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ACVS Phase I Master Deck *Use This* > Chapter 5: Fluids > Flashcards

Chapter 5: Fluids Flashcards

1
Q

Canine blood donors ideally should be erythrocyte antigen ____ and ___, negative if possible? and why is this?

A

1.1 and 7, as a dog is most likely to have a clinically significant transfusion reaction to these.

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2
Q

How many naturally occurring dog erythrocyte antigens have been identified?

A

8

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3
Q

How do you work out how much blood is needed in a transfusion?

A

Vol(ml) = 1.5 x desired PCV x kg BW

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4
Q

What is the blood volume of a dog and of a cat?

A

dog - 90ml/kg
cat - 50ml/kg

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5
Q

Animals with colloid osmotic pressure of <___mmHg may benefit from synthetic colloid administration?

A

<16mmHg

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6
Q

What antigen is associated with incompatible cross match results in cats?

A

Mik antigen

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7
Q

Type A cats rarely have naturally occurring anti-B antibodies, but type B cats often have strong naturally occurring anti-A antibodies - What results if type A blood is given to type B cat?

A

Severe and potentially fatal transfusion reactions and RBC lifespan of aprrox. 1 hour

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8
Q

What are the most common side effects in dogs associated with synthetic colloid administration?

A

coagulopathies - decrease in factor 8 and vWF, impairement of platelet function, interference with stability of fibrin clots making clot more susceptible to fibrinolysis

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9
Q

Patients with severe head trauma should be administered what fluid?

A

0.9% NaCl - as has higher sodium and is less likely to cause a decrease in osmolarity and subsequent water movement into brain interstitium

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10
Q

What fluid should you use for hyperchloremic metabolic acidosis?

A

0.9% NaCl

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11
Q

Fluid type for patient with severe metabolic acidosis?

A

LRS

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12
Q

what are the two most common transfusion reactions in dogs?

A
  • TACO (transfusion associated circulatory overload)
  • non-hemolytic febrile reactions
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13
Q

Chronic hyponatremia should be corrected slowly (no more than 0.5mEq/L/h)- if not it could result in what?

A

Osmotic demyelination syndrome (central pontine myelinolysis)

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14
Q

Clinical signs of hypernatremia are usually only seen over what number in dogs?

A

170mEq/L dogs
Cats 175mEq/L

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15
Q

Chronic hypernatremia can result in the formation of what?

A

Idiogenic osmoles
- maintain the intracellular osmolarity similar to that of the extracellular and prevent fluid from moving out of the cell
- if the cell was to shrink it can result in vascular damage and hemorrhage within the brain

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16
Q

How is free water deficit usually replaced?

A

FW is most commonly replaced using 5% dextrose in water IV - as dextrose is rapidly metabolized - effectively leaving free water

Loop diuretics can facilitate natriuresis particularly in animals with hypervolemic hypernatremia

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17
Q

potassium moves intracellularly with?
Potassium moves extracellularly with?

A
  • Intracellular: glucose, insulin, catecholamines and metabollic alkalosis
  • Extracellular: metabolic acidosis or hyperosmolarity
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18
Q

What is meant by the term paradoxical aciduria?

A

From vomiting, when chloride is low, sodium is reabsorbed from the kidneys in exchange for K+ and H+ (acids in urine)
- worsens the hypokalemia and metabolic alkalosis

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19
Q

If K+ serum concentration is<3 what can result?
<2?

A

< 3: muscle weakness, cardiac arrythmias and PU
< 2: rhabdomyolysis with increased CK concentrations and respiratory muscle paralysis

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20
Q

Animals with refractory hypokalemia should have what checked?

A

Their serum Mg levels checked and supplementation instituted

21
Q

What are expected ECG changes with K+ of:
5.7-6 ?
7-8.5?
>8.5?
10-12?

A

5.7-6: Spiked T waves and shortened QT interval
7-8.5: Prolonged PR interval and widening of QRS
>8.5: P waves disappear, R-wave amplitude decreases and S-wave prominence increases resulting in a sinoatrial wave
10-12: asystole and atrial fibrillation

22
Q

Treatment options for hyperkalemia? (5)

A

Calcium gluconate - raises threshold membrane potential
Insulin and glucose - moves potassium into the cell
Sodium bicarbonate - moves potassium into the cell
Beta-2 agonists (albuterol or terbutaline) -moves potassium into the cell
Dialysis

23
Q

Kidney failure can cause hypocalcemia how?

A

Reduced ability of kidney to convert 25-hydroxycholecalciferol to vitamin D - resulting in decreased intestinal absorption of calcium

24
Q

Does hypoalbuminaemia affect ionised calcium levels?

A

no

25
Q

What is the most common cause of hypercalcemia in dogs / cats?

A

Malignancy in dogs
Idiopathic in cats

26
Q

HypoMg+ causes?

A

malabsorption: Decrease absorption: pancreatic insufficiency, cholestatic liver disease, short bowel syndrome, generalised malabsorption syndrome or starvation
excessive urinary losses: Renal tubular abnormalities - decreased resorption - renal tubular acidosis, postop diuresis, polyuric renal failure and diuresis,
drugs: aminoglycosides, digoxin, cisplatin and cyclosporin
redistribution: insulin, catecholamines,

27
Q

Causes of hypermagnesemia?

A

Renal failure: acute or chronic
Endocrine disorders: hypoadrenocorticism, hyperparathyroidism, hypothyroidism
Iatrogenic over administration - cathartic, laxatives, antacids

28
Q

Causes of hypophosphatemia?

A

Increased renal loss: primary hyperPTH, Diabetes, eclampsia, diuretic, Cushing’s, hyperaldosteronism
Decreased Gut absorption: vitamin D deficiency, malabsorption, vomiting, diarrhea, phosphate binders and antacids, diet deficiency
Translocation: DKA, insulin admin, glucose, bicarbonate, total parenteral nutrition, refeeding syndrome, hypothermia, resp alkalosis or hyperventilation

29
Q

Causes of hyperphosphatemia?

A

Increased intestinal absorption: vitamin D toxicosis, phosphate containing enemas,
IV over admin
Decreased renal excretion: renal failure, urinary obstruction, uroabdomen, hypoPTH,
Translocation: tumor cell lysis, tissue trauma or rhabdomyolysis, hemolysis, metabolic acidosis
young growing animals
lab error

30
Q

Calculation for corrected Chloride?

A

Cl measured x 146/Na measured - dog

Cl measured x 156/Na measured - cat

31
Q

Causes of hypochloridemia?

A

Excessive loss - GI loss - vomiting, other GI disease - trichuriasis, salmonellosis, duodenal perforation
Renal loss - thiazide or loop diuretics, chronic resp acidosis, HAC
Excessive gain of sodium relative to chloride - sodium bicarbonate administration

32
Q

Causes of hyperchloridemia?

A

Excessive loss: diarrhea
Excessive gain: NaCl, total parenteral nutrition, salt poisoning
Renal chloride retention: renal failure, renal tubular acidosis, Addisons, diabetes, Chronic resp alkalosis and spironolactone
Pseudohyperchloremia - potassium bromide therapy

33
Q

What is Whipple’s triad?

A

Hypoglycemia
Clinical signs of hypoglycemia
Resolution of signs once supplemented

34
Q

Causes of hypoglycemia?

A

Excess insulin: overdose, insulinoma, PNS, toxins and meds - xylitol
Excess glucose use: infection, exercise induced, pregnancy, pns, polycythemia, leukocytosis
Decreased glucose production: liver, neonatal, toy breed, PSS, neoplasia, cirrhosis, glycogen storage disease, Addison’s, betablockers

35
Q

Causes of hyperglycemia?

A

Postprandial hyperglycemia
Endocrine - Diabetes, pancreatitis
Increased gluco-counterregulatory hormones: glucocorticoids, stress, critical illness, catecholamines - pain, exertion, excitement, growth hormones, progesterone, hyperthyroidism
Drugs: adrenocorticotropic, progesterone, xylazine, ketamine, morphine, glucose/dextrose containing fluids

36
Q

What is the only significant volatile acid in the body?

A

Carbonic acid

37
Q

Dissociation of a weak acid is described by what equation?

A

Henderson - Hasselbach Equation

38
Q

In terms of Acid/Base - what is a buffer?
Main buffers in body?
What is the main extracellular buffer?
Main intracellular buffers?
Other part of the body with buffering capacity?

A

A buffer is a weak acid and its conjugate salt that can accept or donate a proton to minimize changes in fluid pH after the addition of a strong acid or base
Main: Bicarbonate, proteins, phosphate
Main extracellular: Bicarbonate - open buffering system
Main intracellular: Hemoglobin, plasma proteins and organic/inorganic phosphate - closed buffering system

Bone also has important buffering capacity in the body.

39
Q

What is the pKa of bicarbonate?

A

6.1

40
Q

How do you calculate anion gap?
What are the causes of increased anion gap?

A

AG = (Na + K) - (Cl + HCO3)
DKA, lactic acidosis, ethylene glycol, salicylate toxicosis, uremic states
(DUELS)
*Albumin can be associated with an increase in AG

41
Q

What are the causes of respiratory acidosis?

What are the acute and chronic compensations?

A

Hypoventilation
- Less commonly increased CO2 production by tissues - (CPR, malignant hyperthermia, heatstroke)

For every 1mmHg increase in PaCO2:

  • acute 0.15mEq/L increase in HCO3
  • chronic 0.35mEq/L increase in HCO3
42
Q

You suspect a patient has a chronic respiratory acidosis - you give oxygen but hypercapnia worsens, why?

A

In some chronic cases the respiratory center is no longer sensitive to elevated CO2 levels
- instead ventilation is driven by hypoxia and so supplemental oxygen may decrease ventilatory drive and worsen hypercapnia

43
Q

What is the compensatory response in acute and chronic respiratory alkalosis?

A

For every 1mmHg decrease in PaCO2:

  • Acute decrease of 0.25mEq/L of HCO3
  • Chronic decrease of 0.55mEq/L of HCO3
44
Q

Causes of metabolic acidosis?

A
  • Normochloremic (increased anion gap): DUELS
  • Hyperchloremic - diarrhea, renal tubular acidosis, giving carbonic anhydrase inhibitors
  • Hypochloremic: Addison’s
45
Q

Compensation for metabolic acidosis?

A

For every decrease 1mEq/L of HCO3 - 0.7mmHg decrease in PaCO2

46
Q

Dose of bicarbonate required to return base deficit to 0 is calculate by what formula?

A

Bicarb Dose = 0.3 x bodyweight (kg) x base deficit (mEq/L)

47
Q

Causes of metabolic alkalosis?

A

Vomiting, suctioning gastric contents, admin of diuretics that induce chloride excretion (Furosemide)
Hyperaldosteronism
Cushing’s

48
Q

What are the four questions to ask in interpreting a blood gas?

A
  1. Is an acid-base disturbance present? (check pH, HCO3, PaCO2)
  2. What is the primary disturbance?
    - alkalosis vs acidosis
    - metabolic vs respiratory
    - Is is compensated? Mixed?
  3. Is the compensatory response appropriate?
    - if not consider a mixed
    4.What underlying diseases are present?

ACVS Phase I Master Deck *Use This* (88 decks)

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