Lung and Kidney

7/28/2019 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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