and hyperventilation.
The first cardiovascular response to hypoxia is an increase in heart
rate and in cardiac output with no changes in stroke volume, and the
arterial blood pressure may temporarily increase. After a few days of
acclimatization, cardiac output reduces to normal values, with still
increased heart rate, so that stroke volume is decreased. In the same
time the systemic vascular resistances increase as a response of the
adrenal medullary activity and the systemic arterial pressure increase,
too. As a consequence of these adaptations
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myocardial workload and oxygen demand increase. Because the
coronary oxygen extraction is normally physiologically high already
at low altitude, the myocardium to adapt to this increased request may
almost exclusively act on coronary vasodilatation enhancing
coronary blood flow. Ultimately, global systolic indices of ventricular
function are preserved or only slightly depressed, with altered
diastolic filling pattern. Even if the relationship between workload,
cardiac output and oxygen uptake is preserved, a decrease in
maximal oxygen consumption and in maximal cardiac output are
observed, which is minimal in acute hypoxia but is more important
after acclimatization. Despite all these consequences, these
adaptations are well tolerated and the high altitude exposure doesn’t
carry risks of myocardial ischemia in healthy subjects.
But there are also intracellular changes that operate to reduce injuries of
hypoxia and provide sufficient oxygenation when a subject is exposed to
altitude. In hypoxic environment, humans are able to switch on activation
of numerous genes to increase oxygen delivery. Recently it has been
shown that the hypoxia-inducible factor hypoxia-inducible factor a family
of transcription factors, plays a pivotal and fundamental regulatory role
in these homeostatic changes both at systemic and cellular levels.
hypoxia-inducible factor acts as the transcriptional activator of
erythropoietin erythropoietin, which increases red blood cell production,
vascular endothelial growth factor vascular endothelial growth factor,
which stimulates vascular development, and other genes which increase
glucose transport and glycolysis to produce energy in the absence of
oxidative phosphorylation.
Another consequence of high altitude is pulmonary hypertension.
The increase pressure in pulmonary artery is caused by the hypoxic
vasoconstriction of pulmonary small arteries and veins and this
response is very variable among humans. The degree of pulmonary
hypertension is generally mild and does not contribute to the
symptoms of acute mountain sickness acute mountain sickness. It can
occur in tourists, as well as in hikers, skiers, and mountaineers.
Interestingly, the increase in pulmonary artery pressure occurs both in
individuals with acute mountain sickness and in those who remain
asymptomatic after the climb. Excessive pulmonary vasoconstriction
play a role in the development of early high-altitude pulmonary edema
high-altitude pulmonary edema and late within weeks right heart failure
at high altitude.
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Lowlanders who ascend to medium or high altitudes may develop
some degree of acute mountain sickness, and the common
symptoms are headache, sleep disorders, gastrointestinal disorders
and dizziness. The degree of susceptibility to this illness varies and
in those with vigorous response it may lead to two potential lethal
ones, high-altitude pulmonary edema and high-altitude cerebral
edema high-altitude cerebral edema. The main cause is hypoxemia
and, thus, the treatment is oxygen administration and, in severe
cases, in addition to appropriate pharmacological treatment if
available, a return to lower altitudes. Acetazolamide administration is
the most widely accepted prophylaxis. Staging the ascent attenuates
the symptoms of acute mountain sickness and, thus, is
recommended as a way to prevent the most serious clinical
conditions as high-altitude pulmonary edema and high-altitude
cerebral edema.
What relate circulatory and hemalologic
to Respiratory adaption
Respiratory adaptations
In all mammalian species, minute ventilation is determined by
oxygen demand, and regulated by neural and chemical stimuli. One
of the latter is the partial pressure of oxygen, a decrease of which is
characteristic of altitude. That have been examined, there is a
significant increase in ventilation upon acute exposure. But it is so
interrelated so it have relation with the circulatory and hemalologic
Circulatory adaptations
In man, immediately upon exposure to altitude, the cardiac output
abruptly increases. This increase results solely from an increase in
heart rate, not from a change in stroke volume.
Hemalologic adaptations
The hematologic adaptations considered in this review are blood
oxygen- carrying capacity and the hemoglobin affinity for oxygen. As
noted
earlier,the increase in oxygen-carrying capacity (i.e., increase in
hemoglobin concentration)
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Conclusion
The high altitude adaptive mechanisms leads to several
conclusions: 1) As a whole, the adaptive process is
extremely complex, being made up on physiological adaption
on breathing. No single component can explain the
completeness of the species adaptation, Each component
must be considered as an element of an interelated system.
It is clearly evident that one form of adaptation influences the
next one. This is exemplified by the position of the oxygen
dissociation curve (physiological adaptation) that is correlated
with Circulatory adaptation and hematological adaptation.
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Reference
1. National Heart and Lung Institute, National Institutes of
Health, Bethesda, Maryland 20014
2. Naeije R. Physiological adaptation of the cardiovascular
system to high altitude. Prog Cardiovasc Di. 2010;52(6):456–
466.
3. Bartsch P, Gibbs JS. Effect of altitude on the heart
and the lungs. Circulation. 2007;116(19):2191–2202.
4. Citation: Donegani E. Effects of high altitude: physiological
adaptations of the heart and lungs. J Cardiol Curr Res.
2014;1(6):175‒176. DOI: 10.15406/jccr.2014.01.00035
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Chapter 2
Gastrointestinal
Tract Disorder
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Introduction
The digestive tract is a long muscular tube that moves food and
accumulated secretions from the mouth to the anus.
The GI tract includes all structures between the mouth and the anus.
The tract itself is divided into upper and lower tracts.
The upper gastrointestinal tract consists of the esophagus, stomach, and
duodenum.
The lower gastrointestinal tract includes most of the small intestine and all of
the large intestine.
so these important part of the body can be attacked by a disease or can
happen disorder of gastrointestinal tract.
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Gastrointestinal Disorders
Gastrointestinal (GI) disorders, including functional bowel diseases
such as irritable bowel syndrome (IBS) and inflammatory bowel
diseases such as Crohn's disease (CD) and colitis, afflict more than
one in five Americans, particularly women. While some GI
disorders may be controlled by diet and pharmaceutical
medications, others are poorly moderated by conventional
treatments. Symptoms of GI disorders often include cramping,
abdominal pain, inflammation of the lining of the large and/or small
intestine, chronic diarrhea, rectal bleeding and weight loss.
Patients with these disorders frequently report using cannabis
therapeutically to address a variety of symptoms, including
abdominal pain, abdominal cramping, and diarrhea. According to
survey data published in 2011 in the European Journal of
Gastroenterology & Hepatology, "Cannabis use is
common amongst patients with IBD for symptom relief, particularly
amongst those with a history of abdominal surgery, chronic
abdominal pain and/or a low quality of life index." More recent
survey data of IBD patients affirms: "[A] significant number of
patients with IBD currently use marijuana. Most patients find it very
helpful for symptom control."
Preclinical studies demonstrate that activation of the CB1 and
CB2 cannabinoid receptors exert biological functions on the
gastrointestinal tract. Effects of their activation in animals include
suppression of gastrointestinal motility, inhibition of intestinal
secretion, reduced acid reflux, and protection from inflammation,as
well as the promotion of epithelial wound healing in human tissue.
Experts suggest the endogenous cannabinoid system plays "a key
role in the pathogenesis of IBD," and that "cannabinoids may,
therefore, be beneficial in inflammatory disorders" such as colitis
and other digestive diseases.
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Observational trial data reports that whole-plant cannabis therapy is
associated with a reduction in Crohn's disease activity and
disease-related hospitalizations. Investigators at the Meir Medical
Center, Institute of Gastroenterology and Hepatology assessed
'disease activity, use of medication, need for surgery, and
hospitalization' before and after cannabis use in 30 patients with
CD. Authors reported, "All patients stated that consuming cannabis
had a positive effect on their disease activity" and documented
"significant improvement" in 21 subjects.
Specifically, researchers found that subjects who consumed
cannabis "significantly reduced" their need for other medications.
Participants in the trial also reported requiring fewer surgeries
following their use of cannabis. "Fifteen of the patients had 19
surgeries during an average period of nine years before cannabis
use, but only two required surgery during an average period of
three years of cannabis use," authors reported. They concluded:
"The results indicate that cannabis may have a positive effect on
disease activity, as reflected by a reduction in disease activity index
and in the need for other drugs and surgery."
In a follow up, randomized placebo-controlled trial, inhaled
cannabis was reported to decrease Crohn's disease symptoms in
subjects with a treatment-resistant form of the disease. Nearly half
of the patients in the trial achieved disease remission. By contrast,
the administration of oral CBD was not found to have a beneficial
therapeutic effect in Crohn’s disease patients in a controlled trial setting.
Based on the available evidence to date, some experts now opine
that modulation of the ECS represents a novel therapeutic
approach for the treatment of numerous GI disorders — including
inflammatory bowel disease, functional bowel diseases, gastrooesophagael reflux conditions, secretory diarrhea, gastric ulcers
and colon cancer.
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Conclusion
As a conclusion Gastrointestinal (GI) disorders is functional bowel diseases such as irritable bowel
syndrome (IBS) and inflammatory bowel diseases such as Crohn's disease (CD) and colitis,
particularly women. While some GI disorders may be controlled by diet and pharmaceutical
medications, others are poorly moderated by conventional treatments. Symptoms of GI disorders
often include cramping, abdominal pain, inflammation of the lining of the large and/or small
intestine, chronic diarrhea, rectal bleeding and weight loss so it can be prevented before the
disorder and it can be treated after the dieses
.
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Reference
1.The National Organization for the Reform of Marijuana Laws (norml.org)
2.https://norml.org/wp-content/uploads/pdf_files/NORML_Clinical_Applications_GI_Disorders.pdf
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Chapter-3
Fluid and Electrolyte
Balance
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Introduction
A typical adult body contains about 40 L of body fluids.
25 L of fluids (or 63%) are located inside body cells, called intracellular fluid ( ICF ).
15 L of fluids (or 37%) are located outside of body cells, called extracellular fluid ( ECF ).
80% of ECF is interstitial fluid (which includes lymph, synovial fluid, cerebrospinal fluid, GI tract
fluids, and fluids in the eyes and ears), and 20% of ECF is blood plasma.
ICF is mostly water and is rich in K+, Mg++, HPO42-, SO42-, and protein anions.
ECF contains more Na+, Cl-, HCO3-, and Ca++.
Concentrations of substances dissolved in ICF and ECF are constantly different because the cell
membrane is selectively permeable, which maintains a relatively unchanged distribution of
substances in different body fluids.
Fluid balance refers to the proper levels of water and electrolytes being in the various body
compartments according to their needs.
Electrolytes are chemical substances that release cations ( positively charged ions) and anions
(negatively charged ions) when they are dissolved in water. Electrolytes serve 4 primary functions
in the body as essential minerals (e.g. iodine, calcium).
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Water balance
Water is the most abundant constituent in the body, varying from 45 % to 75% of body weight.
Water balance occurs when water intake equals water output. A normal adult consumes about
2,500 ml of water daily 1,500 ml in beverages, 750 ml in food, and 250 ml from cellular respiration
and anabolic metabolism. At the same time, this adult is releasing about 2,500 ml of water daily -1,500 ml in urine, 700 ml by evaporation (through the skin and lungs), 100 ml in the feces, and 200
ml in sweating.
Regulation of Water intake
 1. The body loses as little as 1% of its water.
 2. An increase in osmotic pressure of extracellular fluid due to water loss stimulates
osmoreceptors in the thirst center ( hypothalamus ).
 3. Activity in the hypothalamus causes the person to be thirsty and to seek H2O.
Drinking and the resulting distension of the stomach by water stimulants nerve impulses
that inhibit the thirst center.
water is absorbed through the wall of the stomach, small intestine, and large intestine.
The osmotic pressure of extracellular fluid returns to normal.
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Events in regulation of water output
I. Dehydration:
1. Extracellular fluid becomes osmotically more concentrated.
2. Osmoreceptors in the hypothalamus are stimulated by the increase in the osmotic pressure of
body fluids.
3.The Hypothalamus signals the posterior pituitary gland to release ADH into the blood.
4. Blood carries ADH to the kidneys.
5. ADH causes the distal convoluted tubules & collecting ducts to increase water reabsorption.
6. urine output decreases, and further water loss is minimized.
Excess water intake
1. Extracellular fluid becomes osmotically less concentrated.
2. This change stimulates osmoreceptors in the hypothalamus.
3.The posterior Pituitary gland decrease ADH release.
4. Renal tubules decrease water reabsorption.
5. Urine output, increases and excess water is excreted.
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Electrolyte balance






Electrolytes are chemical substances that release cations ( positively charged ions) and
anions (negatively charged ions) when they are dissolved in water. Electrolytes serve 4
primary functions in the body.
as essential minerals (e.g. iodine, calcium).
control osmosis between body compartments by establishing proper osmotic pressure (e.g.
sodium, chloride).
help maintain acid-base balance (e.g. hydrogen ion, bicarbonate ion).
carry electrical current that allows the production of action potentials (e.g. sodium,
potassium).
The most important electrolytes include Na+, K+, Cl-, Ca++, and HPO42-.
Na+ is the most abundant extracellular cation; involved in nerve impulse transmission,
muscle contraction, and creation of osmotic pressure.
Cl- is a major extracellular anion; involved in regulating osmotic pressure between body
compartments, forming HCI in stomach, and involved in the “chloride shift” process in
blood.
K+ is the most abundant cation in ICF; involved in maintaining fluid volume, nerve impulse
transmission, muscle contraction, and regulating pH.
Ca++ is the most abundant ion in the body, located mainly in ECF; a major structural
component of bones and teeth; functions in blood clotting, neurotransmitter release, muscle
tone, and excitability of nervous and muscle tissues.
HPO42- is an important intracellular anion; another major structural component of bones and
teeth; required for synthesis of nucleic acids and ATP, and for buffering reactions.
Level of electrolytes are mainly regulated by hormones:
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
Aldosterone (from adrenal cortex) causes an increase in sodium reabsorption and
potassium secretion at the kidney tubules.
 Parathyroid hormone (PTH) from the parathyroid glands and Calcitonin (CT) from the
thyroid gland regulate calcium balance.
Regulation of electrolyte Intake & output
Electrolyte intake:
Electrolytes are usually obtained in sufficient quantities in response to hunger and thirst
mechanism.
In a severe electrolyte deficiency, a person may experience a salt craving.
Electrolyte output:
Electrolytes are lost through perspiration, feces and urine. The greatest electrolyte loss
occurs as a result of kidney functions.
Quantities lost vary with temp. and exercise.
Electrolyte Balance
 1. Concentrations of Na, K and calcium ions in the body fluid are very important.
 2.The regulation of Na+ and K+ ions involve the secretion of Aldosterone from adrenal glands.
1.
2.
3.
K+ ion concentration increases.
Adrenal cortex is signaled.
Aldosterone is secreted.
4.Renal tubules increase reabsorption of Na+ ion and increase secretion of K+ ions (excretes
K ions).
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5.Na+ ions are conserved and K+ ions are excreted.
 3. Calcitonin from the thyroid gland and parathyroid hormone from the parathyroid glands
regulate Ca+ ion concentration.
- Parathyroid hormone increases activity in boneresorbing cells (osteocytes & osteoclasts)
which increase the conc. of both Ca+ and phosphate ions in extracellular fluids. This hormone
also causes increase absorption of Ca+ and increase excretion of phosphate, from the
kidney.
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Conclusion
The fluid balance can be monitored with a system that is fairly simple but requires meticulous collection of patient data
The pertinent data includes previous fluid and electrolyte balance, intake, output, trends in changes in urine specific
gravity, changes in body weight, serum electrolytes, calcium phosphorus, blood gases, and vital signs. It should be
emphasized that the goal of fluid balance in the first week of life is to achieve a negative balance with an anticipated
weight loss of approximately 10% during the first week of life. This allowance for 1 to 2% per day of weight loss and
1–1.5 mEq/day of sodium loss during the first week of life is essential specifically in premature and sick infants to
avoid overload or dehydration.
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Reference
1.Fluid, Electrolyte, Dr. Ali Ebneshahidi 2009
2.Human Anatomy & Physiology: Fluid & Electrolyte Balance; Ziser, 2004
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Chapter 4
Acid Base Balance
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Introduction
In a healthy individual the extracellular fluid pH change following addition of a metabolic acid or
base, is modified initially by the body’s buffers. Subsequent respiratory compensation, by
excretion or retention of CO2, modifies this change before metabolism of the organic acid or
renal excretion of the acid or alkali returns the plasma bicarbonate to normal. A primary
respiratory acid-base change is modified initially by cellular buffers, with renal compensatory
mechanisms adjusting slowly to this change. However, correction of the respiratory pH disorder
only occurs with correction of the primary disease process
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Acid-base balance
Acids are electrolytes that release hydrogen ions (H+) when they are dissolved in water.
Bases are electrolytes are release hydroxide ions (OH-) when they are dissolved in water.
Acid-base balance is primarily regulated by the concentration of H+ (or the pH level) in body
fluids, especially ECF.
Acid-base balance
Normal pH range of ECF is from 7.35 to 7.45.
Most H+ comes from metabolism -- glycolysis, oxidation of fatty acids and amino acids, and
hydrolysis of proteins.
Homeostasis of pH in body fluids is regulated by acid-base buffer systems (primary control),
respiratory centers in brain stem, and by kidney tubule secretion of H+.
Acid-base buffer systems are chemical reactions that consist of a weak acid and a weak base, to
prevent rapid, drastic changes in body fluid pH. one of the most carefully regulated conc. in the
body is that of H+ ion.
one of the most carefully regulated conc. in the body is that of H+ ion.
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When acid (H+) is added to the blood, the pH
decreases. Then increased acidity (decreased
pH) is minimized by buffers which bind some of
the added H+.
When acid is taken away, blood becomes
more alkaline (pH increases). This change is
minimized by buffers, which release H+ and
replace some of the acid that was lost.
H+ + HCO3H2CO3
H2O +
CO2
 The pair bicarbonate / carbonic acid forms
an important buffer system. H2CO3 (carbonic
acid) is the acid member of the pair because
it can release H+. HCO3- is the base member
of the pair because it can accept H+. This
system is important because two of its
components are rigorously controlled by the
body: the lungs control CO2 and the kidney
control HCO3-.
Chemical Acid-Base buffer systems
1. Bicarbonate buffer system:
Bicarbonate ion (HCO3-) – converts a strong acid into a weak acid.
Carbonic acid (H2CO3) – converts a strong base into a weak base.
Bicarbonate buffer system produces carbonic acid (H2CO3) and sodium bicarbonate (NaHCO3) to
minimize H+ increase, mainly in the blood:
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(1)HCl NaHCO3 H2CO3 NaCl
(2)NaOH H2CO3 NaHCO3 H2O
 Phosphate buffer system: produces sodium hydrogen phosphates
(NaH2PO4 and Na2HPO4) to regulate H+ levels, mainly in kidney tubules and erythrocytes:
(1)HCl Na2HPO4 NaH2PO4 NaCl
(2)NaOH NaH2PO4 Na2HPO4 H2O
 Protein buffer system: relies on the carboxylic acid group of amino acids to release H+, and the
Tubule H secretion of filtered Hco3
amino group to accept H+, mainly inside body cells and in blood plasma.
 Respiratory centers in the pons and medulla oblongata regulate the rate and depth of breathing,
which controls the amount of carbon dioxide
gas (CO2) remained in the blood and body fluid -- e.g. slower berating rate
an increase in
blood CO2 level
an increase in carbonic acid (H2CO3) in blood
more H+ is released
into body fluids
pH of blood and body fluids drops.
 Nephrons react to the pH of body fluids and regulate the secretion of H+ into urine -- e.g. a diet
high in proteins causes more H+ to be produced in body fluids (which lowers body fluid pH), as a
result the nephrons will secrete more H+ into the urine.
Compensation
Compensation is a series of physiological responses that react to acidbase imbalances, by
returning blood pH to the normal range (7.35 –7.45).
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Acidosis & Alkalosis
 Respiratory acidosis: (due to deficiency of CO2 expiration) and respiratory alkalosis (due
to abnormally high CO2 expiration) are primary disorders of CO2 pressure in the lungs.
These may be compensated by renal mechanisms where nephrons will secrete more H+ to
correct acidosis and secrete less H+ to correct alkalosis.
It is due to increased CO2 retention (due to hypoventilation), which can result in the
accumulation of carbonic acid and thus a fall in blood pH to below normal.
 Metabolic Acidosis: increased production of acids such as lactic acid, fatty acids, and
ketone bodies, or loss of blood bicarbonate
(such as by diarrhea), resulting in a fall in blood pH to below normal.
Respiratory Alkalosis:
A rise in blood pH due loss of CO2 and carbonic acid (through hyperventilation).
Metabolic Alkalosis:
A rise in blood pH produced by loss of acids ( such as excessive vomiting) or by excessive
accumulation of bicarbonate base.
Respiratory Excretion of CO2
The respiratory center is located in the brain stem.
It helps control pH by regulating the rate and depth of breathing.
Increasing CO2 and H+ ions conc. stimulate chemo receptors associated with the respiratory
center; breathing rate and depth increase, and CO2 conc. decreases.
If the CO2 and H+ ion concentrations are low, the respiratory center inhibits breathing.
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Renal excretion of H+
Nephrons secrete hydrogen ions to regulate pH.
phosphate buffer hydrogen ions in urine.
Ammonia produced by renal cells help transport H+ to the outside of
the body:
H-NH3 -NH 4
chemical buffer system (Bicarbonate buffer system, phosphate
buffer, and protein buffer system) act rapidly and are the first line of
defense against pH shift.
physiological buffer (respiratory mechanism CO2 excretion), renal
mechanism (H+ excretion) act slowly and are the 2nd line of defense
against pH shift.
Source of H+
a. Aerobic respiration of glucose
produces CO2 , which reacts with water to from carbonic acid.
carbonic acid dissociates to release H+ and bicarbonate ions.
b. Anaerobic respiration of glucose produce lactic acid.
c. Incomplete oxidation of fatty acids releases acidic ketone
bodies.
d. Oxidation of sulfur-containing amino acids produce sulfuric
acid.
e. Hydrolysis of phosphoproteins and nucleic acids gives rise to
phosphoric acid.
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Conclusions
In man the acid-base balance is maintained and
regulated by the renal and respiratory systems, which
modify the extracellular fluid pH by changing the
bicarbonate pair (HCO3 - and PCO2); all other body
buffer systems adjust to the alterations in this pair.
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Reference
1.Acid-Base Balance Dr. Ali Ebneshahidi 2009
2.Text book of Biochemistry for medical students: DM Vasudevan: 7th edition P a g e 3 2 | 32