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RENAL > VII: Acid-Base Disorders > Flashcards

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

A

8-12mEq/L

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
Q

Renal compensation in metabolic acidosis

A

Takes a few days
H+ is excreted as titrable NH4+
New HCO3- synthesized

26
Q

Metabolic alkalosis loss of fixed acid

A

H+ loss from stomach

HCO3- is not stimulated so it stays in blood, HCO3- increase

27
Q

Buffering in ECF and ICF in metabolic alkalosis

A

H+ leaves the cells so K+ enters = hypokalemia

28
Q

Respiratory compensation in metabolic alkalosis

A

Hypoventilation = increased arterial pressure

To increase pCO2

29
Q

Renal correction in metabolic alkalosis

A

HCO3- excreted in urine to decrease [HCO3-] in blood

30
Q

What is complicated about HCO3- excretion during vomiting

A

There is ECF volume contraction which is causing reabsorbtion

31
Q

During ECF depletion (a.k.a vomiting) what happend

A

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
Q

K+ seccretion during ECF contraction can cause

A

Hypokalemia

33
Q

Main cause of repsiratory acidosis

A

Increase in pCO2 due to hypoventilation

34
Q

Buffering in respiratory acidosis mainly by

A

RBC in ICF

35
Q

Renal correction in respiratory acidosis

A

Increase in H+ excretion as NH4+

Increase in HCO3- synthesis

36
Q

Main cause of respiratory alkalosis

A

Loss of CO2 from hyperventilation

37
Q

Buffering in respiratory alkalosis

A

In ICF by RBC

CO2 out of cell to increase concentration

38
Q

Renal compensation in respiratory alkalosis

A

Decrease in H+ excretion

Decrease in HCO3- synthesis

RENAL (9 decks)

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