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Boards: AcidBase/Fluids/Electrolytes > HUNG Electrolytes/Acid-Base > Flashcards

HUNG Electrolytes/Acid-Base Flashcards

1
Q

How does acid base affect iCa level?

A

Acidic pH facilitate dissociation of calcium from protein and increases the amount of iCa in the sample.
Alkaline pH favors calcium binding to protein, thus decreasing the amount of iCa

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2
Q

Which ion is the main intracellular anion?

A

Phosphate

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3
Q

Where is the central osmocenter?

A

Hypothalamus

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4
Q

What are the two stimuli for ADH release?

A

1) Increased plasma osmolarity
2) Decreased effective circulating volume (signals sent by baroreceptors)

  • maintenance of effective circulating volume is always prioritized over maintenance of normal plasma osmolality
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5
Q

What is ADH also called?

A

Arginine vasopressin

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6
Q

Explain how ADH increased renal distal tubules and collection duct water resorption.

A

ADH binds to V2 receptors, which are coupled with stimulatory G proteins (Gs) → activates adenylate cyclase (AC) → stimulates formation of cyclic adenosine monophosphate (cAMP) from ATP → activates protein kinase A and phosphorylation of intracellular proteins → moving aquaporin-2 (AQP-2) to the luminal side of the cell membrane.

On the basolateral side of the cell membrane are other aquaporins, AQP-3 and AQP-4, that permit water to flow out of the cell, although these aquaporins do not appear to be regulated by AVP.

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7
Q

Where do most and second most Na absorption happen in the nephron? What channels do they use?

A

1) Proximal renal tubule (about 67%)
- Co-transport with glucose, AA, phosphate, Na-H antitransporter

2) Ascending loop of Henles (about 25%)
- Na-K-2Cl cotransporter, Na-H antitransporter

3) Distal convoluted tubule (about 5%)
- Na-Cl cotransporter

4) Collecting duct (about 3%)
- Na channel

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8
Q

What stimulate aldosterone and what inhibit it?

A

Stimulation: Angiotensin II, Hyperkalemia, ACTH

Inhibition: Dopamine, ANP

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9
Q

True or False: catecholamine can stimulate proximal renal tubule Na reabsorption through 𝜶1 receptor.

A

True

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10
Q

True or False: catecholamine can stimulate renin release through 𝜶1 receptor.

A

False

𝜷1

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11
Q

True or False: Angiotensin II can stimulate Na-H antiporter in the proximal tubules and facilitate Na reabsorption.

A

True

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12
Q

List 5 drugs that can stimulate ADH release.

A

1) Barbiturates
2) Angiotensin II
3) Beta adrenergic drugs
4) Narcotics
5) Vincristine
6) Tricyclic antidepressant
7) Cholinergic drugs
8) Carbamazepine

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13
Q

What are the three big categories of causes for hypernatremia. List 3 examples for each categories.

A

1) Pure water deficit
- Diabetes insipidus (central/nephrogenic)
- Primary hypodipsia
- No access to water
- High environmental temperature

2) Hypotonic fluid loss
- Extra-renal: GI loss (V/D), third-space loss, burn
- Renal: AKI, CKD, post-obstructive diuresis, diuretic administration

3) Impermanent solute gain
- Salt toxicity
- Hyperaldosteronism
- Hypertonic saline infusion

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14
Q

What is the cause of central diabetes insipidus?

A

Partial or lack of production of ADH (congenital, trauma, neoplasia, idiopathic)

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15
Q

For dogs with central DI, administration of DDAVP can improve the USG and/or osmolarity, but the initial effect may not be very significant. Why?

A

Because of renal medullary wash out → no concentration gradient for water to move

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16
Q

What is the MOA of glucocorticoid, E. coli endotoxemia, hypokalemia, hypercalcemia causing NDI?

A

Inhibit adenyl cyclase on the basal membrane → inhibit aquaporin 2 movement to the luminal membrane → decrease water reabsorption

  • Other causes of NDI: hepatic insufficiency, hyperthyroidism, medullary interstitial amyloidosis (e.g. cats, Sharpei), pyelonephritis, polycystic kidney disease
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17
Q

How does thiazide help with DI management?

A

Thiazide cause mild volume depletion → increase water and Na reabsorption at the proximal renal tubule and decrease the flow to the distal collecting tubule where water is impermeable → decrease urine volume

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18
Q

How does paintballs cause hypernatremia?

A

They usually contain polyethylene glycol, glycerol and sorbitol, which can cause severe osmotic diarrhea

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19
Q

When we correct the chronic hypernatremia or hyponatremia, what is the rate that we shouldn’t exceed?

A

not exceed 10-12 mEq/L per 24 hours

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20
Q

What can cause hyponatremia with high osmolarity?

A

Hyperglycemia, mannitol infusion

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21
Q

What can cause hyponatremia with normal osmolarity (pseudohyponatremia)?

A

Hyperlipidemia
Severe hyperproteinemia

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22
Q

How to calculate osmol gap?

A

Osmol gap = Measured osmolarity - Calculated osmolarity

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23
Q

What is normal osmol gap in dogs and cats?

A

< 10 mOsm/L

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24
Q

What are the common cause of increased osmol gap?

A

Ethylene glycol intoxication, ethanol intoxication

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25
Q

List three differentials for hyponatremic patients that are hypervolemic, euvolemic or hypovolemia.

A

1) Hypervolemic
- CHF
- Advanced CKD
- Cirrhosis
- Nephrotic syndrome

2) Euvolemic
- Psychogenic polydipsia
- SIADH
- Anti-diuretic administration
- Hypotonic fluid
- Myxedema coma

3) Hypovolemic
- Renal: diuretic administration, hypoadrenocorticism
- Non-renal: GI loss, third space loss (guess they can do whatever they want)

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26
Q

Why do some dogs with chronic third space loss develop pseudo-Addison’s?

A

1) Volume depletion cause vasopressin release → increase water reabsorption → hyponatremia
2) Volume depletion cause decrease renal potassium excretion → hyperkalemia

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27
Q

What are the diagnostic criteria for syndrome of inappropriate ADH release (SIADH)?

A
  1. Hyponatremia with hypoosmolarity
  2. Abnormally high urine osmolarity in the presence of plasma hypoosmolarity
    • In psychogenic polydipsia, urine osmolarity will be very low
  3. Normal renal, adrenal and thyroid function
  4. No evidence of hypovolemia or hypervolemia (or third space loss)
  5. Presence of natriuresis despite hyponatremia and plasma hypoosmolarity as a result of mild volume expansion (urine Na concentration usually > 20 mEq/L)
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28
Q

What happens to the brain if hyponatremia is corrected to quickly?

A

Osmotic demyelination

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29
Q

How does hyperadrenorcorticism cause PUPD?

A

Excessive glucocorticoid decrease ADH secretion from the posterior hypothalamus

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30
Q

How does hypercalcemia cause PUPD (5 causes)?

A

1) Affect adenyl cyclase so ADH cannot activate the cascade
2) Increased medullary blood flow
3) Impaired NaCl transport to the loop of Henle
4) Direct stimulation of thirst center
5) Hypercalcemic nephropathy

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31
Q

How does severe liver disease cause PUPD (3 causes)?

A

1) Decrease BUN → decrease medullary solute
2) Decrease metabolism of endogenous hormones (e.g. cortisol, aldosterone)
3) Hypokalemia

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32
Q

How does Addison’s disease cause PUPD?

A

Renal Na loss with medullary solute washout

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33
Q

What are the idiogenic osmoles made from?

A

inositol, glutamine, glutamate

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34
Q

How long does it take for the idiogenic osmoles formation in the brain to fully compensate the hypernatremia?

A

2-7 days

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35
Q

What is the recommended percentage of Na raise in the first day for the patient with symptomatic hyponatremia?

A

no more than 10-15% in the first day

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36
Q

What is the formula to calculate sodium deficit?

A

Sodium deficit (mEq) = (Target Na - Patient Na) x 0.6 x body weight

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37
Q

During the treatment of correcting hyponatremia, correcting potassium is also an important part of the therapy if the patient is hypokalemic. Why?

A

After giving the potassium, the potassium will enter the cell and exchange Na in order to reach electroneutrality.

  • It will also allow Na-K ATPase to function normally? Maybe?
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38
Q

What is the limit rate for Na correction

A

No more than 10 mEq/L in the first 24 hours and no more than 18 mEq/L in the first 48 hours

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39
Q

What is the stabilization therapy for acute hypernatremia with clinical signs?

A

Give D5W at the rate of 7-10 ml/kg/hr to correct the Na at the rate of 2-3 mEq/kg/hr for the initial 2-3 hours or until neurological signs resolve.

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40
Q

What is the stabilization therapy for acute hyponatremia with clinical signs

A

Give 3% HTS at the rate of 1-2 ml/kg over 10-20 min to raise Na by 4-6 mEq/L

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41
Q

Which electrolyte is the major determent of the resting membrane potential?

A

Potassium!
More precisely, the ratio of intracellular K to extracellular K

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42
Q

Which electrolyte has higher permeability to the cell membrane, Na or K?

A

K (100x more permeable than Na)

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43
Q

What is normal resting membrane potential?

A

-90 mV

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44
Q

How does hyperkalemia affect the resting membrane potential?

A

It decreases the resting membrane potential (make it less negative) and make the cell membrane more excitable, but if the new resting membrane potential becomes less than the threshold potential, the cell will depolarize but cannot repolarize → no longer excitable

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45
Q

Draw how does potassium and calcium affecting the resting membrane potential and threshold.

A
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46
Q

How does hypocalcemia affect the threshold potential?

A

It increases the threshold potential (make it more negative) and make the cell more excitable.

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47
Q

Does acidemia increase or decrease membrane excitability?

A

Decrease

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48
Q

True or False: Aldosterone can affect colonic potassium absorption.

A

True

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49
Q

What is the MOA of using terbutaline to treat hyperkalemia?

A

Terbutaline is an 𝜷2 agonist. It will activate the Na-K ATPase on the cell membrane (especially muscles and liver) and increase K uptake by the cell.

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50
Q

How does acid base affect the potassium movement across the cell membrane?

A

Acidosis → K moves to ECF (in exchange of H+)
Alkalosis → K moves to ICF

  • Metabolic acid-base derangement will cause more significant change of K than respiratory.
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51
Q

How many percentage of K is reabsorbed at proximal renal tubule and ascending loop of Henle’s respectively?

A

70% and 10-20%

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52
Q

In the proximal part of the renal tubule, is K transported mainly via transcellular route or paracellular route?

A

Paracellular route

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53
Q

Which part of the nephron/cells is responsible for K secretion?

A

Principle cells at the Connecting tubule and collecting duct

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54
Q

There are two form of intercalated cells at the kidney collecting duct - 𝜶 and 𝜷. What are their functions?

A

𝜶 intercalated cells - secrete acid
𝜷 intercalated cells - secrete bicarb

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55
Q

How does aldosterone affect the potassium secretion in the distal renal tubules

A

1) It stimulates ENaC at the principle cells and increases Na reabsorption → increases Na-K ATPase activity at the basal membrane → facilitates K secretion
2) Directly increase K channel at the luminal membrane

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56
Q

How does aldosterone affect the hydrogen secretion in the distal renal tubules

A

1) It stimulates ENaC at the principle cells and increases Na reabsorption → creates electronegativity → facilitates H secretion at the 𝜶 intercalated cells
2) Directly promotes H secretion by stimulating the H-ATPase at the luminal membrane

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57
Q

True or False: High tubular flow increases K secretion.

A

True

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58
Q

How does hypochloremic metabolic alkalosis cause hypokalemia?

A

Low chloride leads to relatively elevated bicarb in the filtrate in the nephron. The Na reabsorption is decreased at the proximal renal tubule due to hypovolemia from the underlying disease which cause hypochloremia (e.g. GI obstruction). The Na reabsorption at the ascending loop of Henle due to low chloride so Na-K-Cl channels don’t work that well. The Na reabsorption at the distal convoluted tubule is also decreased because of low Cl and Na-Cl channels don’t work well either. There will be increased concentration of Na reaching the connecting tubule and collecting duct. Na will be reabsorbed via ENaC and K as well as H will be exchanged and secreted into the filtrate due to electronegativity.

  • If patient is also hypokalemia already, more hydrogen will be excreted (because K is not enough) and therefore worsening the metabolic alkalosis

Good Reference: https://eclinpath.com/chemistry/acid-base/compensation/renal-concentration/

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59
Q

Does serum or plasma contain higher K level? Why?

A

Serum

Because platelets release K during clotting process

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60
Q

What is the formula to calculate fraction excretion of potassium?

A
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61
Q

What percentage cutoff of FEk is used to differential renal and non-renal cause of hypokalemia?

A

FEk > 4% renal
FEk < 4% non-renal

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62
Q

Which breed of cat can have a inherited hypokalemic polymyopathy?

A

Burmese cat

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63
Q

What are the three big categories of causes for hypokalemia? List three differentials in each category.

A

1) Decreased intake
- Anorexia
- Administration of low potassium fluid

2) Move from ECF to ICF
- Alkalosis
- Insulin administration
- B2 agonist administration
- Catecholamine

3) Increased loss
- GI loss (v/d)
- CKD
- Post-obstructive diuresis
- Diuretic administration
- Primary hyperaldosteronism

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64
Q

How does hypokalemia cause muscle weakness?

A

1) hyperpolarization of the cell membrane
2) vasoconstriction and muscle ischemia (usually during exercise muscle will release K which leads to vasodilation and increase blood flow)

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65
Q

What is the proposed mechanism of hypokalemic nephropathy? What is its characteristics.

A

Characteristics: chronic tubulointerstitial nephritis

Renal vasoconstriction
Reduced medullary blood flow
Impaired renal angiogenesis

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66
Q

True or False: Hypokalemia increases renal ammoniogenesis.

A

True

*chronic metabolic acidosis also causes it

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67
Q

Normally, potassium supplementation shouldn’t exceed what rate?

A

0.5 mEq/kg/hr

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68
Q

What are the three big categories of causes for hyperkalemia? List three differentials in each category.

A

Increased intake
- Unlikely to be the sole cause of hyperkalemia

Move from ICF to ECF
- Insulin deficiency
- Acidosis (acute, mineral)
- Acute tumor lysis syndrome
- Rhabdomyolysis
- Reperfusion injury

Decrease excretion
- Anuric AKI
- Urethral obstruction
- Hypoadrenocorticism

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69
Q

What drugs can cause hyperkalemia?

A

ACEI, ARB (decreased aldosterone release)
Potassium-sparing diuretic
NSAID, heparin
Non-specific 𝜷 blocker (blocked beta adrenergic effect on Na-K ATPase)
Digoxin (inhibit Na-K ATPase)

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70
Q

What are the two main causes of pseudohyperkalemia?

A

Hemolysis
Thrombocytosis

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71
Q

What can we see on ECG in patients with hyperkalemia

A

Tall T wave
Prolonged P-R interval
Widened QRS complex
Atrial stanstill

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72
Q

Explain how does hyperkalemia cause changes on ECG.

A

1) initially, hyperkalemia cause increased resting membrane potential (less negative) → shortens the gap between resting membrane potential and threshold potential → higher cell excitability → shortens action potential duration and the tall T wave.
2) As the hyperkalemia worsens, it can decreased the available Na channels for the phase 0 → decreased Na channels cause decreased depolarization rate of phase 0 → prolonged action potential → widened QRS complex and prolonged PR interval
3) In severe hyperkalemia, resting membrane potential may increase to at the same level or above the threshold potential → unable to depolarize → atrial standstill

Reference:
1. Weiss JN, Qu Z, Shivkumar K. Electrophysiology of Hypokalemia and Hyperkalemia. Circ Arrhythm Electrophysiol. 2017 Mar;10(3):e004667. doi: 10.1161/CIRCEP.116.004667.
2. Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33(1):40-7. PMID: 16572868; PMCID: PMC1413606.

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73
Q

Explained the pathophysiology of osmotic demyelination syndrome.

A

When a patient is hyponatremic, the brain will exhibit some protective mechanism to maintain the brain cell volume. It will first increase the water excretion from the brain parenchyma to the CSF. It will also excrete some iorganic or organic osmoles out of the cells to maintain the similar osmolarity as the extracellular fluid.
When the hyponatremic is being correct, the opposite actions take place. The brain cells will take back the elextrolytes, synthesize intracellular proteins, and synthesize receptors to reuptake the previously secreted organic osmoles. This process usually takes days. So if the hyponatremic is being corrected too quickly, the ECF osmolarity will be markedly higher than the ICF osmolarity, which case net flux of water out of the cells and lead to osmotic demyelination.

74
Q

Which group of cells does the most K locate?

A

Skeletal muscles

75
Q

Does elevated catecholamines cause hyperkalemia or hypokalemia. Why?

A

Hypokalemia
Activation of 𝜷 adrenergic receptors → stimulate Na-K ATPase

76
Q

What are the common arrhythmias seen in hypokalemic patients?

A

Ventricular tachycardia
Ventricular fibrillation
Torsade de pointes

77
Q

What is the major electrolyte complication in digitalis administration? Why?

A

Hyperkalemia
Digitalis block Na-K ATPase to increase the intracellular sodium concentration.

78
Q

If you really need to use sodium bicarbonate to manage hyperkalemia, what is the dose?

A

1-2 mEq/kg slow IV over 15 minutes

79
Q

Describe chloride shift. What the key enzyme that allows it to happen?

A

It is also called Hamburger effect. It describes the movement of the chloride into RBCs while the bicarb moves out of the RBCs in the venous blood. Th source of bicarb is the CO2 that is eliminated by the cells into the plasma and then into RBCs.

Key enzymes: carbonic anhydrase in RBCs

  • The reverse action happens in the pulmonary capillaries
80
Q

Of the Na-K-2Cl transporter at the ascending loop of Henle, which electrolyte delivery is the rate-limiting step?

A

Chloride delivery

81
Q

What is the formula to calculate corrected chloride?

A
82
Q

The change of chloride can result from change of pure water or gain/loss of chloride. What are the four classification of chloride disorder?

A

Concentration alkalosis (free water loss)
Dilution acidosis (free water gain)
Hyperchloremic acidosis
Hypochloremic alkalosis

83
Q

Why patients receiving KBr may have elevated chloride?

A

Because the machine falsely measures Br as chloride → pseudohyperchloremia

84
Q

What is the body distribution of magnesium?

A

99% are intracellular
67% in the bone
20% in the muscles
11% in the other soft tissue
1% are extracellular
55-65% ionized
30-40% protein-bound (mainly albumin)
4-6% complexed form

85
Q

Where is Mg mainly absorbed in the GI tract?

A

Ileum

86
Q

In the kidney, where is Mg mainly reabsorbed?

A

Cortical thick ascending limb of loop of Henle (60%)

  • Very different from other electrolytes!
  • Only 10-15% at the proximal tubule and another 10-15% at distal tubule
87
Q

What factors increase Mg reabsorption in the kidney? What factors decrease Mg reabsorption in the kidney?

A

Increase: PTH, calcitonin, glucagon, ADH, aldosterone, insulin

Decrease: prostaglandin E2, hypokalemia, hypophosphatemia, acidosis

88
Q

What does increased Mg level do to the vessels (vasoconstriction vs vasodilation)? Why?

A

Vasodilation
Mg blocks the Ca channels

89
Q

Does Mg deficit cause neural excitation or inhibition?

A

Neural excitation

90
Q

True or False: Magnesium can block the NMDA receptors in the CNS.

A

True

91
Q

What is the two most common causes of hypermagnesemia?

A

Renal insufficiency
iatrogenic

92
Q

List 5 functions of Mg.

A

1) Cofactor for many ion channels (e.g. Na-K ATPase)
2) Help in depolarization of muscles & neurons
3) T-cell activation
4) Control oxidative phosphorylation
5) Affect Ca movement across the mitochondria
6) Cofactor for the DNA and RNA polymerase → important for protein synthesis
7) Cofactor for insulin release and function

93
Q

What are the three mechanisms of the cells maintain cytosolic Mg level?

A

1) Intracellular protein-binding of Mg
2) Influx or efflux of Mg through the Mg-Na antitransporter or TRPM channels on the cell membrane
3) Sequestration or release from the organelles

94
Q

What ECG abnormalities can be observed in Mg deficiency?

A

A fib
V-tach
SVT
Torsade de Pontess

95
Q

List 3 treatment for Mg excess.

A

1) IV fluid to promote diuresis
2) 10% Calcium chloride 100 ml/kg slow IV over 20 minutes
3) Peritoneal dialysis

96
Q

True or False: Hypercalcemia can induce renal vasoconstriction which leads to decreased GFR

A

True

97
Q

What is the proposed mechanism of increased gastrin level in hypercalcemic dog?

A

Hypercalcemia → decreased GFR → decreased gastrin excretion

98
Q

What are the differentials for hypercalcemia?

A

Hyperparathyroidism
Osteolytic disease
Granulomatous disease (e.g. blastomycosis)
Spurious
Idiopathic
Youth
Addison’s disease
Renal disease
Vitamin D toxicity

99
Q

Why does patients with granulomatous disease develop hypercalcemia?

A

the macrophages and giant cells in the granulomatous disease can produce 1𝜶-hydroxylase

100
Q

What are the most common neoplasia that can cause hypercalcemia in dogs?

A

T-cell lymphoma
Apocrine gland anal sac adenocarcinoma
Multiple myeloma

101
Q

What are the most common neoplasia that can cause hypercalcemia in cats?

A

Lymphosarcoma
SCC

102
Q

How do you treat hypercalcemia?

A

1) IV fluid to facilitate calciuresis
2) Glucocorticoid - decrease bone Ca reabsorption, GI absorption and increase urine Ca excretion
3) Furosemide
4) Bisphosphonate - directly decrease osteoclast activity & induce osteoclast apoptosis

103
Q

List 5 differentials for hypocalcemia.

A

1) Eclampsia
2) CKD
3) Hypoalbuminemia
4) Hypoparathyroidism
5) Ethylene glycol intoxication
6) Acute pancreatitis
7) Massive blood transfusion (citrate intoxication)
8) Sepsis
9) GI disease (e.g. PLE)

104
Q

How long does it take for oral calcitriol to effect?

A

1-4 days
* dose 30-60 ng/kg/d

105
Q

What is the dose for daily oral calcium supplementation?

A

25-50 mg/kg/d elemental calcium divided into a few doses

106
Q

How does respiratory alkalosis affect the serum phosphorus level?

A

It decreases serum phosphorus level due to activate intracellular phosphofructokinase → promote glycolysis → increase intracellular phosphorus demand

107
Q

Where are Ca and Phos being reabsorbed mainly in the nephron?

A

Calcium: distal renal tubules
Phosphorus: proximal renal tubules

108
Q

How does hypophosphatemia affect the oxygen delivery to the tissue? Why?

A

Hypophosphatemia will decrease 2-3 DPG production → increase oxygen affinity to the hemoglobin → decrease oxygen unloading to the tissue

109
Q

What are the two major clinical consequences of hyperphosphatemia?

A

Hypocalcemia
Soft tissue mineralization

110
Q

What are the concentrations of potassium and phosphorus in potassium phosphate?

A

Potassium: 4.4 mEq/ml
Phosphorus: 3mmol/ml

111
Q

What is the cutoff number for [Ca] x [P] solubility product for increased risk of soft tissue mineralization?

A

> 60

112
Q

How low does the GFR need to be will us see hyperphosphatemia in CKD patient?

A

20% or less

113
Q

What ECG changes can be seen in patients with hypercalcemia?

A

Widened QRS complex
Widened T wave
Prolonged PR interval
Shorten QT interval
Shorten or absent ST segment

Bradyarrhythmias

114
Q

True or False: Ionized hypocalcemia is a poor prognostic indicator in dogs with sepsis.

A

True

115
Q

Can you give calcium subQ or not? why?

A

No! Never!
Can cause severe skin necrosis and abscess formation

116
Q

What is the CRI rate for calcium supplementation?

A

1-3 mg/kg/hr elemental Ca

117
Q

What electrolyte is the second most abundant intracellular cation?

A

Magnesium

118
Q

True or False: Acute pancreatitis can cause hypocalcemia by saponification but not magnesium.

A

False

It can cause both hypocalcemia and hypomagenesemia.

119
Q

True or False: Hypomagnesemia can predispose patient to digoxin-induced arrhythmias.

A

True

Both inhibit Na-K ATPase

120
Q

How can hypomagnesemia affect the potassium, sodium and calcium?

A

Hypokalemia
Hyponatremia
Hypocalcemia

121
Q

How dose hypomagnesium and hypermagnesium affect the PTH?

A

Hypomagnesium PTH in

122
Q

If the patient has concurrent hypocalcemia with hypomagnesemia, which Mg solution should you give? Why?

A

You should give MgCl2 instead of MgSO4.
Because SO42- can chelate with calcium and make hypocalcemia worse.

123
Q

What are the endocronipathies that can cause hypomagnesemia?

A

Hypothyroidism
Hypoadrenocorticism
Hyperparathyroidism

124
Q

What is one of the earliest signs of magnesium overdose?

A

Hyporeflexia (neuromuscular blockade effect)

125
Q

What is the most common form of inorganic phosphate in the blood?

A

Monohydrogen phosphate (HPO42-)
Dihydrogen phosphate (H2PO4-)

85% for both

126
Q

What is the major inorganic form of phosphate in the RBCs?

A

2,3-DPG

127
Q

How dose salicylate toxicity affect the phosphorus?

A

Salicylate inhibits oxidative phosphorylation and Kreb’s cycle → initially cause hyperphosphatemia → later becomes hypophosphatemia due to renal excretion

128
Q

How does hypophosphatemia cause rhabdomyolysis?

A

ATP depletion → loss of muscle cell integrity

129
Q

which is the most important transporter for phosphorus reabsorption in kidney?

A

Na-PO4 cotransporter at the proximal renal tubule

130
Q

The Na-PO4 cotransporter at the nephron is inhibited by metabolic acidosis or alkalosis?

A

metabolic acidosis

131
Q

What is hungry bone syndrome and when does it commonly happen?

A

A state of profound hypocalcemia after parathyroidectomy or parathyroid ablation

132
Q

Hypomagnesemia can cause platelet activation or inhibition?

A

Platelet activation

133
Q

What are the consequences of metabolic acidosis?

A

1) Decreased protein synthesis & function
2) Arterial vasodilation
3) Decreased cardiac contractility
4) Impaired coagulation
5) Altered CNS function
6) Decreased renal & hepatic blood flow
7) Insulin resistance
8) Decrease response to catecholamines

134
Q

What is the osmolarity of sodium bicarb?

A

2000 mOsm/L

135
Q

What is the mEq/ml of Na and bicarb in the 8.4% NaHCO3? how much mmol/L are they?

A

1 mEq/ml of Na and bicarb
1000 mmol/L

136
Q

List 10 potential adverse effects from sodium bicarbonate administration.

A

1) Hypernatremia
2) Hypervolemia
3) Hyperosmolarity
4) Paradoxical intracellular acidosis
5) Hypercapnea
6) Phlebitis
7) Increase oxygen affinity to hemoglobin
8) Increase lactate production
9) Hypokalemia
10) Hypocalcemia (ionized)

137
Q

Explain paradoxical intracellular acidosis

A

When sodium bicarbonate is given to a weakly acidic environment, CO2 is formed. Because of high permeability of CO2 across the cell membrane, CO2 may enter the cell, bind to water and cause intracellular acidosis by releasing hydrogen ion.

138
Q

What is the formula for sodium bicarbonate dose?

A

Sodium bicarbonate dose (mmol) = 0.3 x body weight x base deficit (mmol/L)

139
Q

True or False: According to current recommendation, sodium bicarbonate can be considered in lactate acidosis if pH < 7.0.

A

False

Sodium bicarbonate is not recommended in treating lactate acidosis regardless of pH

140
Q

What does RECOVER guideline recommend in terms of sodium bicarbonate administration in CPCR?

A

Sodium bicarbonate in not recommended routinely but can be considered in prolonged CPCR > 10-15 minutes without ROSC.

141
Q

What are the three approaches to evaluate acid-base status?

A

1) Henderson-Hasselbalch equation (traditional approach)
2) Stewart approach
3) Semiquantitative approach

142
Q

When a blood-gas sample is exposed to air or has a big air-bubble in it, how will the PO2 and PCO2 change?

A

PO2 will increase
PCO2 will decrease

143
Q

What is the Henderson-Hasselbalch equation?

A
144
Q

What is the equation for anion gap?

A

Anion gap = (Na + K) - (Cl + HCO3-)

145
Q

What is the definition of Base Excess (BE)?

A

The amount of acid or base needed to add to an oxygenated whole blood sample to restore the pH to 7.4 at 37C and pCO2 of 40 mmHg.

146
Q

What does increased BE and decreased BE mean?

A

Increased BE: alkalosis
Decreased BE: acidosis

147
Q

What is the unit of base excess?

A

mEq/L or mmol/L

148
Q

What is the benefit of use BE to access acid-base status?

A

it’s independent of the change of respiratory system

149
Q

What is the normal range for BE?

A

0 ± 3

150
Q

What does TCO2 mean in blood gas?

A

It means the total CO2 in the blood no matter what forms they are. The majority of CO2 exists as bicarbonate in the blood.

151
Q

What is the correlation between TCO2 and HCO3-

A

TCO2 is 1-2 mmol/L higher than HCO3-

152
Q

Describe the two types of metabolic acidosis according to the AG.

A

Hyperchloremic acidosis (normal AG):
- The cause of acidosis is due to loss of bicarb from GI tract or kidney
- Secretive diarrhea, renal tubular acidosis, dilutional, acidosis

Normochloremic acidosis (high AG):
- The cause of acidosis is due to increased unmeasured anion
- DUEL: lactate, ethylene glycol, ketone bodies, uremia, sulfate, phosphate

153
Q

What is normal AG in dogs and cats?

A

Dog: 18 (12-24) mmol/L
Cat: 24 (13-27) mmol/L

  • 12-20 mmol/L in ER textbook
154
Q

What compose of normal unmeasured anion and cation?

A

UA: albumin, phosphate
UC: Mg, Ca

  • Hypoalbuminemia can mask increased unmeasured anion
155
Q

True or False: Severe hypokalemia can cause metabolic acidosis.

A

False

Metabolic alkalosis

156
Q

Where is the main site for bicarb reabsorption in the nephron?

A

Proxima renal tubule

157
Q

Name 3 examples for each acid-base imbalance.

A

Metabolic acidosis
- DKA
- Ethylene glycol toxicity
- AKI

Metabolic alkalosis
- Sodium bicarb overdose
- Upper GI obstruction & vomiting
- NG tube suctioning
- Loop diuretic administration cause renal acid loss

Respiratory acidosis
- Cervical spinal cord injury leading to hypoventilation
- Pneumothorax
- Diaphragmatic hernia
- Anesthesia & sedative cause hypoventilation
- NM junction disease

Respiratory alkalosis
- Pain & panting
- Anxiety & panting
- Severe hypoxemia

158
Q

Name four buffers in the blood.

A

1) Bicarbonates
2) Phosphates
3) Hemoglobin
4) Plasma protein

159
Q

What are the three “independent” variables that determine acid-base status in the Stewart approach?

A

1) pCO2
2) Strong ion difference (SID)
3) Total weak acid (Atot)

160
Q

What is the definition of strong ion in the Stewart approach and what are the five common strong ions?

A

The ion that are dissociated at physiologic pH

Na, K, Cl, Mg, Ca

  • Some references include lactate and ketoacids
161
Q

What is the equation for SID?

A

SID = (Na + K + Ca + Mg) - Cl

162
Q

Does increased SID indicate metabolic acidosis or alkalosis?

A

Metabolic alkalosis

163
Q

Which solution has the highest SID? 0.9% NaCl, LRS, sodium bicarbonate.

A

Sodium bicarbonate > LRS > 0.9% NaCl

164
Q

What are the two main variables in Atot?

A

albumin, phosphate

165
Q

In dogs, what are the net protein charge for total protein and albumin, respectively?

A

Total protein: 0.25 mEq/g
Albumin: 0.42 mEq/g

166
Q

In cats, what are the net protein charge for total protein and albumin, respectively?

A

Total protein: 0.19 mEq/g
Albumin: 0.41 mEq/g

167
Q

Does increased Atot indicate metabolic acidosis or alkalosis?

A

Metabolic acidosis

168
Q

In the Stewart approach, what is strong ion gap (SIG) used for?

A

It is used to evaluate the unmeasured anions (e.g. lactate, sulfates, ethylene glycol, ketones)

169
Q

What is the equation for SIG?

A

1) SIG = SID - Atot - bicarbonate
2) Dog: Simplified SIG = (albumin x 4.9) - AG
3) Cat: Simplified SIG = (albumin x 7.4) - AG

170
Q

Does increased SIG indicate metabolic acidosis or alkalosis?

A

Metabolic acidosis

171
Q

What are the five metabolic acid-base abnormalities that can be identified by the Stewart Approach?

A

1) Increased SID - metabolic alkalosis
2) Decreased SID - metabolic acidosis
3) Increased Atot - metabolic acidosis
4) Decreased Atot - metabolic alkalosis
5) Increased SID - metabolic acidosis

172
Q

What is the benefit of using SIG to evaluate acid-base than using AG?

A

SIG is independent of albumin level → more sensitive in identifying unmeasured anion especially in hypoalbuminemic patient

173
Q

What is semi-quantitative approach also called?

A

Stewart-Fencl approach

174
Q

What is the semi-quantitative approach?

A

It evaluates the acid-base status based on assessing the effect of five different parameters on the base excess

175
Q

What are the five parameters in the Stewart-Fencl approach?

A

1) Free water effect (marked by Na concentration)
2) Chloride effect
3) Albumin effect
4) Phosphate effect
5) Lactate effect

  • Needs to measure pH, pCO2, BE
176
Q

What are the formula for the effect of each parameters in the Stewart-Fencl approach? What does the positive sum mean?

A

1) Free water effect = (Measured Na - Normal Na)/4
2) Chloride effect = Normal chloride - Corrected chloride
* Corrected chloride = Measured chloride x (Normal Na/Measured Na)
3) Albumin effect = (Normal albumin - Measured albumin) x 4
4) Phosphate effect = (Normal phosphate - Measured phosphate)/2
5) Lactate effect = Measured lactate x (-1)

Sum = free water effect + Chloride effect + Albumin effect + Phosphate effect + Lactate effect

Positive sum = alkalotic influence in BE

177
Q

An excess free water will cause acidosis or alkalosis?

A

Acidosis (dilutional acidosis)

178
Q

Does an increased chloride effect indicate acidosis or alkalosis?

A

Alkalosis

179
Q

According to Stewart-Fencl Approach, does a decreased albumin concentration indicate acidosis or alkalosis?

A

Alkalosis

180
Q

How does atrial natriuretic peptide (ANP) work at the kidneys?

A

It increases the GFR by dilating the afferent arterioles and constricting the efferent arterioles.

181
Q

What is normal anion gap in dogs and cats?

A

Dog: 12-24 (average: 18) mEq/L
Cat: 13-27 (average: 24) mEq/L

182
Q

When calculate the sodium bicarbonate dose, how do you calculate base deficit?

A

Base deficit = 24 - patient’s bicarbonate concentration

Boards: AcidBase/Fluids/Electrolytes (13 decks)

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