Acid Base Homeo Flashcards

(52 cards)

1
Q

Three primary systems that regulate H concentration

A
1 chemical acid-base buffer system of body fluids (combine with acid or base to prevent excessive changes in H concentration)
2 respiratory center (removal of CO2 and carbonic acid)
3 kidneys (excrete and adjust H ion conc)
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2
Q

H concentration is kept at a low level in the ecf bec

A

All activities of enzyme system in the body are influenced by H.

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3
Q

pH and relationship with H ion

A

pH is inversely proportional to the H concentration

Low pH High H concentration
High pH Low H concentration

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4
Q

pH =

A

pH = -log [H]

pH = log 1/[H] = -log[H]

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5
Q

Any substance that can reversibly bind H

A

Buffer

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6
Q

How are buffers able to minimize H conc

A

When H conc increases, the reactions goes to the right more H ions binding with buffer to make a weak acid as long as the buffer is available.

When the H concentration decreases, the reaction shifts toward the left and H is released from buffer.

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7
Q

Bicarbonate buffer system 2 ingredients

A

1 weak acid H2CO3

2 bicarbonate salt NaHCO3

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8
Q

Carbonic acid is formed by reaction

by the enzyme

A

CO2 + H2O <=> H2CO3

Carbonic anhydrase

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9
Q

Carbonic anhydrase is present in

A

Walls of lung alveoli

Epithelial cell of renal tubules

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10
Q

H2CO3 is a buffer bec it can ionize quickly to form

A

H2CO3 <=> H + HCO3

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11
Q

NaHCO3 is also a buffer in the ECF bec it ionizes quickly to form

A

NaHCO3 <=> Na + HCO3

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12
Q

Bicarbonate buffer system equation

A

CO2 + H2O <=> H2CO3 <=> H + HCO3 + Na

Weak dissociation of carbonic acid yields few H conc

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13
Q

Adding strong acid to the bicarbonate buffer solution is buffered by

yielding greater amounts of H2O and CO2.

Elimination of CO2 from ECF is by

A

HCO3

respiration (hypervent)

The opposite occurs if a strong base is added. There will be dec CO2 and inc HCO3 that is compensated by inc renal excretion of HCO3.

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14
Q

Henderson Hasselbach =

A

pH = 6.1 + log HCO3/0.03xPCO2

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15
Q

Henderson Hasselbach calculates

A

pH of soln if the molar concentration of HCO3 and PCO2 are known

defines determinants of normal pH regulation and acidbase balance of ECF

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16
Q

Increase in HCO3 causes

Inc in PCO2 causes

A

pH to rise shifting acid base balance toward alkalosis

pH to decrease shifting acid-base balance toward acidosis

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17
Q

HCO3 is regulated mainly by

PCO2 is controlled by

A

Kidneys

Rate of respiration

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18
Q

When two components of buffer system are equal, the pH according to the Henderson-Hasselbach is

A

equal to pK (dissociation constant) 6.1 of bicarbonate buffer system

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19
Q

Buffer power is determined by

A

Amount and

relative concentration of buffer component

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20
Q

The buffer system is most effective when

region in titration curve

A

pH is near the pK

center

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21
Q

Most important extracellular buffer

A

Bicarbonate buffer system

22
Q

Phosphate buffer system is important in tubular fluids and kidneys and ICF bec

A

1 phosphate becomes greatly concentrated in tubules inc buffering power of phosphate system
2 tubular fluid has low pH than ECF bringing operating range of buffer close to pK 6.8 of system

23
Q

In RBCs hemoglobin is a buffer:

A

H + Hb <=> HHb

24
Q

60-70% of chemical buffering of body fluids inside the cell is a result of

A

intracellular protein buffer

but delayed due to slow diffusion of Bicarbonate and H through cell to buffer ECF

25
Whenever there is change in H concentration in ECF, balance of all buffer systems change at same time.
Isohydric Principle Any condition changing the balance of one buffer system changes the balance of others bec the buffer actually buffers one another by shifting H back and forth.
26
Non volatile acids from protein metabolism are so
Bec they are not excreted by lungs not H2CO3
27
Reduction in ECF H concentration causes failure of kidney to
reabsorb filtered HCO3 | inc excretion of HCO3 to raise H conc back to normal
28
Kidneys regulate ECF H conc through 3 mechanims
secretion of H reabsorption of filtered HCO3 production of new HCO3
29
80-90-% bicarb reabsorption and H secretion occurs in H secretion and bicarb reab occur in all parts of the tubules except
PCT thin limbs LOH
30
H is secreted in PCT, thick ascending LOH and early DT by
Na-H counter transport | Secondary active transport
31
H secretion and HCO3 reabsorption:
CO2 diffuses or formed by metabolism in tubular epithelial cell CO2 + H2O by carbonic anhydrase into carbonic acid Then dissociates into H and HCO3 H is secreted from cell into lumen by Na-H exchanger Na moves into cell and H moves out into lumen The HCO3 in the cell moves downhill at the basolateral membrane into interstitial fluid and peritubular capillary Net result: for every H secreted into lumen, a bicarb entes the blood
32
Transport of bicarbonate across basolateral membrane is facilitated by
1 NaHCO3 co transport in PCT | 2 Cl-HCO3 exchange in late segment of PCT abs TAL, CT, CD
33
Each time a H is formed in tubular epithelial cell,
a bicarb is formed and released back into the blood
34
During acidosis excess H is buffered in tubules by
phosphate | ammonia
35
In distal tubule and cd tubular epithelium intercalated cells secretes H by
active transport by H-transporting ATPase
36
In acidosis, excess H supposedly excreted in the tubule when all HCO3 are exhausted is combined with
Phosphate and ammonia buffers to generate new HCO3 helping replenish lost HCO3 or excreted as Na salt NaH2PO4 carrying excess H
37
Ammonia in kidney comes from
glutamine for each molecule of glutamine in PCT two ammonia are secreted in urine and two bicarbonate are reabsorbed into blood
38
In the collecting duct, ammonia buffering
for each ammonia excreted a new HCO3 is generated and added to the blood
39
With chronic acidosis, the dominant mechanism by which acid us eliminated is
excretion of ammonia also most important mechanism of generatinf bicarb in chronic acidosis
40
Inc H secretion and HCO3 reabsorption
``` Inc PCO2 inc H Dec HCO3 Dec extracellular fluid Inc angiotensin II Inc aldosterone Hypokalemia ```
41
Dec H secretion and HCO3 reabsorption
``` Dec PCO2 Dec H and Inc HCO3 Inc ECF Dec Angiotensin II Dec Aldosterone Hyperkalemia ```
42
In metabolic acidosis, the compensations
1 inc ventilation rate dec PCO2 | 2 renal comp by adding HCO3 to ECF
43
In respi alkalosis, primary compensation:
1 reduction in plasma HCO3 by renal excretion
44
In metabolic alkalosis, primary compensation:
1 dec ventilation raising PCO2 | 2 inc renal excretion of HCO3
45
Renal tubular acidosis (Metabolic Acidosis) assoc d/o
1 chronic renal f 2 Addison’s disease dec aldosterone 3 Fanconi
46
Most frequent cause of metab acidosis
Diarrhea bec of large amounts of sodium bicarb excretion in feces
47
Ingestion of acids contribute to formation of metabolic acidosis
Aspirin | Methyl alcohol lambanogz
48
Diuretics except CA inhibitors cause metabolic alkalosis bec
Inc fluid flow in tubule promotes Na reabsorption which is coupled with H sec and inc bicarb reabsorption Also aldosterone excess (Conn’s)
49
Anion gap formula
Anion gap = Na - (Cl + HCO3)
50
Anion gap inc if
unmeasured anions rise (albumin, phosphate, sulfate) unmeasured cations fall (Ca, Mg, K) N= 8-16
51
Metabolic acidosis with Normal Anion Gap 4
diarrhea renal tubular acidosis carbonic anhydrase inhibtors addison’s
52
Metabolic Acidosis with inc anion gap normochloremia
``` DM Lactic acidosis Chronic renal failure Aspirin poisoning Methanol poisoning Ethylene glycol Starvation ```