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DT3-Exam 3 > Electrolyte & Acid Base Disorders +Cases-- Leah** > Flashcards

Electrolyte & Acid Base Disorders +Cases-- Leah** Flashcards

1
Q

Blood pH is determined by the levels of what two substances in the plasma?

A
  • carbonic acid

- bicarbonate

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2
Q

What is the normal blood pH

A

7.4 (7.35-7.45)

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3
Q

What equation is used to determine blood pH?

A

pH= pKa + log [A-]/[HA]

where A- is bicarbonate and HA is CO2

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4
Q

What two organs are responsible for secreting acid in response to the body’s needs?

A
  • kidneys (secrete H+/ titratable acid)

- lungs (secrete CO2)

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5
Q

Heroin overdose is a classic example of what acid base disorder?

A

respiratory acidosis

-hypoventilation prevents release of CO2

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6
Q

Is the metabolic disturbance cause by heroin OD usually compensated for?

A
  • No, heroin OD = acute respiratory acidosis, and this cannot be compensated for by the kidneys.
  • renal compensation takes 48-72 hours to begin.
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7
Q

In what order are the four arterial blood gas findings generally listed and presented in the clinic?

A

pH, CO2, O2, %O2 sat
*He will make this clear on the exam, but in real life/ during rounds, they like you to just read off values in this order.

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8
Q

What would you expect the serum bicarb level to be in the case of respiratory acidosis secondary to heroin OD?

A
  • normal, because kidneys don’t have time to compensate for the acidosis.
  • hypoventilation does not change bicarb values.
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9
Q

How do you treat acute respiratory failure? (2)

A
  • intubation
  • mechanical ventilation
  • Before running tests*
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10
Q

Three steps for ABG evaluation

Yes, his PPT has 6, Ive just group them nicely.

A
  • Use pH and pCO2 to determine primary disorder.
  • calculate ion gap, esp important in met. acidosis
  • check for compensation/ clues to mixed disorders
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11
Q

What is the formula for anion gap?
What is the normal value?
What does a high anion gap most generally mean?

A

Na- (Cl + HCO3) = 4-12 (normal)

  • High gap = some extra negatively charged substance in the blood.
  • Could be ketones, lactate, ethylene glycol, etc.
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12
Q

A patient in sepsis would most likely present with what metabolic derangement?
Would there be compensation?

A
  • metabolic acidosis w/ high anion gap, due to lactate build up.
  • often see respiratory compensation (LOW CO2, tachypnea)
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13
Q

A type 1 diabetic is most at risk for what type of metabolic derangement?
Would you see compensation?

A
  • metabolic acidosis with high anion gap due to ketone build up
  • may also see metabolic alkalosis due to vomiting and respiratory acidosis due to CNS depression over time (both induced by high ketones in the blood)

*Respiratory compensation may be present, but with time, CNS depression makes this harder to accomplish.

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14
Q

What ABG values can best be used to determine the presence of respiratory compensation?
Renal compensation?

A
  • respiratory compensatory changes seen by examining pCO2
  • renal compensatory changes seen by examining HCO3

*Remember, HCO3 is not directly measured by a blood gas but can be calculated using ABG.

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15
Q

We get normal value sheets, but for quick reference/ to be familiar, what are normal pH pCO2 and HCO3 values?

A
  • pH: 7.35-7.45
  • pCO2: 34-45
  • HCO3: 22-28
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16
Q

Treatment of DKA:

A

-IV bolus insulin + fluids

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17
Q

CO2 is a product of _______.
Titratable acid is a product of _____.
How are these two substances removed?

A
  • CO2: cellular metabolism, removed by lungs

- titratable acid: protein catabolism, removed by kidneys

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18
Q

In what part of the nephron is H+ secreted?

A

-H+ is secreted in the collecting duct, especially in the presence of aldosterone.

*Remember H+ and K+ follow each other!
If H leaves the duct, K leaves too.
This is why aldo antagonists are K+sparing diuretics

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19
Q

Which diuretic causes hyponatremia?

hypocalcemia? hyperuricemia?

A
  • thiazides cause hyponatremia and hyperuricemia

- loops cause hypocalcemia

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20
Q

Acetalozamide: mechanism of action and classic use

A

carbonic anhydrase inhibitor, classically treats mountain sickness by inducing ^Cl metabolic acidosis –> stimulates compensatory respiratory drive!!

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21
Q

How effective is renal compensation?

A
  • slow, takes up to 72 hours

- cannot handle large acid loads

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22
Q

How effective is pulmonary compensation?

A
  • rapid, takes place nearly instantly via chemoreceptor stimulation of respiratory drive
  • can handle much larger acid load than the kidneys
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23
Q

Function of compensation?

A
  • corrects pH
  • ASSUME THAT IT NEVER OVERCORRECTS!!!!!!
  • If you are suspecting “over correction”, you should really be thinking of a second disorder.
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24
Q

What is an example of “false overcompensation”

A
  • respiratory alkalosis in sepsis.
  • we know lactate = metabolic acidosis sepsis + respiratory compensation.
  • HOWEVER, if alkalosis is present, you should assume that there is a SECOND DERAGEMENT caused by the sepsis, NOT overcompensation by the lungs.

Summary: diagnose the patient with metabolic acidosis + respiratory alkalosis, NOT over compensation.

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25
Q

1 Cause of lactoacidosis

A

-failure to perfuse organs

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26
Q

1 Causes of ketoacidosis (3)

A
  • DKA
  • starvation
  • alcohol intox
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27
Q

Cause of metabolic acidosis that are NOT related to lactate or ketones (2)

A
  • loss of bicarb: renal failure or diarrhea

- toxic ingestion: ethylene glycol, methanol, salicylates

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28
Q

What metabolic acidoses have HIGH anion gaps?

A

-lactoacidosis, ketoacidosis, ingestion of some toxins (i.e. ethylene glycol)

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29
Q

What metabolic acidosis have NORMAL anion gaps?

A

-loss of bicarb: diarrhea or renal failure

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30
Q

The degree of anion gap should correlate to?

A

-the degree of bicarb decrease

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31
Q

Four causes of metabolic alkalosis

A
  • diuretics RX QUESTION
  • alkaline ingestions
  • vomiting (HCL loss)
  • primary and secondary hyperaldosteronism
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32
Q

How do diuretics induce metabolic alkalosis

A

-Cl wasting diuretics cause increased bicarb reabsorption

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33
Q

Three causes of respiratory acidosis

A
  • CNS depression
  • OBSTRUCTIVE DISEASE exacerbation
  • *EXCEPT NOT ASTHMA, ASTHMA = alkalosis**
  • neuromuscular disorders
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34
Q

Five causes of respiraory alkalosis

A
  • PE, asthma
  • salicylates
  • sepsis
  • hypoxia
  • hyperventilation
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35
Q

Two examples of combined metabolic derangement

A
  • sepsis: metabolic acidosis + respiratory alkalosis +also occasionally met. alkalosis (vomiting)
  • DKA: metabolic acidosis + metabolic alkalosis + respiratory alkalosis (eventual acidosis w resp depression)
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36
Q

Normal levels of compensation BY THE LUNGS in metabolic acidosis and alkalosis

A
  • metabolic acidosis: CO2 down by 1.25 mmHg for every 1 meq/L HCO3-
    (acidosis: 1.25:1)
  • metabolic alkalosis: CO2 up by 0.75 “…”
    (alkalosis: 0.75:1)
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37
Q

When might compensation fail to appropriately occur?

A
  • neuro diseases
  • drug intoxication

*This is different than the body just not being able to compensate for an extreme amount of acid.

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38
Q

Normal levels of compensation by the kidneys in acute or chronic respiratory derangement:

A

acidosis:
- acute bicarb ^ 1 for every 10 CO2 ^
- chronic bicarb ^ 4 for every 10 CO2 ^
(1: 10, 4:10 in acidosis)

alkalosis:
- acute bicarb DOWN 2 for every 10 CO2 decrease
- chronic bicarb DOWN 4 for every 10 CO2 decrease
(2: 10, 4:10 in alkalosis)

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39
Q

In the event of metabolic acidosis AND alkalosis, what findings would be seen on arterial blood gas?
When might this actually happen?

A
  • anion gap change would NOT be proprtional to the change in bicarb
  • NORMAL bicarb w/ very HIGH anion gap

-this happens when a patient is in DKA OR septic w/puking

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40
Q

7.30/ 50/ 60/ O2 sat not listed
Bicarb: 27
This is an example of?

A
  • low pH= acidosis
  • high CO2, normal bicarb
  • RESPIRATORY acidosis, uncompensated.
41
Q

7.47/ 30/ 80/ O2 sat not listed
Bicarb: 19
This is an example of?

A

-high pH = alkalosis
-CO2 low, bicarb low
respiratory alkalosis with metabolic compensation
(likely chronic because bicarb is significantly low.)

42
Q

7.37/ 28/ 70/ O2 sat not listed
Bicarb: 15
This is an example of?

A

-pH on the low end of normal
-CO2 is low
-bicarb is low
metabolic acidosis with respiratory compensation

43
Q

7.45/ 47/ 70/ O2 sat not listed
Bicarb: 32
This is an example of?

A
  • pH on the high end of normal
  • CO2 is high, bicarb is high
  • metabolic alkalosis with respiratory compensation
44
Q

If the PCO2 and the bicarb change in the same direction the disorder is usually?
If hey change in opposite directions?

A

same direction: metabolic

opposite direction: respiratory

45
Q

Major intracellular and extracellular cations?

A
  • Just remember, its like there’s a banana floating around in the salty sea.
  • Na extracellular fluid, K intracellular
46
Q

Abnormalities in sodium CONCENTRATION reflect?

A

-problems with free water handling, not sodium handling.

47
Q

Definition of hyper and hyponatremia

A

hyper:&raquo_space;145, too much water

48
Q

Most common cause of hypernatremia

A

not drinking enough, esp in the elderly/ chronically ill who cannot drink on their own

49
Q

PE findings assc with hypernatremia (4)

A
  • volume depletion = tachycardia and low BP
  • dry mucous membranes
  • thirsty and lethargic
  • poor skin turgor
50
Q

Describe the TYPICAL urine findings assc with hypernatremia

A

-high osmolality because patient is trying to retain fluid

51
Q

When might a patient have hypernatremia and DILUTE urine?

A

-diabetes insipidus, due to LOSS of ADH

52
Q

Treatment of symptomatic hypernatremia: (2)

A

IV fluids, hypotonic solutions

goal = stabilize the hypotension

53
Q

Hyponatremia is usually ______ ________, in comparison to hypernatremia.

A

physiologically complex, whereas HYPERnatremia often just involved poor fluid intake!!

54
Q

PE findings assc with hyponatremia (2)

A
  • usually asx unless severe

- nausea, H/A and neurodeficits may occur at very low levels

55
Q

Three types of hyponatremia

A
  • hypovolemic
  • hypervolemic
  • euvolemic
56
Q

Urine osmolality is a surrogate for what?

Urine Na is a surrogate for what?

A
  • osmolality ~ ADH activity

- Na ~ volume status

57
Q

Three causes of HYPERvolemic hyponatremia

A

-CHF, cirrhosis, nephrotic syndrome

58
Q

One cause of euvolemic hyponatremia

A

-SiADH, i.e. small cell lung cancer

59
Q

What would be the OPPOSITE of SiADH?

A

-Diabetes insipidus, pituitary condition

60
Q

Cause of HYPOvolemic hyponatremia

A

-Thiazide diuretics

61
Q

Treatment for SiADH

A

-fluid restriction

62
Q

How is symptomatic HYPOnatremia treated?

A
  • slow replacement with HYPERtonic saline

- must do this SLOWLY to prevent pontine demyelination (locked in syndrome)

63
Q

When might K+ shift across cellular membranes? (3)

A
  • When there are changes in pH
  • acidosis = HYPERkalemia
  • alkalosis= HYPOkalemia
64
Q

Causes of hyperkalemia? Which is most common? (6)

A
  • # 1: renal failure*
  • excess intake
  • acidosis
  • lack of aldosterone
  • severe volume depletion
  • drugs
65
Q

What causes pseudohyperkalemia?

A

-lysed RBCs spill K+ in blood sample tube

66
Q

HYPERkalemia EKG changes?

HYPOkalemia EKG changes?

A
  • hyper: tall, peaked T wave

- hypo: prolonged QT interval, risk of torsades

67
Q

Treatment of HYPERkalemia in the presence of EKG changes: (3)

A
  • calcium gluconate (only for weird EKG)
  • insulin and albuterol to shift K+ into cells
  • resin to increase K+ excretion

*or dialysis if cause is acute renal failure

68
Q

Four causes HYPOkalemia

A
  • diuretics
  • diarrhea
  • alkalosis
  • Mg deficiency

DDAM GIRL, YOU HYPOKALEMIC.

69
Q

Symptoms of severe HYPOkalemia (2)

A

-arrythmia and muscle twitches

70
Q

Test that is not useful for K+ levels

A

urine concentrations

71
Q

Treatment of HYPOkalemia; what do we avoid?

A
  • Gradually give ORAL K+

- AVOID IV KCl: causes sclerosis

72
Q

Mg is a cofactor for?

A

-ATPases

73
Q

Causes of Mg deficiency (3)?

A
  • CKD
  • Diuretics
  • alcoholism
74
Q

Low Mg can cause low _____.

A

K+

75
Q

Avoid Mg loading in ______.

A

renal disease

76
Q

What are the three types of RTAs?

A

Type I- distal
Type II- proximal
Type IV- hyperkalemic

77
Q

What is the defect in type I RTA? What is the urine pH? K+ levels?

A

distal a-intercalated cells cannot secrete H+; urine is basic (5+); K+ is LOW

78
Q

What is the defect in type II RTA? What is the urine pH? K+ levels?

A

proximal tubule cannot reabsorb bicarb; urine is normal (acidic) because distal tubule compensates for the defect. K+ is still low.

79
Q

What is the defect in type IV RTA? What is the urine pH? K+ levels?

A

Lack of Aldo or resistance to Aldo; predominately seen in diabetes; urine is acidic (normal pH) but LOW IN AMMONIA! type (4) is low in NH(4); K+ is HIGH due to low aldosterone

(similar to giving a K+ sparing diuretic!)

80
Q

What RTA can cause calcium stones?

What RTA can cause rickets/osteomalacia?

A

Type I- causes stones

Type II- causes hypophosphatemic rickets

81
Q

What are some causes of type I RTA?

A 
Autoimmune disease (i.e. Sjorgens) 
Chemotherapy, Amphotericin, Analgesics 
Obstruction
82
Q

Type II RTA causes (2)

A
  • carbonic anyhdrase inhibitors

- Fanconis Symdrome

83
Q

Most common/important cause of type IV RTA?

A

DM

84
Q

Describe total body weight compartments (water, non-water mass, ECF/ICF/plasma)

A

Total Body Water –> 60% body weight
Of the water –> 2/3 ICF; 1/3 ECF
Of th ECF –> 1/4 is plasma

(60, 40, 20 rule–> 60% body weight = H20, 40% = intracellular, 20%= Extracellular)

85
Q

Diuretics most likely to cause hyponatremia?

A

Thiazides

86
Q

Findings assc with diabetes insipidus:

A

Hypernatremia; dilute urine

87
Q

Over what period of time should you correct hyponatremia?

When is this most important?

A

48 hours –> slow to prevent pontine myelinolysis

esp in pre menopausal females

88
Q

HIV drug assc with kidney stones

A

Indinavir

89
Q

Hallmark presentation of kidney stones

A

Flank pain and blood in the urine

90
Q

What is the urinary ion gap?
When is it useful?
What is it essentially a surrogate for?

A

[(Na+K) -Cl]
Used in non ion gap metabolic acidosis (i.e. Diarrhea)
Essentially a surrogate for ammonia

91
Q

If someone is HYPERnatremic, what should their urine look like (assuming they are healthy?)

A

Concentrated, HYPERnatremia suggests a lack of free water– the body should be trying to RETAIN Fluid (via ADH).

One example of this failing is Diabetes insipidus

92
Q

Which is a bigger problem: hypotension or hypernatrmia?

A

Hypotension! If you have both in a patient, correct the hypotension first.

(Although I’m a little confused because I think you give fluids to both hypotensive and hypernatremic patients……..)

93
Q

What two things can all diuretics cause?

A

volume depletion, pre-renal azotemia

94
Q

What are the primary uses of:

  • thiazides
  • Loops
  • K+ sparing
  • Mannitol
  • CAi
A
  • thiazides: HTN
  • Loops: edema
  • K+ sparing: hyperalo, weak-antiHTN, reduce renal/CHF mortality
  • Mannitol- increased ICP, trauma, renal failure
  • CAi- mountain sickness, glaucoma
95
Q

What is the mechanism of action for:

  • Thiaizdes
  • Loops
  • Triameterene
  • Spiro
A
  • Thiaizdes: block NaCl transport at DCT, CD
  • Loops: block Na/K/2Cl transport at LOH
  • Triameterene: block Na/K transport at CD
  • Spiro: Blocks aldosterone
96
Q

What acid base carbonic anhydrase inhibitors cause?

A

Metabolic acidosis

97
Q

Diuretic than can prevent kidney stone?

A

Thiaizdes, because decreased amount of Ca in urine

98
Q

Loop used in patients allergic to sulfa drugs

A

Ethacrynic acid

99
Q

Metabolic changes assc with thiazides

A
  • low Na, K

- high Ca, Uric acid, glucose

DT3-Exam 3 (9 decks)

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