lung and kidney
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Definition:pH is defined as potential of H+ Ionconcentration in body fluid. The amount of
H+ ion concentration is so low in the bodyhence it is expressed asve logarithm tobase of the H+ ion concentration inmEq/lit.
pH = log 1/ [H+ ]= - log [H+ ]
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Balance of H conc. In ECF .
To Achieve Homeostasis .
Balance Between :
The H Intake or Production
The H Removal
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Arterial blood = 7.35 7.45
Can be explained as follows;
Normal value of H+ ion conc. is about
40nEq/lit.
40 nEq/lit = 0.00000004 Eq/lit.
Therefore pH = - log [0.00000004]
= 7.4
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Acidosis = Decrease in arterial PH ( 7.45)
Due to excess base .
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Molecules containing H atoms that can release(donate) H ions in solutions .
Example : HCL . Hydrogen ions are the toxic end product of
metabolism and they adversely affect all physicaland biochemical cellular process in our body.
Strong acids :- Completely dissociate : (HCL , H2SO4 )
Weak acid :- Partially dissociate : ( H2CO3)
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An Ion that accept a H ion .An example of a base is the Bicarbonate
( HCO3 ) .
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Substances that Neutralize acids or bases.
Chemical Reactions which Reduce the
effect of adding acid or base to a solution
H .
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Three Systems in the body :
1) Buffers in blood .
2) Respiration through the lungs .
3) Excretion by the kidney .
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These buffer systems serve as a first line
of defense against changes in the acid-
base balance :
- HCO3(Regulated by Renal and
Respiratory) .
- Protein
- Phosphate- Hemoglobin
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Acidic and Basic Amino acid in plasma and
cell protein act as buffers .
HB is an important buffer , cant be
regulated physiological .
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Both Intra and Extra cellular phosphate act
as a buffer . But its role is minor compared
to HB or HCO3.
Intracellular buffers are needed because H
doesnt cross Plasma Membrane .
Intracellular PH is more acidic . (7.2)
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Hydrogen Ion Excretion in Kidney
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Buffering of hydrogen ions in urine
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Decrease H ion secretionand HCO3 ion reabsorption
Increase in H ion secretionand HCO3 ion reabsorption
PCO2PCO2
H , HCO3H , HCO3
ECF volumeECF volume
Angiotensin IIAngiotensin II
AldosteroneAldosterone
HyperkalemiaHypokalemia
Factors that increase or decrease H secretion and HCO3Reabsorption by renal tubules :
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Maintaining Normal PH by maintaining
constant PCO2 .
Normal gas Exchange and ventilation .
Controlled by chemoreceptors .
PCO2 PH
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Tubular Mechanisms of H+
Tubular Reabsorption of HCO3 .
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Blood PH
Blood PCO2
Blood HCO3
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Compensation
-If underlying problem is metabolic :Hyperventilation and Hypoventilation mechanisms
will help through Respiratory Compensation .
-If the problem is Respiratory , Renal mechanisms, then Renal mechanisms will help through
Metabolic Compensation .
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-Principal effect of acidosis is Depression of
the CNS through the decrease in synaptic
transmission .
- Generalized Weakness .- Deranged CNS is the greatest thread .
- severe acidosis causes :
1- Disorientation
2- Coma
3- Death
Acidosis
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Alkalosis-Causes over excitability of the central and peripheralnervous systems .
-Numbness
- Lightheadedness
It can cause :- nervousness .
- muscle spasms or tetany .
- convulsions
- loss of consciousness
- death .
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Acid/base
disorders
Primary change Compensatory change Timescale
of
compensat
ory change
Metabolic
acidosis
Decrease in
plasmabicarbonate
concentration
Decrease in pCO2 (hyperventilation) Minute/hour
s
Metabolic
alkalosis
Increase in
plasma
bicarbonate
concentration
Increase in pCO2 (hypoventilation) Minute/hour
s
Respiratory
acidosis
Increase in pCO2 Increase in renal bicarbonate
reabsoption : increase in plasma
bicarbonate concentration
Days
Respiratory
alkalosis
Decrease in
pCO2
Decrease in renal bicarbonate
reabsoption : decrease in plasma
Days
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Metabolic acidosis Ketoacidosis
Lactic acidosis
Renal failure (inorganic acids) Severe diarrhea (loss of bicarbonate)
Surgical drainage of intestine (loss of bicarbonate)
Renal loss of bicarbonate (renal tubular acidosis
type 2) Impairment of renal H+ excretion (renal tubular
acidosis type 1)
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Respiratory acidosis Chronic obstructive airways disease
Severe asthma
Cardiac arrest Depression of respiratory center (opiats)
Weakness of respiratory muscles (poliomyelitis,
MS)
Chest deformities
Airway obstructive
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Metabolic alkalosis Vomitting (loss of hydrogen ion)
NGT suction
Hypoklaemia IV administration of bicarbonate (after cardiac
arrest)
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Respiratory alkalosis Hyperventilation (anxiety, fever)
Lung diseases associated with hyperventilation
Anemia Salicylate poisoning
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Disorder pH pCO2 Bicarbonate
Metabolic acidosis Decrease Decrease
(respiratory
compensation)
Decrease
(primary change)
Respiratory
acidosis
Decrease Increase (prymary
change)
Increase
(metabolic
compensation)
Mixed Excessive
decrease
Increase
(respiratory
acidosis)
Decrease
(metabolic
acidosis)
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Disorder ory
alkalosis)
pH pCO2 Bicarbonate
Metabolic
alkalosis
Increase Increase
(respiratory
compensation)
Increase (primary
change)
Respiratory
alkalosis
Increase Decrease
(primary change)
Decrease
(metabolic
compensation)
Mixed Excessive
increase
Decrease
(respiratory
alkalosis)
Increase
(metabolic
acidosis)
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