VII: Acid-Base Disorders Flashcards

1
Q

Respiratory disorder due to

A

pCO2

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2
Q

Metabolic disorder due to

A

[HCO3-]

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3
Q

Metabolic acidosis HCO3- and pH

A

Low [HCO3-] and low pH

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4
Q

Compensation of metabolic acidosis (pCO2)

A

Hyperventilation to eliminate CO2 (decreased pCO2)

Kidney will compensate to increase HCO3- but it will take longer

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5
Q

Metabolic alkalosis

A

High [HCO3-] and high pH

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6
Q

Compensation for metabolic alkalosis

A

Hypoventilation to keep the CO2 (increase pCO2)

Kidney will secrete HCO3- to decrease its concentration in blood

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7
Q

Respiratory acidosis pCO2 and pH

A

High pCO2 and low pH

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8
Q

Compensation for respiratory acidosis

A

Synthesize more HCO3-

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9
Q

Cause of respiratory acidosis

A

Hypoventilation causing CO2 retention

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10
Q

Respiratory alkalosis

A

Low pCO2 and high pH

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11
Q

Compensation for respiratory alkalosis

A

Kidney will stop producing HCO3-

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12
Q

Cause of respiratory alkalosis

A

Hyperventilation causing CO2 loss

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13
Q

Mechanisms to maintaining blood pH in normal range

A

ICF and ECF buffers (HCO3-)
Respiratory compensation
Renal compensation

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14
Q

Use of anion gap of plasma

A

In diagnosis of acid-base disorders

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15
Q

Bases of anion gap

A

[cations] must equal [anions]
Na+ HCO3- and Cl-
So any unmeasured anions will make up for the “gap”

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16
Q

Calculation of plasma anion gap

A

[Na+] - ([HCO3-] - [Cl-])

17
Q

Normal range of anion gap

18
Q

During metabolic acidosis, what happens to the anion gap

A

There is a loss of [HCO3-] and because the system has to be in equilibrium, there will be an unmeasured anion replacing the lost HCO3-

19
Q

Anion gap increased during

A

Diabetic ketoacidosis

Lactic acidosis

20
Q

If HCO3- replaced by Cl-

A

Hyperchloremic

21
Q

Main cause of metabolic acidosis

A

Gain of non-volatile H+

22
Q

Buffering of H+ excess by HCO3-

A

In ECF, HCO3- has decreased so there is buffering in ICF of H+ with organic anions or K+
Use of K+ to buffer can cause hyperkalemia

23
Q

Respiratory compensation of metabolic acidosis

A

Hyperventilation to decrease pCO2

24
Q

Consequence of hyperventilation in arterial pressure

A

Arterial pressure drops

25
Renal compensation in metabolic acidosis
Takes a few days H+ is excreted as titrable NH4+ New HCO3- synthesized
26
Metabolic alkalosis loss of fixed acid
H+ loss from stomach | HCO3- is not stimulated so it stays in blood, HCO3- increase
27
Buffering in ECF and ICF in metabolic alkalosis
H+ leaves the cells so K+ enters = hypokalemia
28
Respiratory compensation in metabolic alkalosis
Hypoventilation = increased arterial pressure | To increase pCO2
29
Renal correction in metabolic alkalosis
HCO3- excreted in urine to decrease [HCO3-] in blood
30
What is complicated about HCO3- excretion during vomiting
There is ECF volume contraction which is causing reabsorbtion
31
During ECF depletion (a.k.a vomiting) what happend
Increase in HCO3- reabsorption Increase in angiotensin II to increase Na+/H+ exchange and HCO3- reabsorption Increase in aldosterone for H+ secretion, HCO3- reabsorption and K+ secretion
32
K+ seccretion during ECF contraction can cause
Hypokalemia
33
Main cause of repsiratory acidosis
Increase in pCO2 due to hypoventilation
34
Buffering in respiratory acidosis mainly by
RBC in ICF
35
Renal correction in respiratory acidosis
Increase in H+ excretion as NH4+ | Increase in HCO3- synthesis
36
Main cause of respiratory alkalosis
Loss of CO2 from hyperventilation
37
Buffering in respiratory alkalosis
In ICF by RBC | CO2 out of cell to increase concentration
38
Renal compensation in respiratory alkalosis
Decrease in H+ excretion | Decrease in HCO3- synthesis