Acid Base Homeo Flashcards

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
Q

Whenever there is change in H concentration in ECF, balance of all buffer systems change at same time.

A

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
Q

Non volatile acids from protein metabolism are so

A

Bec they are not excreted by lungs not H2CO3

27
Q

Reduction in ECF H concentration causes failure of kidney to

A

reabsorb filtered HCO3

inc excretion of HCO3 to raise H conc back to normal

28
Q

Kidneys regulate ECF H conc through 3 mechanims

A

secretion of H
reabsorption of filtered HCO3
production of new HCO3

29
Q

80-90-% bicarb reabsorption and H secretion occurs in

H secretion and bicarb reab occur in all parts of the tubules except

A

PCT

thin limbs LOH

30
Q

H is secreted in PCT, thick ascending LOH and early DT by

A

Na-H counter transport

Secondary active transport

31
Q

H secretion and HCO3 reabsorption:

A

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
Q

Transport of bicarbonate across basolateral membrane is facilitated by

A

1 NaHCO3 co transport in PCT

2 Cl-HCO3 exchange in late segment of PCT abs TAL, CT, CD

33
Q

Each time a H is formed in tubular epithelial cell,

A

a bicarb is formed and released back into the blood

34
Q

During acidosis excess H is buffered in tubules by

A

phosphate

ammonia

35
Q

In distal tubule and cd tubular epithelium intercalated cells secretes H by

A

active transport by H-transporting ATPase

36
Q

In acidosis, excess H supposedly excreted in the tubule when all HCO3 are exhausted is combined with

A

Phosphate and ammonia buffers to generate new HCO3 helping replenish lost HCO3

or excreted as Na salt NaH2PO4 carrying excess H

37
Q

Ammonia in kidney comes from

A

glutamine

for each molecule of glutamine in PCT two ammonia are secreted in urine and two bicarbonate are reabsorbed into blood

38
Q

In the collecting duct, ammonia buffering

A

for each ammonia excreted a new HCO3 is generated and added to the blood

39
Q

With chronic acidosis, the dominant mechanism by which acid us eliminated is

A

excretion of ammonia

also most important mechanism of generatinf bicarb in chronic acidosis

40
Q

Inc H secretion and HCO3 reabsorption

A
Inc PCO2 inc H
Dec HCO3
Dec extracellular fluid
Inc angiotensin II
Inc aldosterone
Hypokalemia
41
Q

Dec H secretion and HCO3 reabsorption

A
Dec PCO2
Dec H and Inc HCO3
Inc ECF
Dec Angiotensin II
Dec Aldosterone
Hyperkalemia
42
Q

In metabolic acidosis, the compensations

A

1 inc ventilation rate dec PCO2

2 renal comp by adding HCO3 to ECF

43
Q

In respi alkalosis, primary compensation:

A

1 reduction in plasma HCO3 by renal excretion

44
Q

In metabolic alkalosis, primary compensation:

A

1 dec ventilation raising PCO2

2 inc renal excretion of HCO3

45
Q

Renal tubular acidosis (Metabolic Acidosis) assoc d/o

A

1 chronic renal f
2 Addison’s disease dec aldosterone
3 Fanconi

46
Q

Most frequent cause of metab acidosis

A

Diarrhea bec of large amounts of sodium bicarb excretion in feces

47
Q

Ingestion of acids contribute to formation of metabolic acidosis

A

Aspirin

Methyl alcohol lambanogz

48
Q

Diuretics except CA inhibitors cause metabolic alkalosis bec

A

Inc fluid flow in tubule promotes Na reabsorption which is coupled with H sec and inc bicarb reabsorption

Also aldosterone excess (Conn’s)

49
Q

Anion gap formula

A

Anion gap = Na - (Cl + HCO3)

50
Q

Anion gap inc if

A

unmeasured anions rise (albumin, phosphate, sulfate)
unmeasured cations fall (Ca, Mg, K)

N= 8-16

51
Q

Metabolic acidosis with Normal Anion Gap 4

A

diarrhea
renal tubular acidosis
carbonic anhydrase inhibtors
addison’s

52
Q

Metabolic Acidosis with inc anion gap normochloremia

A
DM
Lactic acidosis
Chronic renal failure
Aspirin poisoning
Methanol poisoning
Ethylene glycol 
Starvation