Module 2, Part 1 of 3 Flashcards

1
Q

Acid-Base Balance

A

-body fluids vary i pH but the range of each fluid is mainly limited by a variety of buffer systems

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2
Q

Major Mechanisms to Control pH in Body

A

-buffer systems (molecular control of free H+)
-exhalation of CO2
-kidney excretion of H+

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3
Q

Buffer Systems

A

-prevent rapid, drastic changes in pH
-do not remove or create H+
-old or release H+ to regulate changes in body pH

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4
Q

Carbonic Acid-Bicarbonate Buffer System

A

CO2 + H2O = H2CO3 = HCO3- + H+

-ph too low (high H+), reaction driven to left

-pH too high (low H+) reaction is driven to right

-CO2 excreted in lungs
-H+ excreted in kidneys/urine

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5
Q

Protein Buffer System

A

-more effective than phosphate and bicarbonate buffer
-carboxyl group COOh can act like an acid and release H+
-amino grop NH2 can act like base and combine with extra H+
-proteins make up most of solute in intracellular fluids and plasma

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6
Q

Phosphate Buffer System

A

-phosphates are major anions in intracellular and extracellular fluid
-phosphate buffers produce H+ or OH-
-monohydrogen phosphate acts as a weak acid to buffer strong acids and H+
H+ - HPO4 –> H2PO4

-dihydrogen phosphate acts as weak acid to buffer a strong base
H2PO4 + OH –> HPO4 + H2O

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7
Q

Bicarbonate and CO2 Levels

A

-cells produce tiny amount of H+ and huge amounts of CO2
-high CO2 means low pH
-bicarbonate buffer converts CO2 to H+ to balance equilibrium
-bicarbonate and H+ can make carbonic acid that turns to CO2 and H2O when CO2 levels are low

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8
Q

Na+/H+ Antiporter in the Proximal C.T (Kidney)
*regulates pH

A

-can take NA from pee into kidney cells through capillaries
-can send H out through pee
-bicarbonate can be released into bloodstram

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9
Q

Lung Exhalation of CO2 Regulates Blood pH

A

-blood and tissue pH can be modified by changing rate and depth of breathing
-increase breathing rate/depth is an increase in blood pH
-as CO2 declines with increased breathing, more H+ from the blood and extracellular fluid combines with bicarbonate to balance equilibrium

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10
Q

-ve Feedback for pH Control

A
  1. decreased blood pH (high H+ concentration)
  2. receptors (central chemoreceptors in medulla oblongata and peripheral chemoreceptors in aortic and carotid bodies)
  3. control centre (respiratory area in medulla oblongata)
  4. effectos (diaphragm contracts more forcefully and frequently so more CO@ is exhaled)
    -less H2CO3 forms and fewer H+ present so blood pH increases
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11
Q

H+ excretion in collecting ducts

A

-collecting ducts are the last part of the kidney so if something is put there, it is most likely excreted as urine
-bicarbonate can easily be sent out as urine
-proton pump in apical membrane pushes H+ out of cell and into fluid in tubule lumen to become urine

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12
Q

High H+ Concentration in Lumen

A

-high H+ can be buffered by available NH3 ammoniato become ammonium NH4 which is less acidic

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13
Q

Kidney Excretion of H+

A

-kidneys reabsorb lost bicarbonate that can buffer H+by proximal convuluted tubules
-kidneys directly excrete H+ in urine as the major way to eliminate excess quickly
-renal failure can cause death rapidly due to its role in pH balance and body will become too acidic

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14
Q

Blood pH Levels

A

normal pH of blood is 7.35-7.45
-acidosis = less than 7.35
-alkalosis = more than 7.5
-around pH blood 7.00, severe depression of CNS and comma occur
-above 7.45, excitability of nervous tissue; convulsions and death

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15
Q

Respiratory Acidosis

A

-elevation of blood Co2 (pco2) above 45mmhg
-due to lack of removal of Co2 from blood
-ex. pulm. edema, trauma to respiratory centres, airway obstruction, dysfunction of respiratory muscles
-renal compensation inloves increasing H+ exretion and HCO3 reabsortion to raise pH

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16
Q

Respiratory Alkalosis

A

-Co2 too low below 35mmhg
-hyperventilation, pulm disease, pregnancy
-renal compensation invloves decreasing exretion of H+ and decreasing reapsorbion of bicarbonate

17
Q

Metabolic Acidosis

A

-nonrespiratory acidosis so not CO2 levels
-indicated by blood bucarboante ion concentration being too low (below 22) so H+ accumulates
-causes: kidney failing to remove H+ from prtoein metabolism, or ketosis from diabetes/dieting
-respiratory compensation by hyperventilating

18
Q

Metabolic Alkalosis

A

-blood bicarb levels too high (above 26) but not because of CO2
-causes = vomitting, diuretic use, excessive intake of alkaline drugs
-respiratory compensation by hypoventilating

19
Q

In Binder Chart

A

on metabolic acidosis from Jan 22

20
Q

Acid-Base Imbalance Diagnosis

A

if acidosis is present:
-respiratory so elevated PCO2
-metabolic so decreased bicarbonate

if alkalosis is present:
-respiratory so reduced PCO2
-metabolic so increased bicarbonate

21
Q

Acid-Base Imbalance in Pregnancy and Birth

A
  1. mother respiratory alkalosis during pregnancy
  2. fetal metabolic or respiratory acidoses in pregnancy
  3. newborn metabolic acidosis and aspyxia (no oxygen so unconscious or dead) during birth process
22
Q

Acid-Base Imbalance in Pregnancy and Birth Continued

A

pregnancy = constant state of respiratory alkalosis due to increased breathing rate
-increased breathing results mainly from progesterone which causes an increased sensitivity to CO2
-pregnancy PCO2 typically around 30 because hyperventilation keeps it low
-renal compensation lowers bicarb

23
Q

Newborn Acid-Base Imbalance

A

-foetal oxygenation and pH generally decline during the course of normal labour due to changes of placental function
-severe asphyxia may cause brain damage

24
Q

APGAR CHART - pull it up

A

-birth asphyxia and hypoxia are related to baby’s appearance and respiratory function is observed by APGAR
-MUST order lab evidence for foetal metabolic acidosis
-low APGAR scores (0-3) longer than 10 minutes correlate to negative neurological outcomes such as cerebral palsy and more
-metabolic acidosis (pH less than 7.00) must be present to define hypoxia
-neonatal neurological unjust can include: seizure, coma and multiorgan failure