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Renal > Acid Base > Flashcards

Acid Base Flashcards

1
Q

What is an acid?

A

substance that can donate H+

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2
Q

What is a base?

A

a substance that can accept H+

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3
Q

What are the 2 types of acids we produce?

A 
carbonic = can be converted to CO2 = can be eliminated in the lungs
non-carbonic = cannot be converted to CO2 = must be excreted in kidney
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4
Q

Carbonic acids are made from the metabolism of ____

A

fats and carbohydrates

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5
Q

Non-carbonic acuds are made from the metabolism of _____

A

proteins and phospholipids

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6
Q

When we’re in a neutral balance, if we make 100 meq of acid, we’ll use 100 meq of _______ to stay stable.

A

bicarbonates

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7
Q

Non-carbonic acids combine with _____ to be excreted by the kidney

A

buffers and anions

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8
Q

What is the clinical pH range?

A

7.8 and 6.8

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9
Q

What measures dissolved CO2 + bicarb conc in venous samples?

A

total CO2 conc

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10
Q

Why is pH outside of 7.8 to 6.8 incompatible with life?

A

bc every enzymes won’t work outside this range

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11
Q

T or F: total CO2 conc always exceeds plasma bicarb conc.

A

True

total CO2 is dissolved CO2 + bicrab

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12
Q

What is the normal bicarb conc?

A

24 mEq/L

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13
Q

What is the difference between acidemia and acidosis?

A

acidemia is a condition and acidosis is a process

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14
Q

What is the equation for the bicarb buffer sys?

A

CO2 + H2O H+ + HCO3-

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15
Q

What is the key extracellular buffer?

A

bicarbonate

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16
Q

Are humans an open or closed system? WHy is this important?

A

open (if we were closed out pH would be 6.1 = death)

*pH based on buffering ability of bicarb

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17
Q

What is the formula for determining pH?

A

(pH) H+ = 24 (CO2) / (HCO3)

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18
Q

What is the H+ when the pH = 7.4?

A

40 nEq/L

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19
Q

What is the trick to determine the H+ from the pH value?

A

80 - last 2 digits of pH to the right of the decimal pt

ex: pH 7.5 = H+ 30 nEq/L

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20
Q

What is the normal pH range?

A

7.35 to 7.45 (or 7.4)

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21
Q

What is the normla pCO2?

A

36-44 mmHg (40 mmHg)

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22
Q

Decreased bicarb is the primary dysfuction in ______

A

metabolic acidosis

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23
Q

Increased bicarb is the primary dysfuction in ______

A

metabolic alkalosis

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24
Q

Metabolic disorders directly alter the conc of _______

A

bicarbonate

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25
Q

Respiratory disorders directly alter ______

A

CO2

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26
Q

Increased CO2 is the primary dysfunction of _______

A

respiratory acidosis

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27
Q

Decreased CO2 is the primary dysfunction of _______

A

respiratory alkalosis

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28
Q

T or F: The effects of bicarbonate as buffer is immediate in onset

A

T

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29
Q

What is the buffer effect in respirators disorders?

A

acidosis: bicarb increases
alkalosis: bicarb decreases

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30
Q

T or F: Buffers completely prevent pH changes.

A

F: they just attenuate, do not completely prevent the pH change

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31
Q

What is the isohydric principle?

A

all buffers change in the same direction

*if you know what one buffer system did (bicarb), you know what they all did

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32
Q

What is the buffer pair of the bicarb system? Where in the body does it act?

A

H+ donor: H2CO3
H+ acceptor: HCO3-

In ECFV

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33
Q

What is the buffer pair in the phosphate system? Where in the body does it act?

A

H+ donor: H2PO4
H+ acceptor: H2PO4 2-

In urine

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34
Q

What is the buffer pair in the ammonia system? Where in the body does it act?

A

H+ donor: NH4+
H+ acceptor: NH3

In urine

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35
Q

What is the buffer pair in the protein system? Where in the body does it act?

A

H+ donor: protein
H+ acceptor: protein

In ICFV

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36
Q

What do the buffer systems in the kidney do?

A

eliminate H+ in urine

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37
Q

What is the role of secondary (compensatory) mechanisms?

A

With a disturbance in pH, we need a whole body response above and beyond the buffer system to bring the pH back toward normal

*it is a second line of defense to maintain normal pH

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38
Q

T or F: compensatory mechanisms are invariable present in simple acid-base disorders.

A

T

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39
Q

What does the absence/dysfunction of a compensatory mechanism imply?

A

the pt has a mixed disorder

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40
Q

The respiratory system compensates for metabolic disrders by _____

A

altering CO2 (via lungs)

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41
Q

How is a respiratory disorder compensated?

A

alter bicarb levels

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42
Q

What is the difference in response time between respiratory compensation mechanisms and metabolic compensation mechanisms

A

the respiratory system can compensate very rapidly by inc CO2 levels when bicarb increases and vice versa

The metabolic compensation in the kidney takes longer

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43
Q

D. Intracellular buffers take longer to take effect, on the order of (mins, hours, days(

A

2-4 hours

44
Q

What is the fastest compensation mechanism?

A

bicarbonate in ECFV

45
Q

What is the 2nd fastest compensation mechanism?

A

change of RR to change CO2 levels in lungs

46
Q

how efficient is the respiratory compensatory mechanism

A

extremely efficient – even tiny changes in the pH, sensed by H+ sensors in the brainstem will result in ventilatory changes

47
Q

Tell whether the following increase or decrease in metabolic acidosis:

pH
HCO3-
pCO2

A

pH: decrease
HCO3-: decrease (primary)
pCO2: decrease (compensatory)

48
Q

Tell whether the following increase or decrease in metabolic alkalosis:

pH
HCO3-
pCO2

A

pH: increase
HCO3-: increase (primary)
pCO2: increase (compensatory)

49
Q

Tell whether the following increase or decrease in respiratory acidosis:

pH
HCO3-
pCO2

A

pH: decreases
HCO3-: increase (compensatory)
pCO2: increase (primary)

50
Q

Tell whether the following increase or decrease in respiratory alkalosis:

pH
HCO3-
pCO2

A

pH: inc
HCO3-: decrease (compensatory)
pCO2: decrease (primary)

51
Q

What are the 3 golden rules of simple acid-base disorders:

A

1) PCO2 and HCO3 always change in the same direction.
2) The secondary physiologic compensatory mechanisms must be present. If not, it’s a mixed disorder
3) The compensatory mechanisms never fully correct pH, they bring toward normal. If they did overcorrect, then it’s a mixed disorder again

52
Q

What is the process that reduces plasma bicarb conc?

A

metabolic acidosis

53
Q

What are the 6 causes of metabolic acidosis?

A
  1. increased acid generation (lactic acid, ketoacid, ingestion of acids)
  2. loss of bicarbonate (GI = diarrhea and intestinal fistulas; Renal = RTA type II)
  3. decreased acid excretion (impaired NH4+ excretion)
  4. renal failure/reduced GFR decreases NH4+ excretion
  5. RTA type I (deficient ATPase and cannot excrete H+)
  6. RTA type IV (hypoaldo)
54
Q

What induces respiratory acidosis?

A

induced by hypercapnia (decreased alveolar ventilation/hypoventialtion) that causes and inc in CO2

55
Q

In term of the buffering mechanisms, what happens during respiratory acidosis?

A

rapid rise in plasma HCO3-

kidney minimizes the change in extracellular pH by inc NH4+ excretion, generating new bicarb ions (slow response, takes 2-3 days)

56
Q

What are some causes of acute respiratory acidosis?

A

anesthesia
seditive overdose
blocked airway

57
Q

What are some causes of chronic respiratory acidosis?

A

COPD
smoking
chronic muscular dystrophy
scoliosis that changes chest wall morphology

58
Q

What process reduces CO3 due to increased alveolar ventilation?

A

respiratory alkalosis

59
Q

Describe the buffering mechanism that goes on during respiratory alkalosis

A

rapid lowering of bicarb
then the kidney responds (1-2 days) by reducing net acid excretion (elim bicarb into the urine or decreases ammonium excretion)

60
Q

What is a process that raises plasma bicarb substantially?

A

metabolic alkalosis

61
Q

What is the etiology of metabolic alkalosis?

A
  1. loss of H+ from GI tract (vomiting)
  2. loss of H+ into urine (loop or thiazide diuretics)
  3. excessive urinary net acid excretion (primary hyeraldosteronism)
62
Q

WHat is the most common cause of chronic respiratory alkalosis?

A

pregnancy

63
Q

What are causes of respiratory alkalosis?

A

acute CNS diseases (stroke, meningitis, or trauma)

acute respiratory alkalosis:
early CHF
pneumonia
pulmonary emboli

64
Q

Acute respiratory acid base disorders always have a greater change in pH than chronic disorders because ….

A

A. Acute respiratory acid base disorders always have a greater change in pH than chronic disorders because the compensatory kidney mechanism is SLOW!!

65
Q

How are respiratory acid base disorders differentiated as acute or chronic?

A

if bicarb conc has changed by…
1-2 mEq = acute
4-5 mEq = chronic

66
Q

T or F: The Na levels (and therefore plasma osmolarity) is directly changed by respiratory acid-base disorders.

A

F: Na is NEVER changed DIRECTLY by acid-base disorders

67
Q

T or F: Plasma Cl- is never directly changed by respiratory acid-base problems.

A

F: plasma Cl- changes inveselt with plasma HCO3 in respiratory acid base disorders

68
Q

T or F: B. Excessive urinary net acid excretion (primary hyperaldosteronism or adrenal adenoma) makes blood progressively alkalemic. Explain.

A

T: bc because aldosterone also influences H+ secretion

69
Q

Excessive urinary net acid excretion (primary hyperalsosteronism) makes blood progressively (acidemic or alkalemic) because aldosterone also influences H+ secretion.

A

alkalemic

70
Q

How can metabolic alkalosis be assc with inc BP or volume explansion?

A

metabolic alkalosis caused by primary hyperaldosteronism bc aldo also regulates Na to inc its reabs. (it also makes blood more alkalemic bc it inc H+ excretion)

71
Q

Whar are the only 2 disorders that cuase a blood sample to have bicarb > 30?

A

metabolic alkalosis and chronic respiratory acidosis (where they kidney is compensating)

72
Q

If someone has metabolic alkalosis, and they have been vomiting/are volume contracted, what will thier urine chloride levels be?

A

low Urine Cl-

73
Q

If someone has metabolic alkalosis, and they are hypervolemic, what do we think the cause of there alkalosis may be?

A

inappropriate secretion of acid into urine (urine Cl- >20 meq/L)

74
Q

If a person has metabolis alkalosis due to primary hyperaldosteronism, will TB C- be low or high? Will giving them NaCl and water be helpful?

A

they would have excess total body Cl an giving them NaCl and water would not be helpful

75
Q

What does urine Cl tell you?

A

if a person has metabolic alkalosis,

Cl- responsive (giving them saline will fix the problem) have urine Cl 20 meq/l

76
Q

Describe how bicarb is reabsorbed

A

90% of FL of bicarb is reabs in the PCT:
*Na going in (via Na:H antiport) is the driving force

CO2 to diffuses into the cell or it enters via aquaporin 1 channels
CO2 combines with OH to form HCO2 via carbonic anahydrase which is then moved into ISF via Na-HCO3-CO3- cotransporter

77
Q

Low pH drives bicarb reabs to (inc or decrease)

A

increase

78
Q

High pH drives bicarb reabs to (inc or decrease)

A

decrease

79
Q

What drugs blocks carbonic anahydrase enzyme?

A

acetazolamide

80
Q

If a pt is taking acetazolamide, how could their pH be affected?

A

it blocks this Carbonic Anhydrase enzyme which will decrease the bicarb that is able to be reabs –> pH will decrease bc there will be less bicarb in the plasma to buffer it

81
Q

acetazolamide will block the reabs of …

A

Na and bicarb

82
Q

T or F: we absorb all of the bicarb that the kidney makes

A

T

83
Q

T or F: for every new molecule of bicarb that is made, a proton is excreted into the urine

A

T

84
Q

What transporter secretes bicarb into the urine?

A

Cl-/bicarb

85
Q

When do the H+:K+ ATPase perform more efficiently?

A

acidemia or excess also

86
Q

What cells secrete bicarb (into urine)? What part of the nephron are they found?

A

beta-intercalated cell of the cortical collecting duct

87
Q

What role the alpha intercalated cells play in renal acid-base balance?

A

they secrete H+ into the urine via H:K ATPase and make bicarb that is absorbed into the ISF thru bicarb:Cl- antiports

88
Q

What type of cells do strict vegetarians have more of? Why?

A

Beta intercalated cells because their diet is more alkaline and therefore need to get rid of more HCO3- so that it doesn’t bind up the H+ they have

89
Q

Describe the movement of Na in the principal cell.

A

lumen –> epithelial cell –> ISF

Na channel —> Na:K ATPase –>

90
Q

What drugs and hormones work at the principal cells?

A

Amiloride and Triamterene inhibit the luminal Na channel here.
Aldosterone also works here.
Spironolactone and Epleronone (competitive antagonists of aldosterone) work on the blood side.

91
Q

What are the 2 fates of the anions from strong acids (that fully dissociates at physiological pH)?

A

excretedf into the urine (creates normal plasma anion gap with inc plasma Cl-)

A- is reabs as an unmeasured anion (inc plasma anion gap, minimal change in plasma Cl-)

92
Q

Why does Cl- stay they same when bicarb drops to buffer lactate when its present from poor perfusion?

A

because electroneutrality is maintained (the bicarb combined with equal amts of lactate to maintain neutrality in the body)
* but there wil be an inc AG to 20

93
Q

Why does urine Cl- drop when bicarb is lost in the stool?

A

When bicarb is lost in the stool, electroneutrality is no longer balanced. Therefor`e, Cl- needs to be reabsorbed to maintain electro- homeostasis

(loss of bicarb = “there is no unmeasured anion so to keep elecroneutrality, so the kidney has to reabsorb more Cl-“

94
Q

What do increases in the plasma anion gap from the normal value of10 -12 meq/l clinically reflect?

A

increased circulating unmeasured anions in the plasma.

95
Q

What are the major causes of increased antion gap (with metabolic acidosis)?

A
  1. renal failure
  2. lactic acidosis
  3. ketoacidosis
  4. Ingestions of aspirin, ethylene glycol, methanol
96
Q

What are the 3 major causes of normal gap metabolic acidosis?

A
  1. RTA
  2. diarrhea
  3. some cases of chronic renal failure
97
Q

Describe the assessment of low seum bicarb conc

A
  1. check arterial blood gases to exclude chronic respiratory alkalosis
  2. calculate serum AG
  3. raised AG= lactic acidosis
    diabetic acidosis
    alcoholic acidosis
    starvation ketoacidosis
    poisoning
    uremic acidosis
  4. normal AG –> calculate urine AG
  5. positive UAG = RTA/problem with kidney acidification
  6. negative UAG = GI bicarb losses (diarrhea)
98
Q

How is phosphate homeostasis maintained?

A

urinary excretion of dietary phosphate

99
Q

What is an effective urinary buffer?

A

monobasic phosphate

100
Q

How much H+ is excreted with phosphate daily?

A

10 - 40 meq

101
Q

What is most frequently increased to handle an increased acid load/physiological needs?

A

ammonium

102
Q

NH4+ is ______ which is why it is trapped in the urine

A

lipid insoluble

103
Q

Looking at two people, one with a low GFR and one with a normal GFR.

If you give them both an acid load, there’s only a slight drop in bicarb in the healthy person compared to a steep drop in plasma bicarb in the pt with the lower GFR. Why?

A

because the healthy person can drastically increase the NH4+ excretion they do not become acidotic. The person with the impaired GFR cannot secrete NH4+ as well

104
Q

How is SIADH different than acid base disorders?

A

both Na and Cl would decreas (proportionally) in SIADH

it is acid base when Na is constant and Cl- is out of whack

105
Q

Describe the law of electroneutrality.

A

Na conc is NOT directly altered by acid-base disorders
plasma Cl- is altered in all acod-base disorders (except inc SAG met acidosis)

Therefore, if Na cocn stays constant but Cl-conc changes, an acid base disorder is present

Renal (33 decks)

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