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PSIO EXAM 3 > acid base notes > Flashcards

acid base notes Flashcards

1
Q

what is acid base balance

A

maintenance of Hydrogen concentration in extras cellular fluids

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2
Q

why is HCL a stronger acid

A

more Hydrogen concentration is liberated

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3
Q

gastric HCL pH

A

.8

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4
Q

pancreatic juice pH

A

8.0

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5
Q

maximal urine acidity pH

A

4..5

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6
Q

arterial blood pH

A

7.45

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7
Q

venous blood pH

A

7.35

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8
Q

principal extracellular buffer

A

HCO3-

acid version is H2CO3

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9
Q

As long as respiration keeps pace with metabolism, there is no

A

gain or loss of H+

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10
Q

Respiratory Acidosis and Alkalosis begin in

A

the lung

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11
Q

Metabolic Acidosis and Alkalosis begin with

A

HCO3- blood abnormalities

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12
Q

decrease in HCO3- Can result from

A

gain in fixed acid

or loss of HCO3- from kidney or GI track

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13
Q

decrease in HCO3- Can is called

A

Metabolic acidosis

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14
Q

metabolic acidosis sequence of everts

A

there is a gain of fixed acid and an accumulation of H+, this results in buffering in which the excess H is buffered by HCO3 which produces a decrease in HCO3- and pH

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15
Q

gain in fixed acid

A

most often the cause
can be a result of
increased production (lactic acid, ketoacids)
ingestion (salicylic acid)
or the inability to excrete fixed acid from the metabolism

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16
Q

metabolic acidosis response

A

hyperventilation to decrease the concentration of CO2
if we decrease CO2 we should be able to shift the eq right and decrease H concentration and raise the concentration of HCO3

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17
Q

Calculating Anion Gap

A

AG = [Na+] – ([HCO3-] + [Cl-])

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18
Q

normal anion gap value

A

12 plus minus 4

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19
Q

if an unmeasured anion is present

A

the serum gap is increased

ex Lactate, salicylate, protein, phosphate, sulfate, citrate

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20
Q

Hyperchloremic metabolic acidosis

A

concentration of Cl- will increase to replace lost HCO3- (both negatively charge, concentration gradient) and the serum anion gap will appear normal

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21
Q

Disorders that increase the AG generate

A

non-volatile acids (lactic acid, etc.) which reduce HCO3- concentrations, which is the opposite of what we want
H+ from non-volatile acids neutralizes some Bicarb

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22
Q

causes of high anion gap

A 
Methanol
Uric Acid (Uremia)
DKA
Propylene glycol (vehicle for IV infusions)
Iron Tablets
Lactic acid
Ethylene glycol
Salicylates
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23
Q

causes of normal anion gap

A

Renal Tubular Acidosis (RTA Type 2)
GI Bicarbonate Loss (Diarrhea)

reduction in concentration of HCO3-

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24
Q

In some types of metabolic acidosis, an organic anion is increased

A

Since it is acidosis, HCO3- is decreased, but this is offset by an increase in unmeasured organic anions
Occurs in diabetic ketoacidosis, lactic acidosis, salicylate poisoning, methanol poisoning and chronic renal failure.

25
Q

Normally, ketoacids are oxidized to

A

CO2 and water, with CO2 eliminated through ventilation

26
Q

DKA

A

production of ketoacids exceeds oxidative capacity and they accumulate
Ketoacids dissociate in blood, yielding carboxylate anion and H+

27
Q

DKA chemically

A

H+ reacts with HCO3- , reducing HCO3-, and increasing CO2.

28
Q

peripheral chemoreceptors in DKA

A

increased ventilation to initiate a compensatory fall in PCO2

29
Q

Pulmonary compensation

A

Involves peripheral and central chemoreceptors that control the rate of ventilation

30
Q

DKA treatment

A

I.v. fluids and insulin, K+ level monitored to watch from correction of hyperkalemia with the treatment

31
Q

diarrhea

A

metabolic acidosis
Diarrheal fluid has a high concentration of HCO3-
Under normal conditions, the luminal Na+/H+ exchanger in the jejunal absorbs sodium bicarbonate and stool has small amounts of bicarbonate.
development of diarrhea and increased stool volume and several hundred millimoles of bicarbonate may be lost on a daily basis.

32
Q

Secretory Diarrhea

A

metabolic acidosis
HCO3- is also secreted but acid in colon produced by bacteria is neutralized; stool pH near neutral
The Cl- that is secreted from the crypts in the intestine stimulates the Cl-/HCO3- transporter but we have a loss a lot of HCO3 so the IC HCO3 will leave and move in CL
This transporter will reabsorb the Cl- while secreting the HCO3.
Thus, the patient ends up with a hyperchloremic metabolic acidosis due to the loss of HCO3 that can only be replaced by adding new HCO3 made by the kidney. So, while there is CL- secretion from the crypts, some of this Cl- gets reabsorbed, while the major secretory anion ends up being HCO3.

33
Q

Metabolic Alkalosis caused by

A 
by an increase in HCO3- 
Can result from:
Loss in fixed acid  (Most often the cause!)
Loss from GI tract (vomiting)
Loss from kidney (hyperaldosteronism)
or gain of HCO3 (ingestion of NaHCO3)
34
Q

vomiting sequence

A

loss of fixed acids, loss of H+, this causes bicarbonate that would normally be removed from blood and added to GI tract to neutralize HCL and remains in the blood causing an increase pH

35
Q

metabolic alkalosis response

A

hypoventilation to increase CO2 and H+

36
Q

why does vomiting cause hypokalemia

A

vomiting causes a loss of gastric HCl, in the ECF volume contraction aldosterone is increased so K+ secretion out of the cell is also increased and results in hypokalemia

37
Q

respiratory alkalosis response

A

decrease the H+ excretion in urine and decrease the HCO3- production to overall increase the H+ concentration and stop hyperventilation

38
Q

Metabolic rules for compensatory responses

A

acidosis 1.3

alkalosis .7

39
Q

respiratory acidosis acute and chronic rules for compensatory responses

A

.1, .4

40
Q

respiratory alkalosis acute and chronic rules for compensatory responses

A

.2, .4

41
Q

Secondary responses to respiratory disorders involves the

A

kidneys altering plasma HCO3 conctraion by altering the excretion of H+ but this take 2 to 3 days

42
Q

Secondary responses to metabolic disorders involves

A

changes in the rate of ventilation which is a quick response

43
Q

Renal Mechanisms in Acid/Base Balance

A

Reabsorption of HCO3-
Excretion of H+
Excretion is accompanied by synthesis and reabsorption of new HCO3-

44
Q

Excretion of H+

A

Excreted as titratable acid (buffered by urinary phosphate)

Excreted as NH4+

45
Q

ynthesis and reabsorption of new HCO3-

A

This replenishes the HCO3- stores that were used in buffering H+

46
Q

Renal Response Diabetic Ketoacidosis

A

Arterial H+ is elevated
Na+-H+-exchanger in proximal tubule is active to dump H+
Plasma HCO3- is low, thus all filtered HCO3- is reabsorbed
Additional HCO3- needs to be generated since HCO3- is low to begin with.
H+ needs to be excreted through titratable acid and NH3. Both will be stimulated, and as H+ is excreted, HCO3- will be added to the blood.
When the entire acid load has been excreted, HCO3- will be restored to normal and the acid base status will be normal.

47
Q

NH3 diffusion/ collecting duct

A

NH3diffusesfrom its high concentration in the medullary interstitial fluid into the lumen of the collecting duct
Combines with the secreted H+to form NH4+
NH4+is not lipid soluble and thus is trapped in the tubular fluid and excreted

48
Q

Thick Ascended limb Reabsorption of NH4+

A

Reabsorption occurs via the tri-transporter, where NH4+ substituted in for K+.

In the less acidic tubular cell, NH4+ dissociates to NH3 and H+ and NH3 diffuses to the medullary ISF

49
Q

Proximal tubuleNH4+is secretion

A

Glutaminase metabolizes glutamineto glutamate andNH4+
Glutamate is metabolized toα-ketoglutarate, which is ultimately metabolized to CO2and H2O and then to HCO3− (which we need)
NH3diffuses from cell to lumen, and the H+is secreted into the lumen on the Na+-H+exchanger.
NH3and H+recombine into NH4+

50
Q

Acidosis and hypokalemia stimulate

A

glutamine catabolism allowing new HCO3-to neutralize blood.

51
Q

Excretion of H+ as NH4+

A

Three segments of the nephron are involved

52
Q

HCO3- Reabsorption in the Proximal Tubule

A

99.9% of filtered HCO3- is reabsorbed

Ensures that this major extracellular buffer is conserved rather than excreted

53
Q

Most filtered HCO3- reabsorbed

A

in proximal tubule

54
Q

Excretion of H+ as Titratable Acid

A

H+excreted with urinary buffers
Inorganic phosphate is the most important of these buffers
85% of the filtered phosphate is reabsorbed; 15% of the filtered phosphate is left to be excreted as titratable acid

Both H+-ATPase and H+-K+-ATPase secrete H+
Secreted H+ reacts with a phosphate anion (HPO42-) and is then excreted as titratable acid (H2PO4)
For each H+excreted as titratable acid, onenewHCO3−is synthesized and reabsorbed

55
Q

The H+secreted is produced in the renal cells from

A

CO2 and H20

use the carbonic anhydrase enzyme

56
Q

Maintenance of Metabolic Alkalosis Chloride depletion

A

Cl- lost in gastric fluid; if NaCl not replaced, Na+ conservation takes place, increasing HCO3- reabsorption in PT
Na+ reabsorbed distally (via aldosterone

57
Q

Maintenance of Metabolic Alkalosis K+ depletion

A

Causes K+ to leave cells

58
Q

Maintenance of Metabolic Alkalosis ECF volume contraction

A

Reduced filtered load of HCO3-

59
Q

Sustained mineralocorticoid excess

A

occurs from maintenance of metabolic alkalosis

PSIO EXAM 3 (8 decks)

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