Fluid, Electrolytes, Acid-Base Flashcards

1
Q

Metabolic consequences of persistent hyperCa?

A

Soft-tissue mineralization
Renal failure

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2
Q

DDx for hyperCa in dogs & most common cause?

A

Malignancy (LSA, AGASACA) most common
DDx hypoA, primary hyperPTH, hypervit D, osteolysis, granulomatous disease, (iatrogenic, spurious)

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3
Q

What are the general principles of the strong ion approach (SIA)? List independent & dependent variables with this approach.

List advantages over using SIA over traditional methods to assess acid-base status.

A

Principles:
- Electroneutrality must be maintained.
- AB status is primarily determined by the lungs (which alter pCO2) & kidneys (which alter strong ions).

Independent variables (altered by processes outside the body):
- pCO2: altered by alveolar ventilation.
- Strong ions: fully dissociated at normal pH, exert no buffering effect. Na+, Cl– most abundant (affected by renal excretion & absorption). Also Ca2+, Mg2+, organic acids (e.g. β-HB, lactate).
- Non-volatile weak acids (or Atot): not fully dissociated at physiologic pH. E.g. proteins, phosphate.

Adv:
- More physiologic cf traditional method of assessing AB status. - Optimal method for determining the best treatment for AB abnormalities.

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4
Q

Define strong ion difference (SID).

What does a high vs low SID indicate?

A

SID = difference between negatively & positively charged strong ions. Represents influence of strong ions on pH & HCO3–; also expressed as BE.
Represented by equation:

SID (inorganic) = Na+ + H+ = Cl– + OH–
OR
SID (inorganic) = Na+ – Cl–corr = OH– – H+.

High SID - alkalosis (increased OH– or decreased H+). Due to loss of Cl– (metabolic alkalosis) or gain of Na+ (contraction alkalosis).

Low SID - acidosis (decreased OH– or increased H+). Due to gain of Cl– (hyperchloremic metabolic acidosis) or a loss of Na+

The influence of strong ions on pH & HCO3– is expressed as the strong ion difference (SID) and BE.

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5
Q

Characteristic electrolyte & AB changes seen with pyloric outflow obstruction?

Other differentials for such changes?

A

Hypochloremic metabolic alkalosis.

Pyloric outflow obstruction (foreign body, tumor, pyloric hypertrophy)
Gastric stasis, upper intestinal obstruction, duodenal stasis, pancreatitis, removal of large volumes of gastric contents by nasogastric suctioning.

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6
Q

Consequences of phosphorus deficiency? (Name 3)

A

Hemolytic anemia
Decreased mobility
Metabolic acidosis

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7
Q

What is a respiratory condition that can trigger SIADH?

A

Aspiration pneumonia

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8
Q

Major complication associated with HCO3 administration? Mechanism?

A

Worsening acidosis.
Based on equation: HCO3 + H+ <–> H2CO3 <–> CO2 + H2O
HCO3- admin –> equation shifts R –> more CO2 produced. If patient cannot increase RR & effort to remove CO2 excess –> excess CO2 diffuses into CNS (very soluble) –> equation shifts back to L –> parodoxical CNS acidosis + increase serum H+ –> decreases blood pH (reflex respiratory acidosis).
Also excess HCO3- created –> renal excretion –> possible metabolic alkalosis (esp if renal dysfunction)

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9
Q

HypoCl - causes?

A

Pseudo - marked elevated TP & lipemia, measurement of halides (Br, I, fluoride)
Steroids (HAC or drugs) - mild
Thiazides, loop diuretics (Cl- renal loss disproprionate to Na+)
GI losses (V+) or upper GI obstruction/stasis (also hypoNa)
Chronic respiratory acidosis
Fluid administration with high Na+

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10
Q

Hyperchloremia - causes?

A

GI losses of Na > Cl + concurrent HCO3- loss (D+, sequestration of intestinal contents - remember bile, pancreatic & duodenal secretions are rich in HCO3-)
Hypoalb (hyperCl likely occurs in response to mild alkalosis 2’ to this)

Renal Cl- retention (causes involving decreased H+ secretion & HCO3- reabsorption):
- Early CKD
- RTA (both proximal + distal) - primary (congenital) vs acquired (hypoA, renal tubular dz)
- Spironolactone tx (similar to hypoA - effects of aldosterone)
- Chronic respiratory alkalosis
- Ketoacidosis (usually during DKA recovery phase - excretion of ketoacid anions as Na+ & K+ salts, Cl- retained in place of them)

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11
Q

High anion gap metabolic acidosis - causes?

A

‘LUKE, E includes other toxins’
1. Increased phosphorus (renal failure)
2. Toxicities - ethylene glycol, salicylate (aspirin), metaldehyde
3. Organic acidosis - lactic acidosis, renal failure, DKA, uremia

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12
Q

NaHCO3- administration
- Indications
- Adverse effects

A
  1. Indications
    - HCO3-losing diseases (RTA, D+ - uncommon)
    - Severe metabolic acidosis i.e. pH <7.15 & HCO3- <12mEq/L (e.g. uremic AKI, NOT DKA or lactic acidosis).
    - Refractory hyperK.
    - Contrast-induced nephropathy (some evidence that prevents?)
  2. AE
    - Hypervolemia, hyperNa (hypertonic solution > volume expansion), hypotension (if rapid admin undiluted)
    - Ionized hypoCa (pH changes > iCa binds to albumin)
    - HypoK (K+ translocates into cells due to binding of iCa-alb)
    - Respiratory acidosis (increased CO2 production; can occur if unable to increase ventilation appropriately)
    - Paradoxical intracellular/CNS acidosis (CO2 pdtn)
    - Phlebitis/thrombosis if peripheral v. admin (shouldn’t give >600mOsm/L solution but undiluted = 2000mOsm/L)
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13
Q

NaHCO3 supplementation - equation?

A

0.6 x BW(kg) x (desired [HCO3-] - measured [HCO3-]) = ____mmol/L

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14
Q

What is osmolal gap (OG)? What is normal in dogs, and what are causes of an elevated OG?

A

Difference between measured - calculated osmolality (measured usually slightly higher as includes additional osmoles in plasma other than Na, urea & glucose).
Normal </= 10mOsm/kg.
Elevated due to:
- Exogenous solutes in the plasma (e.g. ethylene glycol)
- Reduced fraction of plasma water 2’ to high plasma triglycerides or proteins (e.g. myeloma proteins)

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15
Q

Equation to calculate plasma osmolality?

A

Plasma osmolality = 2 [Na+] (mEq/L) + ([Glucose] (mg/dl)/18) + ([BUN] (mg/dl)/2.8)

*[Na+] is in mmol/L
Glucose & urea = ineffective osmoles, so contribute to osmolality but not tonicity

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16
Q

What are the diagnostic criteria for SIADH? (Hint: think osmolality)

A
  • Excluded other causes of hypoNa
  • Concurrent plasma hypo-osmolality (hypoNa) + inappropriately HIGH urine osmolality. Urine [Na+] >20mEq/L. As natriuresis occurs despite hypoNa
  • Adequate renal and adrenal function
  • Absent hypovolemia, ascites, or edema
  • Correction of hyponatremia with fluid restriction.
17
Q

In a hypoNa animal, how does urine osmolality and/or urine [Na+] help to differentiate cause?

A

HypoNa + uOsm >100mOsm/L - indicates impaired H2O excretion. (natriuresis occurs despite hypoNa to reduce circulating vol from H2O retention)

HypoNa + uOsm <100mOsm/L - usually primary PD (normal renal urine diluting ability), low solute intake (rare)

Urine [Na] < 20mEq/L suggests hypovolemia. So >20mEq/L expected for SIADH, diuretics, hypoaldos, renal failure (body is not in Na retaining state).

18
Q

List 5 characteristics of hyperglycemic hyperosmolar syndrome (HHS)?

A
  • BG >540- 600mg/dL; 30-34mmol/L
  • Serum osmolality >325-350mOsm/Kg
  • Profound dehydration, with progressive CNS depression
  • +/- mild acidosis, but usually blood pH >7.3 & [HCO3-] >15mEq/L
  • Variable ketosis
19
Q

What are the main roles of the endothelial glycocalyx?

A

Forms a layer over the luminal surface of endothelial cells. Maintains the vascular permeability barrier.
- Shield vascular walls from direct exposure to blood flow
- Mediate shear stress–dependent NO (NO) production
- Promotes retention of vascular protective enzymes
- Preserves IV concentration of coagulation inhibition factors
- Immunomodulatory - prevents leukocyte adhesion & binding of chemokines,
cytokines & GFs to the endothelium

20
Q

What are the tissue safety factors preventing interstitial oedema in health?

What pathological changes occur with oedema formation?

A
  1. ISF hydrostatic P is slightly negative (-3mmHg) - holds tissues together (suction like effect)
  2. IS has low compliance - small changes in ISF volume significantly increases ISF HP significantly (prevents further fluid entry into IS)
  3. Lymphatic flow increases 10-50x when capillary P increases/fluid accumulates in tissues > carries away large amounts of fluid & proteins > prevents ISF P from rising into the positive range
  4. Lymphatics carry away protein in the ISF > decreases ISF colloid osmotic pressure & thus prevent further accumulation of ISF.

Increased capillary hydrostatic P, lymphatic obstruction etc.
> fluid enters ISF > when ISF pressure rises >0mmHg, tissue compliance increases markedly so allows large amts of ISF to accumulate with only small increase in pressure

21
Q

What life-threatening complication may occur if hypertonic saline is administered too rapidly?

A

Vagally mediated bradycardia, CPA

22
Q

What are the 2 types of lactic acidosis?

A

Type A: tissue hypoxia (hypoperfusion 2’ to decreased effective circulating volume)
Type B: not related to tissue hypoxia or hypoperfusion.

Fundamental problem is the inability of mitochondria to process the amount of pyruvate it is presented with.

23
Q

Which 3 synthetic colloids are commonly used in vet med?
How do molar ratio (degrees of substitution), C2:C6 ratio & molecular weight affect efficacy of synthetic colloids?

A

Hetastarch (450kDa) > pentastarch (260kDa) > tetrastarch (130kDa)

Higher C2:C6 ratio –> slower degradation by amylase, more soluble product.
Higher MW & higher molar ratio > prolonged volume effect (stays longer in IV space), but associated with more SE.

24
Q

What are the complications of colloid therapy?

A
  1. Fluid overload esp if concurrent dz with increased vascular permeability (smaller colloid particles alb etc. extravasate through leaky vessels into interstitium > lower plasma COP > oedema/third spacing) delayed protein clearance in lungs.
  2. Nausea, hypotension with rapid infusion (cats)
    **3. Anaphylaxis & allergic reactions
  3. ARF**
  4. Impaired hemostatic disturbances (platelet dysfunction - decr integrin αIIbβ3 expression > decr fibrinogen binding; decr FVIII & vWF - accelerated elimination, interference with fibrin clot stablisation)
  5. Contributes to hyperchloridemic metabolic acidosis if suspended in 0.9% saline
25
Q

What factors stimulate vs inhibit PO4 tubular reabsorption?

A

Stimulate - GH, IGF-1, insulin, thyroid hormone
Inhibit - PTH, FGF-23 (direct effect on Na-P co transporter), incr serum P

(NB: insulin, dextrose, bicarbonate increases PO4 intracellular uptake)

26
Q

Where are vitamin D receptors predominantly located in the kidneys?
Where is Ca & Mg predominantly reabsorbed in the kidneys?

A

VDRs most abundant in DTs (less in PTs & glomerular podocytes)
Ca: PCT , Mg: LOH 65%

27
Q

What electrolyte derangements may occur with hyperthyroidism?

A

Hyperphos, hypoMg