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Auburn ECC > Acid/Base/Fluid/Lyte > Flashcards

Acid/Base/Fluid/Lyte Flashcards

1
Q

Free water deficit calculation?

A

TBW x (serum Na / normal serum - 1)

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2
Q

Normal SID in dogs vs cats

A

dog: 27 mEq/L cat: 30 mEq/L

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3
Q

What toxins cause type B lactic acidosis?

A

cyanide ethanol ethylene glycol

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4
Q

For every 100 mg increase in glucose, sodium decreases by?

A

1.6 (pseudohyponatremia)

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5
Q

Myelinolysis lesions in dogs vs people?

A

dog: thalamus people: pons (hence “central pontine myelinolysis”)

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6
Q

Boag, JVIM, 2005. Dogs with linear FBs were more likely to have what e-lyte abnormality?

A

Hyponatremia. Study also found hypochloremic metabolic alkalosis found in most regardless of GI or jejunal FB. 25% hypokalemic

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7
Q

death and severe complications of hyponatremia typically occur when the serum Na concentration is less than what?

A

120 meq/L

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8
Q

what gradient of water between the plasma and brain in dogs can result in translocation of water between plasma and the brain in dogs?

A

30-35 mOsm/kg gradient

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9
Q

when hyponatremia is chronic, brain volume is adjusted toward normal via what mechanisms?

A

loss of potassium and organic osmolytes from cells

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10
Q

what are the clinical signs of acute water intoxication?

A

weakness, incoordination, and seizures

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11
Q

T/F- acute water intoxication likely occurs only if the patient has an underlying cause of impaired water excretion at the time of water load?

A

true

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12
Q

severe symptomatic hyponatremia of acute onset (clinical signs)

A

death, cerebral edema, seizures

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13
Q

what is the maximum recommended rate of correction of chronic hyponatremia?

A

>10-12 meq/L in 24 hrs

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14
Q

name the type of injury that occurs to the brain when chronic hyponatremia is corrected too quickly

A

demyelination or myelinolysis

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15
Q

where in the brain are lesions often found with demyelination from sodium correction?

A

pons, thalamus, subcortical white matter, cerebellum

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16
Q

list the MRI abnormalities associated with demyelination

A

hyperintense area on T2, hypointense on T1, not enhanced with contrast

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17
Q

list the clinical signs that have been reported & associated with myelinolysis?

A

lethargy, weakness, ataxia, progressing to hypermetria and quadriparesis, loss of CPs, dysphagia, trismus, decreased menace

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18
Q

What mechanism causes a hyponatremic patient to excrete solute-free water via the kidneys when they are volume resuscitated?

A

volume repletion in hypovolemic patients abolishes the nonosmotic stimulus for vasopressin release and allows the animal to excrete solute-free water via the kidneys- this itself tends to correct hyponatremia

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19
Q

in edematous hyponatremic patients, what treatments should be considered?

A

dietary sodium restriction, diuretic therapy or 0.9% NaCl in combination with a diuretic for rapid correction of hyponatremia

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20
Q

How do AVP receptor antagonists work?

A

block either V2 or V1/V2 receptors and increase free water excretion by the kidneys; they normalize serum Na in patients with non-osmotic release of AVP causing euvolemic (SIADH) or hypervolemic (CHF, liver failure) hyponatremia

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21
Q

Why are infusion site reactions common with administration of conivaptan, a V2/V1A receptor antagonist?

A

the pH of the drug is very low

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22
Q

T/F- vasopressin Rc antagonists have been shown to improve survival in patients with CHF?

A

false, but they do promote aquaresis and correct hyponatremia in this population

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23
Q

Which other drugs should be cautiously administered when giving conivaptan?

A

other CYP450 inhibitors such as ketoconazole

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24
Q

what is normal water intake for dogs? cats?

A

dogs- 90 ml/kg/day cats- 45 ml/kg/day

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25
Q

what is normal urine output for dogs? cats?

A

20-45 ml/kg/day for dogs and cats

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26
Q

what are the most common causes of PU/PD in dogs and cats?

A

chronic renal failure, diabetes mellitus, hyperadrenocorticism, hyperthyroidism

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27
Q

contraindications for water deprivation test?

A

azotemia, clinical dehydration, +/- severe polyuria b/c they could become rapidly dehydrated

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28
Q

Briefly describe a water deprivation test

A

-empty bladder + collect baseline data (body weight, hct, TP, skin turgor, osmolality, urine osmolality, USG) -withhold water and monitor data every 2-4 hours -stop test once animal concentrates urine or loses more than 5% body weight -if 5% body weight, give 0.25-0.5 U/kg aqueous vasopressin

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29
Q

At 5% body weight, what are the typical values for USG, urine osmolality and urine/plasma osmolality ratio in normal dogs and cats?

A

dogs- USG 1.050-1.076, urine osm 1787-2791, urine/plasma osm 5.7-8.9 cats- USG 1.047-1.087, urine osm 1581-2984

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30
Q

T/F- during a water depriv test, normal dogs and dogs with psychogenic polydipsia should show no response to ADH administration?

A

true

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31
Q

Describe the aqueous vasopressin test

A

IV infusion of aqueous vasopressin (pitressin) at 10 mU/kg is given over 60 min. Bladder is emptied and USG is measured at baseline and q30 min for 3 hrs.

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32
Q

Define COP

A

Force generated when 2 solutions with different concentrations of colloids are separated by a semipermeable membrane

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33
Q

What is albumin’s contribution to COP?

A

65-80%

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34
Q

What is the Gibbs-Donnan effect?

A

Sodium’s constribution to COP b/c they are noncovalently bound to negatively charged albumin

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35
Q

What besides albumin and sodium contribute to COP?

A

globulins, fibrinogen, hemoglobin, RBC (<5%)

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36
Q

Odunayo, JVECC, 2011. COP in WB vs. plasma. Main findings?

A

plasma COP * lower than whole blood COP with mean difference 0.5 mm Hg; regardless both in reference range (21-25 mm Hg); no diff in sex, decreased slightly when frozen, hemolysis had no effect

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37
Q

Hayes, JVECC, 2011. What significantly affected TPP readings?

A

hypercholesterolemia and hyperglycemia

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38
Q

An increase in serum glucose by ___ assc’d with increase in refractometer TPP of ____. Hayes, JVECC, 2011

A

10 mmol/L0.23 g/dL

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39
Q

An increase in serum cholesterol of 38.6 mg/dL (1 mmol/L) assc’d with increase in refractometer TPP of ____.

A

0.14 g/dL

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40
Q

TPP < 58 g/L was highly specific for serum hypoalbuminemia and hypoproteinemia. T/F Hayes, JVECC, 2011

A

T - 84% specificitynonlinear relationship

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41
Q

What formula predicted toal protein by refractometer?

A

serum protein (g/L) = 0.3 + 0.84(refractometer TP)

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42
Q

How does refractometer work?

A

measures angle of refraction b/t air and aqueous solution

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43
Q

Mechanisms of iHCa in trauma patients.

A

CalciuresisDilution following fluidsCellular uptake of calciumChelation with citrate in blood productsAberrations in hormones and electrolytes that regulate iCa

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44
Q

Holowaychuk, JVECC, 2011. Significant differences in iHCa trauma patients.

A

higher HR, lower SBP, higher ATT, higher systems score, lower HCO3, higher BE, higher lac, higher creat, higher mortality, longer in hospital, needed more transfusion, colloid, oxygen, vasopressor

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45
Q

The trauma system scores uses what 6 body systems?

A

skin, appendage, thorax, head, abdomen, spine

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46
Q

iHCa (<1.25) found in __% trauma patients. Holowaychuck, 2011, JVECC

A

16%

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47
Q

What are the 3 independent variables in Stewart AB?

A

Atot, pCO2, SID

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48
Q

What is Atot?

A

total plasma concentration of nonvolatile weak buffers such as albumin, globulins, and phosphate

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49
Q

What is SID?

A

Difference in charge between fully dissociated and therefore nonreactive or nonbuffering strong cations and strong anions at physiologic pH

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50
Q

What is the strong ion gap?

A

SIDa - SIDeSIDa: Na, K, Ca, Mg, Cl, lactateSIDe: HCO3, albumin, phosphate

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51
Q

SIG increased by ______ and decreased by ______.

A

unmeasured anions, unmeasured cations

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52
Q

What was the mean and derived ref range for SIG using SIDa-SIDe? Fettig, JVECC, 2012

A

mean 7.13; RR: 1.85-10.61

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53
Q

What was the mean and derived reference range for SIG using (alb) x 4.9-AG? This formula derived from Atot and Ka on healthy dogs. Fettig, JVECC, 2012

A

mean -0.22, RR: -5.36-5.18

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54
Q

SIG in vivo is usually…

A

positive due to an excess of unmeasured anions compared to unmeasured cations

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55
Q

BE takes into account…

A

free water, chloride, protein, and phosphate concentrations

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56
Q

T/F. A simple conversion factor can convert SIG1 to SIG2.

A

F - values are not interchangable and conversion factor cannot be used

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57
Q

What are the two methods to correct hyponatremia?

A
  1. Sodium deficit [(desired change)] x TBW2. Adrogue-Madias to determine estimation of effect of infusing a 1 L bag of fluids:(desired change) = (infusate Na - serum Na) / (TBW +1)
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58
Q

How do you calculate free water deficit?

A

TBW x (serum Na/normal sodium - 1)

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59
Q

For every 100 mg increase in glucose, sodium decreases…

A

1.6 - pseudohyonatremia

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60
Q

How much sodium does 23.4% have in mEq/ml

A

4

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61
Q

Myelinolysis lesions in dogs are typically found where?

A

thalamus (pons in humans)

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62
Q

What are the most common reasons for a Na/K less than 27:1

A

renal failure, hypoadrenocorticism, GI dz (whips, salmonella, duodenal perforation)also chronic chylothorax, lung lobe torsion, neoplastic pleural effusion, pregnancy in greyhounds

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63
Q

What is the most notable adverse metabolic effect of hypokalemia?

A

glucose intolerance, insulin release impaired

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64
Q

Cardiac effects of hypokalemia.

A

High intracellular to extracellular K induces state of electrical hyperpolarization leading to prolongation of the the action potential. This may predispose to atrial and ventricular tachyarrhythmias, AV dissociation, and ventricular fibrillationPredisposes to dig induced cardiac arrhythmias and causes myocardium to be refractory to class 1 antiarrhythmics

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65
Q

How do you treat a normovolemic, hyponatremic patient in an emergency setting of hyponatremia (chronic)?

A

mannitol along with furosemide to ensure that electrolyte free water is excreted along with the mannitol; goal = increase sodium no more than 10 mEq/L during first 24 hours

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66
Q

Causes of pseudohyperkalemia

A

thrombocytosis, leukocytosis, Akita dogs (their RBC have a fxnal Na-K ATPase so have high intracellular K),

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67
Q

Drugs that promote hyperkalemia

A

ACE inhibitors, Beta blockers, K sparing diuretics

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68
Q

Complexed calcium is bound to…

A

phosphate, bicarbonate, lactate, citrate, oxalate

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69
Q

Principle actions of PTH

A

increased tubular reabsorption of calcium, increased osteoclastic bone resorprtion, increased production of 1,25(OH)2D3

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70
Q

Calcitonin

A

Produced by thyroid gland in response to hypercalcemia, acts on bone to inhibit osteoclastic bone resorption activity

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71
Q

Effects of alkalosis and acidosis on ionized calcium?

A

alkalosis decreases iCa (b/c more bound to protein)acidosis increases iCa (b/c less bound to protein)

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72
Q

Clinical signs of hypercalcemia

A

PU/PD (dogs only), anorexia, constipation, lethargy, weakness, ataxia, obtundation, listlessness, muscle twitching, seizures, coma

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73
Q

ECG findings of hypercalcemia

A

prolonged PR interval, widened QRS, shortened QT, shortened or absent ST, widened T wave, bradyarrhythmias that progress to complete heart block, asystole, cardiac arrest

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74
Q

Most common cause of hypercalcemia in dogs vs cats?

A

dogs cancercats idiopathic

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75
Q

Why is 0.9% saline the fluid of choice for hypercalcemia?

A

Additional sodium ions present competition for calcium and result in reduced renal tubular calcium reabsorptionFurosemide enhances urinary calcium loss

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76
Q

Mechanism of hypercalcemia in fungal disease

A

due to dysregulated production of 1,25-(OH2)D3 (calcitriol) by activated macrophages trapped in pulmonary alveoli and granulomatous inflammation.

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77
Q

Steroid MOA for hypercalcemia

A

reduces bone resorption, increases urinary loss, decreases intestinal calcium absorption

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78
Q

Calcitonin MOA for hypercalcemia

A

decreases osteoclast bone resorption

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79
Q

Bisphosphonates MOA for hypercalcemia

A

Decreases osteoclast activity and bone resorptionEx: pamidronate, zoledronate, alendronate (oral)

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80
Q

Calcimimetic MOA

A

Activate the calcium sensing receptor and therefore decrease PTH

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81
Q

ECG abnormalities of hypocalcemia

A

decreased inotropy and chronotropy (bradycardia), prolonged QT interval (d/t proloned ST segment), deep, wide T waves, or AV block

82
Q

Serum magnesium breakdown

A

66% (cats) 63% (dogs) ionized, 4-6% complexed to anions, 30-31% protein bound

83
Q

Where is most Mg absorbed in GI tract?

A

jejunum and ileum

84
Q

Where is most Mg absorption in kidney?

A

LoH

85
Q

ECG changes of hypomagnesemia

A

prolongation of PR interval, widening of QRS, depression of ST, peaking of T wave

86
Q

What effect does magnesium have on acetylcholine release?

A

Hypomagnesemia increases acetylcholine release and enhances the excitatiblity of nerve and muscle membranes; also increases intracellular content of skeletal muscle

87
Q

Mg relationship to Ca

A

Hypomagnesemia impairs PTH release and enhances calcium movement from extracellular fluid to bone

88
Q

Endocrinopathies associated with hypermagnesemia

A

hypoadrenocorticism, hyperparathyroidism, hypothyroidism

89
Q

ECG findings of hypermagnesemia

A

prolonged PR and widened QRS

90
Q

Hypermagnesemia results in varying degrees of….

A

neuromuscular blockade

91
Q

How do you treat hypermagnesemia

A

Stop exogenous sourcesCalcium salts are direct antagonists of Mg at NM jxnSaline diuresis +/- furosemideSevere signs - anticholinesterase

92
Q

How do glucose and insulin affect Ph

A

shifts intracellular and trapped as glucose-6-phosphate

93
Q

Endocrinopathies associated with hyperphosphatemia

A

Hypoparathyroidism, GH excess (acromegaly, hyperthyroidism)

94
Q

What is base excess?

A

the amt of strong acid or base needed to restore plasma pH of iL of blood to 7.4 at a PaCO2 of 40 mm Hg and temperature of 37 Cprovides a measure of metabolic component independed of changes in PCO2

95
Q

What is the expected compensation for metabolic acidosis?

A

PCO2 decreases by 0.7 mm Hg for every 1 mEq/L decrease in bicarb +/-3

96
Q

What is the expected compensation for metabolic alkalosis?

A

PCO2 increases by 0.7 mm Hg for every 1 mEq/L increase in bicarb +/- 3

97
Q

What is the expected compensation for acute vs. chronic respiratory acidosis?

A

Bicarb increases 0.15 (acute) or 0.35 (chronic) per 1 mm Hg increase in PCO2

98
Q

What is the expected compensation for acute vs. chronic respiratory alkalosis?

A

Bicarb decreases 0.25 (acute) or 0.55 (chronic) per 1 mm Hg decrease in PCO2

99
Q

What is TCO2?

A

sum of bicarb, carbonic acid, and dissolved CO2 in the system

100
Q

When acidosis occurs without an increase in AG, the cause is

A

hyperchloremiaSo, hyperchloremic metabolic acidosis = normal AG acidosis whereas a normochloremic metabolic acidosis = high AG acidosis

101
Q

Increased SID =

A

alkalosis

102
Q

Decreased SID =

A

acidosis

103
Q

SID estimated by…

A

Na - Cl

104
Q

SID really ….

A

Na+K+Ca+Mg-Cl-other strong anions

105
Q

Causes of hyponatremia

A

sodium loss thru vomiting or diarrhea, 3rd space loss, nephrotic syndrome, hypoadrenocorticism, CHF, psychogenic polydipsia, diuretic administration, hypotonic fluid use, SIADH

106
Q

Sodium contribution to A/B

A

Hyponatremia is acidifying Hypernatremia is alkalinizing Change BE = 0.25 (dog sodium-normal sodium)Change BE = 0.22 (cat sodium-normal sodium)Hyponatremia decreases BE (more negative)Hypernatremia increases BE (less negative)

107
Q

Chloride contribution to A/B

A

Hypochloridemia is alkalinizingHyperchloridemia is acidifyingCorr Cl / pet Cl = Normal Na / pet NaChange BE = Normal Cl - pet’s ClHypochloridemia will increase BE (less negative)Hyperchloridemia will decrese BE (more negative)

108
Q

Protein’s contribution to A/B

A

Hyperproteinemia is acidifying Hypoproteinemia is alkalizingChange BE = 3 (Normal protein - Pet’s protein)Change BE = 3.7 (Normal albumin - Pet’s albumin)Hyperproteinemia increases BE (more negative)Hypoproteineia decreases BE (less negative)

109
Q

Phosphorus’s contribution to A/B

A

Hyperphosphatemia is acidifyingHypophosphatemia is alkalinizingChange BE = 0.6 (Normal Ph - Pet’s Ph)Hyperphosphatemia increases BE (more negative)Hypophosphatemia decreases BE (less negative)

110
Q

d-lactate

A

metabolic product of bacterial metabolism, also reported to be clinically significant in humans with short bowel syndrome, cats with propylene glycol, DM cats, EPI cats

111
Q

l-lactate

A

isomer produced metabolically in dogs and catsmany hospital analyzers only measure l-lactate, so d-lactate would be recognized as a metabolic acidosis w/ an increased AG not accounted by routine lactate measurement

112
Q

What is the purpose of lactate synthesis in aerobic metabolism?

A

to regenerate nicotinamide adenine dinucleotide (NAD) so that glycolysis can procede NAD essential reducing agent for glycolysisLactate can also be transported to liver under aerobic conditions for energy storage via gluconeogenesis and glycogen synthesis –> Involves conversion of lactate to pyruvate in liver (cori cycle) under aerobic conditions to drive Kreb’s cycle

113
Q

What is the difference between A and B lactate?

A

Type A = true hypoxic formType B = nonhypoxic form, occurs in face of adequate oxygen delivery when mitochondrial oxidative fxn is abnormal

114
Q

Causes of Type A lactic acidosis

A

Hypoxemia, anemia, poor perfusion, increased tissue demand (exercise, convulsions, heat stroke)

115
Q

Causes of Type B lactic acidosis

A

Drugs, toxins, hypoglycemia, DM, liver failure, renal failure, LSA, sepsis, inborn errors in metabolism

116
Q

What toxins cause type B lactic acidosis?

A

cyanide, ethanol, ethylene glycol

117
Q

What drugs cause type B lactic acidosis?

A

salicylate, lactulose, beta agonists, nitroprusside, acetaminophen, propylene glycol, phenformin

118
Q

What (other than drugs and toxins) cause type B lactic acidosis?

A

>SIRSDMMalignancy (hematologic) Thiamine deficiency Liver failure Hypoglycemia in newborn errors or metabolism Mitochondrial myopathies

119
Q

What are the metabolic complications of TLS?

A

hyperphosphatemia, hyperkalemia, hypocalcemia, metabolic acidosis

120
Q

When would you expect to hear a mill weed murmur?

A

air embolism

121
Q

What variables decreased in Muir’s study on LRS to anesthetized dogs, JAVMA 2011?

A

PCV, total protein, albumin, hemoglobin, whole blood viscosity

122
Q

Crystalloids with SID of ___ maintain base excess near zero and are considered balanced.

A

24

123
Q

Conclusions of Muir’s study…JAVMA, 2011

A

Conventional rates of LRS to healthy iso’d dogs increase plasma volume and CO and decrease blood viscosity and protein but do not increase rate urine prod’n or produce consistent and significant alterations in mean CVP or arterial BP

124
Q

Boag, JVIM, 2005. Dogs with linear FBs were more likely to have what e-lyte abnormality?

A

Hyponatremia. Study also found hypochloremic metabolic alkalosis found in most regardless of GI or jejunal FB. 25% hypokalemic

125
Q

i-hypoCalc in critically ill dogs (Holowaychuk, 2009, JVIM). Findings?

A

16% critically ill dogs hypocalcemicihypo Ca assc’d with longer ICU and hospital stays, but not with decreased survival. Septic dogs (>3 SIRS criteria and positive culture) more likely to have ihypo Ca

126
Q

Normal value for Atot in dogs vs. cats

A

17.4 +/- 8.6 mmol/L (equivalent to 0.273 mmol/g total protein or 0.469 mmol/g albumin) DOGS24.3 +/- 4.6 mmol/L cats

127
Q

Normal Ka dogs vs. cats

A

0.17 +/- 0.11 x 10^-7 DOGS0.67 +/- 0.4 x 10^-7 CATSKa = dissociation constant for plasma nonvolatile buffers

128
Q

Normal pKa dogs

A

7.77

129
Q

Normal SID in dogs vs. cats

A

27 mEq/L dogs30 mEq/L cats

130
Q

Net protein charge for normal canine plasma

A

0.25 mEq/g total protein0.42 mEq/g albumine

131
Q

What are the 6 primary acid-base disturbances in the strong ion approach?

A
  1. respiratory acidosis2. respiratory alkalosis3. strong ion acidosis (decreased SID)4. strong ion alkalosis (increased SID)5. nonvolatile buffer ion acidosis (increased albumin, globulin, or phosphate)6. nonvolatile buffer ion alkalosis (decreased albumin, globulins, or phosphate)
132
Q

List 3 things that stimulate aldosterone production

A

hyperK, angiotensn II, ACTH

133
Q

List 2 things that inhibit aldosterone production

A

dopamine, atrial natriuretic peptide

134
Q

list 5 idiogenic osmoles

A

taurine, inositol, glutamine, glutamate, sorbitol

135
Q

What is the expected change in serum Na for every 1000 mg/dL increase in serum triglyceride?

A

decrease in Na of 2 mEq/L

136
Q

what is the expected change in serum Na for every g/dL increase in protein above 8 g/dL?

A

decrease in Na by 0.25 meq/L

137
Q

what is the expected decrease in serum Na for every 100 mg/dL increase in serum glucose?

A

Decrease of Na of 1.6 meq/L (or even larger decrease if BG is >400)

138
Q

list the 4 diseases listed in Dibartola that are associated with a hypervolemic, low plasma osmolality hypoNa

A

severe liver disease, CHF, nephrotic syndrome, advanced renal failure

139
Q

list the 7 criteria that must be met in order to diagnose SIADH

A
  1. hypoNa with plasma hypoosmolality
  2. high urine osmolality >100 mOsm/kg
  3. Normal adrenal, renall and thyroid function
  4. presence of natriuresis despite hypoNa and plasma osmolality (urine Na >20 meq/L)
  5. no evidence of hypovolemia
  6. no evidence of ascites or edema, CHF, liver dz etc
  7. correction of hypoNa by fluid restriction
140
Q

where is 60% of Cl reabsorbed in the kidney? (what part of nephron)

A

proximal convoluted tubule

141
Q

in which segment of the nephron does Cl resorption occur transcellularly, which contributes to the lumen-positive transepithelial voltage?

A

thick ascending limb of loop of henle

142
Q

what does the anion gap represent?

A

difference between measured cations (Na & K) and measured anions (Cl & HCO3)

143
Q

what are the 2 types of metabolic acidosis?

A

hyperchloremic (normal anion gap)

normochloremic (high anion gap)

144
Q

what is the equation for corrected Cl?

A

Cl (corrected)=Cl (meas) x [Nanorm/Nameas]

145
Q

in what ways does Cl cause metabolic alkalosis?

A

Decreases in Cl increase SID, which causes metabolic alkalosis

Cl depletion is assoc with increased plasma HCO3

146
Q

what percentage of K is secreted in the urine vs the GI ?

A

90-95% urine

5% GI

147
Q

in general, what effect does acid-base status have on the movement of K from ECF<–>ICF

A

acidosis makes K move from ICF–>ECF

alkalosis makes K move from ECF–>ICF

148
Q

where is a majority (70%) of K reabsorbed?

A

proximal tubule- along with water and Na

149
Q

how much K is reabsorbed in the ascending limb of LOH?

A

10-20%

150
Q

how much of the filtered K is delivered to the distal nephron?

A

10-20%

151
Q

what is the mechanism of K reabsorption in the early proximal tubule?

A

paracellular route via solvent drag; there are still Na/K ATPase channels in basolateral membrane but nothing is actively resorbed through luminal side

152
Q

what are the mechanisms of K reabsorption (From the luminal side) in the loop of Henle?

A

paracellular route AND Na/K/2Cl ATPase on luminal membrane

153
Q

what is the mechanism (tyes of transport) for K in the early distal convoluted tubule?

A

K/CL cotransporter secretes K out of cells into tubular fluid; no reabsorption of K occurs here

154
Q

what is the mechanism of renal K handling in the late distal convoluted tubule and collectng duct??

A

K reabsorbed via paracellular route; no active reuptake; K moves out via luminal K channels b/c of negative potential of tubular lumen

155
Q

what is the most impt hormone affecting urinary K secretion?

A

aldosterone

156
Q

what 3 main factors affect K secretion in th distal nephron?

A

magnitude of chemical concentration gradient for K between tubular cells and tubular lumen

tubular flow rate

transmembrane potential difference across luminal membranes of tubular cells

157
Q

what 2 things (Hormones) inhibit aldosterone release?

A

dopamine and atrial natriuretic factor; both are released in response to volume expansion

158
Q

what effect does aldosterone have on the channels in nephron?

A

increases number of open Na channels on luminal side and number and activity of Na/K ATPase on basolateral side

Also stimulates H ATPase on luminal membrane

159
Q

how does acute acidosis change K secretion and why/how?

A

More H+ ions enter cells so K ions leave cells and enter the ECF; now the cell has less K in it and there is a less favorable chemical concentration gradient to push K out of the cell and into the luminal membrane

**acidosis DECREASES K secretion**

160
Q

what dog breeds have been shown to be “high potassium”, or higher K in their erythrocytes (they have presence of Na/K ATPase activity on mature RBC)?

A

akita, shiba inu, Jindo, shar-pei

161
Q

what electrolyte abnormality potentiates the effects of digoxin toxicity?

A

hypokalemia

162
Q

hypoK renders the myocardium refractory to which class of anti-arrhythmics?

A

Class I

163
Q

why is NaHCO3 potentially effective in the treatment for hyperK?

A

H+ ions leave cells to titrate the HCO3, which moves K into cells (from ECF–>ICF)

**in some studies, HCO3 didn’t work very well to reverse hyperK unless it is given with Na!**

164
Q

what are the 3 major forms of Ca in body?

A

ionized, complexed, and protein bound

165
Q

what is the role of protein-bound Ca?

A

serves as a storage pool or buffering system for iCa; it has no biologic role

166
Q

list 3 important intracellular Ca binding proteins

A

calmodulin, calbindin, troponin C

167
Q

high concentrations of serum and intracellulra iCa inhibits PTH secretion via what mechanism?

A

increased arachadonic acid

168
Q

list the main and other stimuli for PTH secretion

A

hypoCa (main)

epinephrine, isoproteronol, dopamine, secretin, PGE2, nerve ending stimulation

169
Q

draw the Serum Ca2+ vs serum PTH graphic

A
170
Q

Does calcitriol inhibit or stimulate PTH synthesis (assuming normal iCa concentrations)?

A

inhibits

171
Q

what is the half life of PTH?

A

3-5 min

172
Q

List the 4 MAJOR effects of PTH

A
  1. increase blood Ca concentration
  2. increase tubular reabsorption of Ca
  3. increase bone resorption and numbers of osteoclasts on bone surfaces
  4. accelerate formation of principal active vitamin D metabolite calcitriol
173
Q

List 3 PTHrP functions

A
  1. hormone in an endocrine manner in fetus and lactating dams
  2. paracrine factor in many fetal and adult tissues
  3. abnormal hormone in an endocrine manner in adults with humoral hypercalcemia of malignancy
174
Q

what form of vitamin D is the only one that has significant biologic activity?

A

calcitriol

175
Q

list the main functions of calcitriol

A

increases serum Ca and P concentrates, mainly via the small intestine; also some effect on bone and kidneys to reabsorb Ca and P

176
Q

how does pH of sample affect Ca?

A

acidic pH favors dissociation of Ca from protein–>increased iCa in sample

alkaline pH occurs with loss of CO2 and favors Ca binding to protein–>decreased iCa in sample

177
Q

list diseases associated with hyperCa

A
178
Q

types of cancer assoc with hyperCa?

A

lymphoma, AGASACA, multiple myeloma, bone tumors (most common carcinoma that metastasized to bone)

179
Q

what are the 2 mnemonics commonly used to remember hyperCa causes?

A

GOSHDARNIT & HARDIONS

180
Q

WHY is 0.9% NaCl the fluid of choice for tx of hyperCa?

A

It doesn’t contain any Ca & the extra Na causes increased volume expansion, increased GFR and Na competes with Ca for the rental tubular absorption, so more Ca gets lost in tubules

181
Q

Mechanism of steroid administration to help with hyperCa?

A

reducing bone resorption, decreasing intestinal Ca absorption, increasing renal Ca excretion

182
Q

what is the mechanism of bisphosphonates in the tx of hyperCa?

A

decrease osteoclast activity and fxn, decreases bone resorption of Ca

183
Q

clinical signs associated with hypoCa

A
184
Q

treatment options for hyperCa?

A
185
Q

what are the 2 major physiologic mechanisms for controlling osmolality?

A

ADH system & thirst mechanism

186
Q

what adverse effects may be associated with IV MgSO4 bolus administration?

A

hypotension, AV block, BBB, hypoCa (chelation of Ca with sulfate)

187
Q

list the 3 broad categories of causes of Mg depletion

A

increased losses (renal or GI), decreased intake, or alterations in distribution

188
Q

how does massive transfusion potentially lead to hypoMg?

A

citrated blood products can avidly chelate Mg ions when administered in large quantities

189
Q

what is the expected change in PCO2 for every 1 meq/L decrease in HCO3 during metabolic acidosis/

A

decrease PCO2 of 0.7 mm Hg

190
Q

what is the expected change in PCO2 with a 1 meq/L increase in HCO3 during metabolic alkalosis?

A

increase in PCO2 of 0.7 mm Hg

191
Q

what is the expected change in HCO3 during an acute respiratory acidosis?

A

increase HCO3 of 0.15 meq/L per 1 mm Hg increase in PCO2

192
Q

what is the expected change in HCO3 during a chronic respiratory acidosis?

A

increase HCO3 of 0.35 meq/L per 1 mm Hg increase in PCO2 (hopper) OR

3.5 meq/L increase in HCO3 for every 10 mm Hg increase in PCO2 (Dibart)

193
Q

what is the expected change in HCO3 during an acute respiratory alkalosis?

A

decrease HCO3 of 0.25 meq/L per 1 mm Hg decrease in PCO2

OR

2.5 meq/L decrease in HCO3 per 10 mm Hg decrease in PCO2

194
Q

expected change in HCO3 during chronic respiratory alkalosis?

A

decreased HCO3 of 0.55 meq/L per 1 mm Hg decrease in PCO2 or

5.5 meq/L decrease in HCO3 per 10 mm Hg decrease in PCO2

195
Q

what are the major contributors to ATOT

A

albumin and phosphate

196
Q

what does ATOT represent?

A

a value for weak acids; increased value indicates metabolic acidosis; decreased value indicates metabolic alkalosis (most commonly from decreased albumin)

197
Q

what is the SIG?

A

evaluation of unmeasured anions; equals SID-HCO3 - ATOT

198
Q

what does an increased SIG represent?

A

similar to increased anion gap; represnts presence of unmeasured anions (lactate, sulfates, EG, ketones)

199
Q

which is more sensitive to the presence of unmeasured anions in hypoalbuminemic patients- SIG or AG?

A

SIG because it is independent of changes in albumin concentration

200
Q

list the 5 effects that are used in calculations to determine a semi quantitative approach to acid-base?

A

free water effect

chloride effect

phosphate effect

albumin effect

lactate effects

the sum of all these effects are subtracted from the base excess; a negative number means ther is an acidotic influence on BE; a positive number means there is an alkalotic influence

Auburn ECC (26 decks)

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