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Fall 2024 > Therapeutics Exam 3 (Acid/Base) > Flashcards

Therapeutics Exam 3 (Acid/Base) Flashcards

1
Q

What is a normal physiological pH?

A

7.35-7.45

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2
Q

Acid-Base disorders fall into what 2 categories?

A

Metabolic
Respiratory

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3
Q

Kidney/Metabolic acid-base disorders refer to which 2 ions?

A

H+ and HCO3-

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4
Q

Lungs/Respiratory acid-base disorders refer to which 2 ions?

A

CO2 and H2O

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5
Q

Which type of acid-base disorder is easier to overcome? Metabolic or Respiratory?

A

Metabolic
-the lungs compensate much faster than the kidneys
-compensation for a disorder comes from the OPPOSITE SIDE

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6
Q

What is a normal PaCO2 value?

A

35-45 mmHg (40)

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7
Q

What is a normal HCO3 value?

A

22-26 meq/L (24)

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8
Q

What is a normal PaO2 value?

A

95-100 mm Hg

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9
Q

What is a normal SaO2 value?

A

> or = 95%

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10
Q

What are the consequences of acidemia?

A

Cardiac: Decreased output, Impaired contractility, Increased pulmonary vascular resistance

Metabolic: Insulin resistance, Inhibition of anaerobic glycolysis, *Hyperkalemia

CNS: Coma, Altered mental status

Other: Decreased respiratory muscle strength, hyperventilation, dyspnea

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11
Q

What are the consequences of alkalemia?

A

Cardiac: Decreased coronary blood flow, Arteriolar constriction, Anginal threshold, Arrhythmias

Metabolic: *Hypokalemia, Low Ca, Low Mg, Stimulation of anerobic glycolysis

CNS: Decreased cerebral blood flow, Seizures

Other: Decreased respirations

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12
Q

Where does acid come from?

A

Diet (1 mEq/day consumed)

Aerobic metabolism of glucose

Nonvolatile acid formation
-Anaerobic metabolism, Triglyceride oxidation, Metabolism of sulfur-containing amino acids and phospholipids

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13
Q

What are the 3 mechanisms of acid regulation?

A

Buffering
Renal regulation
Ventilatory regulation

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14
Q

What is the body’s first line of defense for acid regulation?

A

Extracellular/Intracellular buffering systems

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15
Q

What are the 3 main buffers in the body?

A

Bicarb/Carbonic Acid
Phosphate
Proteins

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16
Q

What is the principle buffer in the body?

A

Bicarbonate

*present in the largest concentration extracellularly over any of the other buffers

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17
Q

What happens when acid is added to your system?

A

HCO3- picks up H+ and becomes H2CO3 (carbonic acid)

H2CO3 dissociates to CO2 and H2O

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18
Q

How much new bicarb needs to be ingested by the body each day?

A

The body needs new bicarb added to the system in an amount that is equivalent to the H+ load ingested every day

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19
Q

What properties do phosphates have as a buffer?

A

Intermediate onset and capacity

-Slower
-Not as many available compared to bicarb

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20
Q

What properties do proteins have as buffers?

A

Rapid onset
Limited capacity

*very quick but limited
–more effective intracellularly than extracellularly

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21
Q

What are the 2 main purposes of the kidneys?

A
  1. Reabsorb filtered bicarb
  2. Excrete H+ ions released from nonvolatile acids (help regenerate new bicarb through hydrogen excretion)
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22
Q

How much bicarb gets reabsorbed by the body?

A

*Body is supposed to reabsorb all bicarb daily
-should have virtually none present in the urine

*Bicarb is also reabsorbed with no net loss of H+

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23
Q

Where does bicarb reabsorption take place?

A

85-90% is reabsorbed in the proximal tubule

10-15% is reabsorbed via distal tubule or collecting duct

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24
Q

Which enzyme is responsible for the dissociation of carbonic acid to for H2O + CO2?

A

Carbonic anhydrase

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25
Q

H+ Is excreted into the urine/tubular lumen in exchange for what?

A

Na+

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26
Q

How do bicarbonate losses in the urine occur?

A

When anything limits H+ secretion into the proximal tubule lumen and bicarb is not able to convert to carbonic acid, then to H2O + CO2 and get reabsorbed

-ex: carbonic anhydrase inhibitors

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27
Q

How do carbonic anhydrase inhibitors work?

A

-Inhibit activity of carbonic anhydrase
-Carbonic acid is not able to change to H2O + CO2 and cross into the proximal tubule

Note that metabolic acidosis occurs with increased bicarb excretion

*this is a way to correct alkylosis

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28
Q

Why must bicarbonate be generated?

A

Reclamation of all filtered bicarb is not sufficient to maintain normal blood pH

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29
Q

**Where does H+ excretion primarily take place?

A

Distal tubule

*this is a different area than where reabsorption is occurring

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30
Q

What are the 2 ways H+ excreted?

A

Ammonium Excretion
Secreted H+ ions combine with ammonia (NH3) in the distal tubule to make ammonium (NH4+) which cannot cross membranes
-this is excreted

Titratable Activity
Phosphoric acid (HPO4^2-) combines with secreted H+ in the distal tubule to become dihydrogen phosphate (H2PO4-)
It is too big to cross the membrane and gets excreted

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31
Q

Ammonium excretion is able to produce how much bicarb?

A

New HCO3- (40 mEq/day) can be increased to 300 mEq/day

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32
Q

Titratable activity (phosphate H+ excretion) is able to account for how much bicarb?

A

30 mEq/day of new bicarb
*capacity is smaller than ammonium excretion
*cannot be increased because it is limited by the buffer

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33
Q

Hydrogen ion secretion in the distal tubule comprises what % of net acid excretion?

A

50%

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34
Q

How does ventilatory regulation of acid occur?

A

-Rapid onset and large capacity

-Chemoreceptors detect increased PaCO2 and increase the rate and depth of ventilation

-More CO2 is expelled through ventilation

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35
Q

What is the primary change in metabolic acidosis?

A

Decreased HCO3-

Compensation: Decreased PaCO2 (lowers this to blow acid off)

36
Q

What is the primary change in metabolic alkalosis?

A

Increased HCO3-

Compensation: Increased PaCO2 (retains CO2 and breathing slows down)

37
Q

What is the primary change in respiratory acidosis?

A

Increased PaCO2

Compensation: Increased HCO3 (kidneys increase bicarb synthesis)

38
Q

What is the primary change in respiratory alkalosis?

A

Decreased PaCO2

Compensation: Decreased HCO3- (kidneys stop bicarb synthesis)

39
Q

When may a mixed disorder be indicated?

A

If the primary change and compensation arrows do not go in the same direction for a disorder or if values fall out of specified ranges

40
Q

What are the characteristics of metabolic acidosis?

A

Low pH (<7.35)
Low serum HCO3- (<24 mEq/L)
Compensatory decrease in PaCO2

41
Q

What are the 2 types of metabolic acidosis?

A

Anion Gap (when anion gap is high)
Non-Anion gap (when anion gap is normal or low)

42
Q

How do we calculate anion gap?

A

Anion Gap= Na - (Cl + HCO3)

43
Q

What is a normal anion gap?

A

3-11 mEq/L

44
Q

What happens in non-anion gap acidosis?

A

Loss of plasma HCO3- that is replaced by Cl-

45
Q

What are the 3 causes of non-anion gap acidosis?

A

GI bicarb losses
Renal bicarb losses
Reduced renal H excretion

46
Q

What are common causes of GI bicarb loss?

A

Diarrhea *very common
-not enough time to reabsorb bicarb

Pancreatic fistulas/Biliary drainage
-these fluids are rich in bicarb

47
Q

What causes renal bicarb loss?

A

Type II renal tubular acidosis (proximal)
-patients cannot reabsorb bicarb in the proximal tubule due to something happening there (disease or drug)

48
Q

When there is more bicarb loss, what else happens?

A

Increased Na+ and fluid loss
-activates the renin-angiotensin system which leads to hyperaldosteronism
- Aldosterone tries to compensate and K gets excreted, leading to hypokalemia

49
Q

What are the 3 types of Reduced renal H+ excretion that can lead to non-anion gap acidosis?

A

Type 1 RTA
Type IV RTA
Chronic renal failure

50
Q

What are the causes of Type 1 Renal Tubule Acidosis (RTA) [Hypokalemia RTA]?

A

-Damage in the distal tubule, patient cannot regenerate bicarb
-H+ cannot be pumped into the tubule lumen by cells of the collecting duct
-Urine cannot be maximally acidified
-Increased K+ excretion to try and replace H+

51
Q

What are the causes of Type 2 Renal Tubule Acidosis (RTA) [Hypoaldosteronism/ Hyperkalemia RTA]?

A

-Body has low aldosterone/is resistant to it
-Aldosterone stimulates H+ excretion
-Less aldosterone = H+ retention (acidosis)
-Hyperkalemia also leads to H+ retention (acidosis)

52
Q

How does chronic renal failure lead to acidosis?

A

Decreased H+ secretion
Less ammonia production (decreases ability to make bicarb)

53
Q

What things are able to lead to anion gap acidosis?

A

MUDPILES

M: Methanol intoxication
U: Uremia
D: Diabetic ketoacidosis
P: poisoning/Propylene glycol ingestion
I: Intoxication/infection
L: Lactic acidosis
E: Ethylene glycol
S: Salicylate/sepsis

54
Q

What is the cause of anion gap acidosis?

A

HCO3- losses are replaced with another anion besides Cl-

55
Q

After determining anion gap, if a patient has anion gap acidosis what is the next step?

A

Calculate delta gap

56
Q

How do we calculate delta gap?

A

Delta Gap= Patient’s Anion Gap - Normal Anion Gap

57
Q

What does the anion gap tell us?

A

Whether a mixed disorder is present

*When the delta gap is added to a patient’s measured bicarb, the result should be in the normal bicarb range
-If these are added and the result is an elevated HCO3-. it tells you there is metabolic alkalosis with the acidosis

58
Q

What is the most common cause of Anion Gap metabolic acidosis?

A

Lactic acidosis

59
Q

What is lactic acidosis?

A

Lactate is a normal part of anaerobic metabolism
-Essential for tissues needing NAD+ to generate energy

60
Q

Increased lactic acid levels almost aways result from what?

A

Decreased clearance

(not overproduction)

61
Q

What is the normal level of lactic acid?

A

1 mEq/L

62
Q

What is considered a high lactic acid level?

A

> 5 mEq/L

63
Q

What is the main way that lactic acid is eliminated?

A

Gets reconverted to pyruvate (NAD+ to NADH)
Disposed by liver, kidney, and muscle

64
Q

What are the causes of lactic acidosis?

A

Shock
Drugs:
-Ethanol
-Metformin
-NRTIs
-Linezolid, Isoniazid, Propofol, Topiramate, Viekera
-Propylene Glycol
-Seizures
-Leukemia
-Hepatic/Renal Failure
-Diabetes
-Others: Malnutrition, Rhabdomyolysis

65
Q

If a patient has a salicylate toxicity, what can happen?

A

-Respiratory alkalosis (stimulated respiratory drive)
-Metabolic acidosis (accumulation of organic acids)

*pH looks normal

66
Q

What is the treatment for lactic acidosis?

A

Acute bicarbonate therapy

67
Q

What are the indications for giving a patient bicarb?

A

-Hyperkalemia
***pH <7.1 with cardiac arrest after defibrillation, ventilation, and medications have been used
-Overdoses

68
Q

How do we dose bicarb?

A

Dose (mEq) = [0.5 x IBW] x [12 - Actual HCO3]

*note that 12= desired bicarb

69
Q

Once we calculate the bicarb dose, how much is actually administered to the patient?

A

Give 1/3 to 1/2 the calculated dose

**want to be super conservative

70
Q

During cardiac arrest, how much bicarb may be given?

A

1 mEq/kg

71
Q

What is the average dose of bicarb for chronic metabolic acidosis therapy?

A

1-3 mEq/kg/day

72
Q

What are the characteristics of metabolic alkalosis?

A

Increased pH (>7.45)

Increased bicarb (>30 mEq/L)

Compensatory hypoventilation resulting in increased CO2

73
Q

What are the 3 main ways plasma bicarb levels can rise?

A

Loss of acid from GI tract or urine

Administration of bicarb or precursor

Contraction alkalosis (Loss of Cl rich fluid and bicarb poor fluid)

74
Q

What else can contribute to metabolic alkalosis?

A

Volume and Chloride depletion

-decreased blood volume
-decreased ability for kidney to excrete bicarb
-increased ability to reabsorb bicarb in the proximal tubule

75
Q

What are the 2 types of alkalosis?

A

Saline responsive
Saline resistant

76
Q

What urinary chloride indicates saline responsive alkalosis?

A

<10-20 mEq/L

77
Q

What are the 3 causes of saline responsive alkalosis?

A

Diuretic therapy
Vomiting and ng suction
Exogenous bicarb administration or blood transfusion

78
Q

What is the main cause of saline responsive alkalosis?

A

Diuretic therapy
-excretion of NaCl and water is increased
-Extracellular volume contraction results
-This stimulates aldosterone release
-Increases Na reabsorption and H+ and K+ secretion
-H+ secretion leads to bicarb reabsorption
-Hypokalemia stimulates hydrogen ion movement intracellularly while K moves out
-Na+ exchanges with K and gets reabsorbed with bicarb

79
Q

How is alkalosis maintained?

A

Na reabsorption increases which leads to H+ secretion and bicarb reabsorption

Less K+ leads to more H+ secretion and Na+ reabsorption

80
Q

What urinary chloride level indicated saline resistant alkalosis?

A

> 20 mEq/L

81
Q

How is saline resistant alkalosis different from saline responsive?

A

Enhanced renal H+ excretion and bicarb reabsorption

-Difference: No chloride depletion, Cl is normal

82
Q

What are the causes of saline resistant alkalosis?

A

Increased mineralcorticoid activity (Na and K exchange is increased, H+ secretion increases, bicarb is absorbed)

Hypokalemia

Renal tubular chloride wasting

83
Q

How do we treat saline responsive alkylosis?

A

Fluid/electrolyte replacement with NaCl or KCl

84
Q

In patients who cannot tolerate excess fluid or sodium, what can we use for alkylosis?

A

Carbonic anhydrate inhibitors (Acetohexamide)

*note that this can make hypokalemia worse

85
Q

What is an alternative last-line therapy for alkalosis?

A

HCl acid
Ammonium chloride
Arginine monochloride

86
Q

How do we treat saline resistant alkalosis?

A

-Correct hypokalemia
-Decrease dose of mineralcorticoid (hydrocortisone)
-Administer spironolactone
-Correct hyperaldosteronism

87
Q
A

Fall 2024 (16 decks)

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