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Exotics and Emerg > Electrolyte and Acid Base DIsorders > Flashcards

Electrolyte and Acid Base DIsorders Flashcards

1
Q

What is the acronym for the causes of hypercalcemia

A

-H: hyperparathyroidism
-A: addisons
-R: renal
-D: hyper-vitaminosis D
-I: Idiopathic (cats only)
-O: osteolytic
-N: neoplastic
-S: spurious (check bloods again)
-G: granulomatous (usually lumped in somewhere else)

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2
Q

What are some system specific signs of hypercalcemia

A

Renal signs: PU/PD (in dogs), incontinence, urolithiasis (mostly cats), can cause kidney injury
Gastro signs: inappetence, constipation, generally ADR
Neuromuscular: lethargy, exercise intolerance, shivering, muscle twitching, seizures (rare)

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3
Q

What should the approach to hypercalcemia be

A

-Be sure this was not a spurious result: double check calcium value- check ionized and total calcium
-See if clinical signs fit: if not PU/PD, then unlikely to be genuine result
-Look at the patient: if patient is very well, think primary hyperparathyroidism (renoprotective disease). If the patient is unwell, think neoplastic (always check anal sacs), Addisons, renal disease

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4
Q

What other investigations should be done if you have hypercalcemia

A

-Serum biochem: kidney values, globulins, phosphate
-Cytology: peripheral lymph nodes (lymphoma)
-Thoracic imaging: neoplasia or granulomas (mycobacterial disease, lungworm)
-Abdominal imaging: lymphoma, small adrenals, abnormal kidneys, US the parathyroids
-Other bloods: ACTH stim, PTH, PTHRP

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5
Q

How should you treat hypercalcemia

A

Treat the underlying cause!
-primary hyperparathyroidism: surgery or percutaneous ethanol
-Addisons: Pred and DOCP, give hydrocortisone if waiting for ACTH results
-Renal: fluids, renal diet, BP meds
-lymphoma: CHOP, COP, Pred
-Multiple myeloma: melphalan and pred
-Anal sac neoplasia: surgery

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6
Q

What are common and uncommon causes of hypocalcemia

A

-Common causes: parathyroid related, immune mediated, lactating bitch
-Uncommon causes: acute pancreatitis, kidney disease, intestinal malabsorption, urinary tract obstruction

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7
Q

When do we treat hypocalcemia, and what are the acute and chronic treatments

A

-When to treat: when symptomatic or if ionized Ca <.8 mmol/L or total <1.75 mmol/L
-Acute: IV bonus of .5-1.5 ml/kg of 10% calcium gluconate (only calcium to go into vein) delivered over 10-20 mins, then CRI
-Chronic: oral calcium carbonate, calcitriol

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8
Q

Causes of hyperkalemia and pseudohyperkalemia

A

-Hypoadrenocorticism (addisons- mineralocorticoid controls water/electrolytes, missing in Addisons)
-GI disease (salmonellosis, tricuris vulpis)
-AKI or CKD (end stage)
-blockage of the urinary tract
-Drugs (ACEI,telmisartan)
-Acidosis
-Rhadbomylosis
Pseudohyerkalemia:
-severe thrombocytosis
-severe leucocytosis
-Breeds (Akita, shiba) with hemolysis

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9
Q

Treatment of hyperkalemia

A

-IVFT (without potassium at first)
-Dextrose bolus to stimulate endogenous insulin release to drives K+ back into cells
-Regular insulin: for every unit of regular insulin administered 2 grams glucose
-Calcium gluconate for cardio protection

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10
Q

Causes of hypokalemia

A

-prolonged starvation
-IVFT
-DKA patients treated with insulin
-alkalemia
-hypothermia
-rattlesnake envenomation
-catecholamine release
-GI loss
-CKD in cats
-Conns syndrome (cats)

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11
Q

What are clinical signs of hypokalemia

A

-Neuromuscular signs: tremors, ataxia, hyperexcitability
-Cardiac arrhythmias

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12
Q

What are the 3 categories of hypernatremia

A

-Pure water deficiency: normovolemic hypernatremia
-Loss of hypotonic fluid: hypovolemic hypernatremia
-Sodium gain: hypervolemic hypernatremia

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13
Q

What are causes of normovolemic/ pure water deficiency hypernatremia

A

-Usually a “problem upstairs” or neuro disease
-primary hypodipsia/dipsia
-Increased set point for ADH secretion: head trauma or neoplasia or malformation of the diencephalon
-No water available in environment

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14
Q

What are causes of hypovolemic/hypotonic fluid loss hypernatremia

A

-Kidney related (AKI), GI tract related (diarrhea, vomiting)
-If the osmolarity of the fluid lost is similar to ECF then hypernatremia wont develop
-Hypernatremia will develop if fluid loss is uncompensated

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15
Q

What causes hypervolemic (sodium gain) hypernatremia

A

-Salt poisoning (seawater consumption)
-IVFT with sodium excess
-Mannitol
-Conns syndrome (rare)
-Cushings (hypernatremia not seen clinically)
-Rare in general

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16
Q

What are some clinical signs for acute and chronic hypernatremia and how should you treat

A

-Acute: lethargy, coma, disorientation, seizures
-Chronic: largely asymptomatic unless Na super high
-Treat: try to treat in most physiological way first, offer water. Then IVFT, very carefully must not decrease Na by more than 1 mmol every 2 hours

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17
Q

What fluids should be used for hypernatremia

A

-If sodium very high, start with .9% NaCl so that sodium doesn’t drop too quickly
-If sodium not very high, use Hartmann’s
-Need to monitor these patients carefully and check bloods

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18
Q

What is the formula for calculating plasma osmolarity

A

Plasma osmolarity (mosmol/L)= 2(Na) + Urea + Glucose

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19
Q

What osmolarity would you expect for a hyponatremic animal

A

-Would expect animal to be hypotonic, if not something else is wrong
-Hyponatremia generally causes hypotonicity- reflects water retention
-Hypertonic hyponatremia usually caused by diabetics leading to high glucose causing water drawn out and diluting sodium
-Normotonic hyponatremic usually spurious result

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20
Q

What are the steps of dealing with hyponatremia

A

Step 1: calculate plasma osmolarity
Step 2: look at hydration status (hypo, normal, and hypervolemia)

21
Q

What causes hypovolemic hypotonic hyponatremia and what things should you check

A

-Sodium loss exceed water loss because of compensatory water intake
-Check 1: renal losses of sodium- addisons disease
-Check 2: GI losses of sodium (V+/D+)
-Check 3: third spacing of fluids (chylothorax)
-Check 4: fractional excretion of Na/kidney tubular disease
-Check 5: occult blood loss

22
Q

What are the 4 most likely causes of hypervolemic hypotonic hyponatremia

A

1) CHF 2) severe liver disease 3) nephrotic syndrome 4)end stage CKD
-recognition of hypervolemic essential (body cavity effusion, jugular distension, peripheral edema)

23
Q

What to check for normovolemic hypotonic hyponatremia

A

-Check 1: hypotonic fluid administration or antidiuretic
-Check 2: psychogenic polydipsia
-Check 3: syndrome of inappropriate ADH secretion (MUO, thalamic tumors, hydrocephalus)
-Check 4: hypothyroid myxedema coma

24
Q

What are physiological and pathological causes of hyperphosphatemia

A

-Physiological: higher in young dogs, because released from growing bones
-Pathological: enhanced GI absorption (Vit D toxicity), decreased excretion (kidney disease, uroabdomen, hypoparathyroidism, hypoadrenocorticism, hyperthyroidism), trans cellular shifts (rhabdomyolysis, hemolysis, tumor cell lysis)

25
Q

What can hyperphosphatemia induce

A

-Hypocalcemia with clinical signs

26
Q

What are some causes of hypophoshatemia

A

-Decreased GI absorption (hypovit D, phosphate enemas, V+D+)
-Increased renal excretion (DM, hyperparathyroid, diuretics, hyperaldosterone)
-Transcellular shifts (insulin, glucose admin, hypothermia, reseeding syndrome, resp alkalosi)

26
Q

What are some causes of hypophoshatemia

A

-Decreased GI absorption (hypovit D, phosphate enemas, V+D+)
-Increased renal excretion (DM, hyperparathyroid, diuretics, hyperaldosterone)
-Transcellular shifts (insulin, glucose admin, hypothermia, reseeding syndrome, resp alkalosis)
-Hemolyisis (remember when treating DKA patients)
-Resp failure
-seizures

27
Q

What are causes of hypomagnesemia

A

-GI malabsorption: reduced intake, chronic diarrhea, malabsorption
-Renal loss: diuretics, osmotic agents, post obstruction renal diuresis, hyperthyroidism, renal tubular acidosis
-Drugs: gentamycin, ticarcillin, ciclosporin, cisplatin
-Others: a true pancreatitis, lactation, insulin admin, catecholamine release, diabetes and insulin admin

28
Q

How does hypomagnesemia affect the parathyroids

A

-Depletion of magnesium impairs PTH secretion, calcitriol synthesis and increases resistance to PTH
-cell membranes have reduced sensitivity to calcium with low magnesium
-some hypoparathyroidism may be refractory to calcium and vit D therapy if hypomagnesemic
-Hypomagnesemia can enhance renal loss of potassium leading to hypokalemia

29
Q

How should you collect and run bloods when looking for acid base disorders

A

-Check blood gases: arterial blood if want to check oxygen) or venous blood
-Immediately after collection needs to be airtight
-Needs to be run within 15 minutes, ideally as soon as possible

30
Q

What is the Henderson Hasselbalch equation and which side is which

A

H+ and HCO3 = H2CO2 = H2O and CO2
The left side is metabolic side, the right side is respiratory
H+ are nonvolatile acids produced by normal metabolism or proteins and lipids, CO2 is the volatile acid produced by normal protein and fat metabolism
H+ and CO2 are the two sources of acid and are intercalated

31
Q

What is HCO3 in the body and what can it be used to ID

A

-HCO3 is bicarbonate and is the major extracellular buffer. It combines with H+ to produce CO2 which is eliminated through ventilation
- It can be used to ID a metabolic problem: when met acidosis occurs the respiratory system will eliminate more CO2 to produce a resp alkalosis to compensate. With a primary resp disorder the opposite met disorder is generated

32
Q

What is a base deficit/excess and how is it calculated

A

It is the amount of base under or over the normal buffer base.
It is calculated by taking into account the expected change in HCO3 secondary to changes in CO2. Reference range usually -5 to +5 milliequivalents per unit

33
Q

What do you see with a respiratory acidosis

A

-increase in partial pressure of CO2 in the blood
-impaired blood flow
-reduced resp rate/effort
-ventilation/perfusion mismatch
-impaired gas exchange

34
Q

How do you treat respiratory acidosis

A

-Correct underlying disorder, localize to lungs and find out what’s wrong (do not give bicarbonate to treat)

35
Q

What are some causes of respiratory alkalosis and what is the treatment

A

-Caused by an increase in ventilation through which more CO2 is eliminated than generated
-Iatrogneic (over ventilation)
-Severe pain causing tachypnea
-Primary pulmonary disease
-CNS disease causing tachypnea
-Treatment: treat underlying disease

36
Q

What are some causes of metabolic acidosis

A

-Caused by a gain of H+ or loss of HCO3 buffering capacity
-Generally caused by ingestion of an acid, increased production of endogenous acid, or failure to eliminate acid via kidneys

37
Q

What happens chemically within metabolic acidosis

A

-Dissociation of acid yields H+and A-, HCO3 binds with H+ to neutralize it, but A- (anion) remains in solution. Electroneutrality must be maintained so if a negative ion increased then another negative ion must decrease (this is typically chloride)
-This leads to a widening anion gap (difference between measure cations and anions

38
Q

What is the anion gap equation, and what is the reference range

A

AG = (Na + K) - (Cl +HCO3)
reference range: 16 +/- 4

39
Q

What are the top 5 causes of metabolic acidosis and an increase anion gap

A

-Ethylene glycol
-Uremia
-Tissue hypoxia (lactic acid)
-DKA
-Aspirin intoxication

40
Q

What causes metabolic acidosis with normal anion gap

A

Loss of bicarbonate, failure to excrete H+ ions (chloride will increase to maintain electroneutrality), caused by renal tubular acidosis, severe GI disease with bicarbonate loss or NaCl admin
-Often referred to as hyperchloremic metabolic acidosis

41
Q

Treatment for metabolic acidosis

A

-For severe metabolic acidosis (pH<7.15) with decreased HCO3 sodium bicarbonate can be administered (as long as you know resp system can compensate adequately)

42
Q

What causes metabolic alkalosis

A

-Loss of chloride in excess of extracellular fluid volume
-often as a result of upper GI fluid loss or sequestration (obstruction with vomiting)
-rarely sodium bicarbonate or Conns

43
Q

How does loss of chloride lead to renal resorption

A

-Vomiting from obstruction leads to hypovolemia
-Hypovolemia leads to activation of RAAS
-RAAS leads to an increase in renal Na reabsorption
-This leads to Cl or bicarb being absorbed with the Na, but because Cl is sequestered in stomach by obstruction, bicarb is reabsorbed more
-this leads ultimately to a metabolic alkalosis

44
Q

How to treat metabolic alkalosis

A

-Correct underlying disease
-Look for upper GI tract obstruction
-give .9% NaCl as fluid choice

45
Q

What is PaO2 and what does it determine

A

-Measures the dissolved O2 in the blood (not bound to hemoglobin)
-The number of dissolved O2 molecules in plasma determines the saturation of hemoglobin

46
Q

What does SpO2 approximate and what does an SaO2 of 90% equal

A

-SpO2 approximates SaO2
-SaO2 of 90%= PaO2 of 60
The gal of hypoxia treatment is to maintain SpO2>90% and the PaO2 over 60 mmHg

47
Q

What are the 3 steps/rules for looking at a blood gas

A

Step 1: look at the pH- are we normal, acidemic (pH <7.35) or alkalemic (pH>7.45)
Step 2: look at the CO2- does the CO2 follow the disorder (if were academic is the CO2 high: primary resp acidosis, if CO2 low then likely metabolic)
Step 3: look at HCO3- does it follow the disorder (if we are acidemic is the bicarb low: if so think primary met acidosis)

Exotics and Emerg (12 decks)

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