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Clinical Pathology > Monovalent Electrolytes, Anion Gap and Osmolality > Flashcards

Monovalent Electrolytes, Anion Gap and Osmolality Flashcards

1
Q

Na, K, Cl from food/fluid

A
  • metabolism is responsible for ICF ECF
  • ECF is Na/Cl rich and K poor
  • changes in ECF will change plasma electrolyte concentration
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2
Q

Platelets release _____

A

K+

- [K] serum > plasma

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3
Q

Electrolytes and H2O is excreted or lost via

A

Kidneys, skin or respiration

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4
Q

Abnormal [electrolyte] in plasma

A
  • decreased or increased intake
  • ICF ECF
  • increased renal retention
  • increased loss via kidney, skin, alimentary tract, respiration
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5
Q

[Na] in plasma is equivalent to ______

A

[Na] in ECF

  • dependent of total body Na and total body H2O
  • hydration is important for [Na] interpretation! –> H2O follows Na (except in distal nephron without ADH)
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6
Q

How does [K] affect [Na]

A
  • if [K] decreases, [Na] decreases since it enters the cells to keep electrical balance
  • a severe [K] increase would be necessary for [Na] to increase, but severe [K] is not compatible with life
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7
Q

Na concentration is regulated by ______

A

Blood volume and plasma osmolality regulation

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8
Q

Hypovolemia stimulates RAS –> angiotensin 2 and aldosterone

A
  • angiotensin 2 increases Na, K, Cl resorption in proximal tubules
  • aldosterone increases Na resorption in collecting ducts
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9
Q

How does hypovolemia stimulate ADH release?

A

Hypovolemia –> carotid sinus –> baroreceptors –> ADH release –> increased water resorption

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10
Q

How does hypervolemia stimulate ANP release?

A

Hypervolemia –> atrial baroreceptors –> atrial natriuretic peptide –> decreased Na resorption

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11
Q

Hyperosmolality

A

Hyperosmolality –> hypothalamic osmoreceptors –> promotion of water intake and release of ADH –> H2O resorption and Na, K, Cl in ascending loop of Henle

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12
Q

Hypoosmolality

A

Leads to decreased water intake

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13
Q

[Na] self regulation

A
  • decreased –> aldosterone release, increased retention

- increased –> decreased aldosterone release, decreased retention

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14
Q

What is the most important regulator of aldosterone release?

A

[K]!!

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15
Q

Dehydration is equivalent to _____

A

Decreased total body H2O

  • only H2O: decreased intake or loss of free H2O
  • H2O + Na loss: alimentary, renal or cutaneous loss
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16
Q

Hypernatremic, hyperosmolar, or hypertonic dehydration

A

Caused by net hypoosmolar or hypotonic fluid loss

- H2O loss > Na loss

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17
Q

Normonatremic, isoosmolar, or isotonic dehydration

A

Caused by net isoosmolar or isotonic fluid loss

- H2O loss = Na loss

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18
Q

Hyponatremic, hypoosmolar, or hypotonic dehydration

A

Caused by net hyperosmolar or hypertonic fluid loss

- H2O loss < Na loss

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19
Q

Inadequate H2O intake

A

Hypernatremia!!

  • H2O deprivation due to restricted access
  • defective thirst response: hypothalamic dz may damage the osmoreceptor
  • thirst center may be damaged
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20
Q

Pure H2O loss without H2O replacement

A

Hypernatremia!!

  • insensible loss of H2O by panting, hyperventilation, or fever
  • diabetes insipidus (central or nephrgenic) –> unrestricted access to H2O may drink sufficiently to prevetn the hypernatremia
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21
Q

H2O loss > Na loss

A

Osmotic diuretic agents (glucose and mannitol) –> inhibit passive H2O resorption = hypernatremia

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22
Q

Hypernatremia due to the alimentary system

A
  • accumulation of osmotic agents will inhibit H2O absorption
  • phosphate enema will pull H2O from ECF to the colon
  • rumen acidosis causes accumulation of solutes in the rumen –> osmotic movement of H2O into the rumen –> hypernatremia
  • dogs with paintball toxicosis
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23
Q

Na excess with concurrent restricted H2O intake

A
  • salt poisoning: cattle with excessive Na and with concurrent restricted access to H2O –> increased tb-Na = hypernatremia
  • administration of hypertonic saline or Na bicarbonate –> increased tb-Na and hypernatremia
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24
Q

Decreased renal excretion of Na

A

Hyperaldosteronism
- excessive aldosterone promotes excessive renal Na retention –> hypernatremia (and hyperchloremia) may occur if H2O is restricted or defective ADH activity

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25
Q

Decreased renal excretion of Na due to aldosterone

A

Aldosterone escape –> hyperaldosteronism does not typically cause hypernatremia

  • once Na retention occurs, there is corresponding H2O retention = natriuresis –> prevents development of hypernatremia
  • naturiesis may be promoted by ANP
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26
Q

Dehydration with net loss of isotonic fluids

A

Normonatremia

  • alimentary: vomit, diarrhea, sequestration
  • renal: polyuric renal dz with defective tubular functions, osmotic diuresis, increased diuresis
  • cutaneous: profuse sweating in horses
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27
Q

Edema or transudation with net retention of isotonic fluids

A

Creates normonatremia or hyponatremia

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28
Q

Congestive heart failure

A

Forward hypothesis

  • decreased CO –> sensed as decreased effected blood volume –> sympathetic nervous system and RAS
  • continued RAS –> renal resorption of Na and Cl –> increased osmolality, stimulating ADH release and thirst center –> increased H2O intake and hypervolemia
  • if venous hydraulic pressure increases enough = edema/transudation
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29
Q

Hepatic cirrhosis with abdominal transudation

A

Underfilling theory

  • initiating event: increased hydraulic P and loss of H2O and protein rich plasma to peritoneal cavity –> underfilling of vascular spaces and hypovolemia –> RAS and aldosterone release –> increased Na and H2O retention
  • clinically: animal has increased tb-Na, tb-H2O, increases concentration of renin, norepinephrine, and ADH, and reduced renal excretion of Na
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30
Q

Hepatic cirrhosis - Peripheral arterial vasodilation theory

A

Decreased effective blood volume –> RAS –> increases hydraulic pressure in the hepatic sinusoids –> transudation

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31
Q

Nephrotic syndrome

A

Protein losing nephropathy (leads to abdominal transudation)

  • H2O and Na retention mechanism is not understood
  • involves several processes
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32
Q

Hyponatremia occurs due to decreased _____

A

Na/water ratio, or IC to EC water shifting

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33
Q

Na deficit

A

Hypotonic dehydration

  • loss of Na fluid (isotonic) followed by water intake = dilution of Na
  • alimentary loss: vomit, diarrhea, sequestration, excess salivation, canine whipworms, bovine hemorrhagic bowel
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34
Q

Hypoadrenocorticism

A

Low aldosterone –> decreased resorption of Na and Cl –> decreased plasma osmolality and decreased renal medullary hypertonicity –> decreased ability to resorb H2O and hypovolemia
- hypovolemia stimulated ADH release and thirst centers water intake –> dilute ECF Na (and Cl)

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35
Q

Renal loss of Na

A

Prolonged diuresis by diuretics

  • osmotic or by furosemide: Na poor
  • thiazide: Na, K, and Cl loss
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36
Q

Ketonuria

A

Ketone bodies in tubular lumen –> obligate excretion of cations, thus increased excretion of Na

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37
Q

Na wasting nephropathies

A

Especially tubular diseases or pyelonephritis

- mostly seen in horses

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38
Q

Sweating

A

Cutaneous loss in horses

- Na, K, Cl rich = hyponatremia

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39
Q

Third space loss

A

Repeated drainage of chylous throacic effusions

  • acute internal hemorrhage or acute exudation
  • hyponatremia
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40
Q

H2O excess

A

Water retention > Na retention
- edematous disorders: CHF, hepatic cirrhosis, nephrotic syndrome
= hyponatremia

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41
Q

Water ICF –> ECF

A

Marked or persistent osmolality by hyperglycemia or mannitol infusion –> osmotic draw of water into the blood –> dilute Na

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42
Q

Na ECF –> ICF

A
  • acute muscle damage: allows Na to enter cells
  • concurrent influx of water and total Ca and efflux of K and PO4
  • results in hypovolemia, hypocalcemia, hyperkalemia, hyperphosphatemia
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43
Q

Na IV –> EV

A

Uroperitoneum

- urine is Na and Cl poor –> diffusion of Na and Cl to peritoneal cavity

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44
Q

K depletion

A

Total K loss due to :

  • GI and renal disorders
  • K from ICF to ECF
  • electrical neutrality maintained by: Na moving from ECF to ICF
  • Cl from ICF to ECF with K –> low intracellular osmolaltiy –> water shifts from ICF to ECF and dilutes plasma Na
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45
Q

Potassium concentration is dependent on

A

Total body K and movement into and out of cell in response to changes in acid-base status

  • most cells are K rich, due to Na/K ATPase pump
  • plasma K regulated via ECFICF and renal excretion
  • intake and absorption, loss in feces and sweat
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46
Q

[K] should be interpreted with consideration of ____

A

Acid base status

  • an inorganic acidosis (renal failure, some diarrheas, ammonium chloride administration) may cause hyperkalemia shift ICF to ECF
  • organic acidosis will not typically cause hyperkalemia
  • treatment of acidosis may cause hypokalemia
  • metabolic alkalosis may cause mild hypokalemia
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47
Q

____ and ____ promote K uptake

A

Epinephrine and insulin

  • Na/K ATPase pump
  • hyperkalemia –> cellular uptake of K
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48
Q

Renal excretion of K

A

Typically resorbed before distal nephron

  • secreted by principal cells of collecting tubules, promoted by aldosterone
  • hyperkalemia and angiotensin 2 are major stimulants of aldosterone secretion –> increased flow rate promotes secretion, slow flow inhibits it
  • hypochloremic states: resorption of Na without Cl establishes electrochemical gradient that promotes K secretion
  • ADH promotes K secretion
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49
Q

Shifting of K ICF –> ECF

A
  • metabolic inorganic acidosis: when H moves in
  • rhabdomyolysis: selenium deficiency, malignant hyperthermia, seizures, strenuous exercise
  • massive intravascular hemolysis
  • hypertonicity: diabetes mellitus
  • pseudo-hyperkalemia: in vitro hemolysis (horses, Akitas, Shibas)
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50
Q

Increased total body K

A
  • renal insufficiency: oliguric, anuric (decreased flow of tubular fluid –> decreased secretion)
  • urinary tract obstruction or leakage: K enters ECF and is not removed (seen in cats)
  • trimethoprin-induced K retention, blocks luminal Na channels –> K sparing diruetics
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51
Q

Hypoaldosteronism

A

Decreased activity of Na/K ATPase pumps

- decreased resorption of Na and decreased movement of K

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52
Q

Repeated chylous effusion drainage

A

May be related to hyponatremia + hypovolemia –> less Na resorbed in the distal nephron, less K excretion

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53
Q

Acidotic

A

Normokalemia

  • inorganic (renal failure, diarrhea): expected to increase concentration = hypokalemia
  • organic: may not have hyperkalemia due to increased K excretion or shift into cells with organic anions
54
Q

Alkalotic

A

Expected to decrease concentration, thus it suggests concurrent hyperkalemia (usually causes normokalemia)

55
Q

Hypokalemia due to metabolic alkalosis

A

K into cells when H moves out (minor)

  • hypovolemia –> renin angiotensin aldosterone system –> increases secretion of K
  • bicarbonaturia –> excretion of cations (including K)
  • anorexia or vomiting –> decreased intake of K
  • increased insulin activity: cellular uptake of K
56
Q

Decreased total body K due to increased excretion

A

Renal loss

  • increased tubular flow
  • increased renal excretion of anions (ketones, lactate, bicarbonate)
  • vomiting or sequestration of H and Cl that causes hypochloremic metabolic alkalosis: excess bicarb in distal nephron –> promotes tubular K secretion
57
Q

Hyperaldosteronism

A

Promote renal K secretion by stimulation of Na/K ATPase pump

58
Q

Hypokalemia is also caused by

A
  • increased excretion via increased alimentary loss
  • increased excretion via increased cutaneous loss
  • hypokalemic renal failure in cats
59
Q

Na:K ______ may be diagnostic of hypoadrenocorticism

A

<27, 25, or 22

60
Q

Decreased Na:K due to hypoadrenocortisim

A

Decreased aldosterone

  • hyponatremia by increased renal excretion
  • hyperkalemia by decreased renal secretion
61
Q

Decreased Na:K due to diarrhea

A

Dogs, cats, and horses

  • hyponatremia by intestinal loss
  • hyperkalemia may occur by acidemia associated with bicarb loss
  • in whipworm infections, pseudo-Addison’s dz occurs
62
Q

Decreased Na:K due to renal failure

A

Decreased ability of tubules to resorb Na and secrete K (oliguria)

63
Q

Decreased Na:K due to urinary tract obstruction or uroperitoneum

A

Na may diffuse into peritoneal fluid and creates hyponatremia

  • mild hyponatremia might be present in obstruction
  • hyperkalemia occurs because of acute oliguria or anuria –> decreased tubular secretion of K
64
Q

Decreased Na:K due to diabetes mellitus with ketonuria

A

Hyponatremia due to osmotic diuresis –> increased Na excretion and plasma dilution
- hyperkalemia not expected

65
Q

Decreased Na:K due to third space loss

A

Hyponatremia due to dilution by retained water

- hyperkalemia may result from decreased renal excretion or a shift from ICF to ECF due to an associated acidosis

66
Q

Chloride concentration

A
  • serum [Cl} = ECF [Cl} –> influenced by Na and HCO3

- controlled by renal resorption and secretion, and alimentary tract functions

67
Q

Hyperchloremia typically occurs with _____

A

Hypernatremia

  • occasionally concurrently with low bicarb (metabolic acidosis)
  • changes in Cl: related to attempts to maintain electrical neutrality
  • increased [Na] –> increased [Cl]
  • decreased [HCO3] –> increased [Cl}
68
Q

Hyperchloremia due to water deficit

A

Cl is the major anion to maintain electrical neutrality in the ECF –> increased Na will lead to increased Cl
- water deprivation or loss (same as Na)

69
Q

Excess Cl

A
  • increased intake of Cl with restricted water (salt poisoning)
  • decreased renal excretion of Na: hyperaldosteronism (rare)
70
Q

Hyperchloremic metabolic acidosis - alimentary

A
  • vomiting, diarrhea with loss of intestinal secretions

- cattle with esophageal obstruction (cannot ingest saliva) –> loss of Na and HCO3 (Cl poor solution)

71
Q

Hyperchloremic metabolic acidosis - renal

A
  • proximal tubule acidosis: less HCO3 allows more Cl to be reabsorbed
  • distal renal acidosis has impaired ability to secrete H –> inability to reabosorb HCO3 and secrete Cl
72
Q

Respiratory alkalosis (chronic)

A

Compensatory change to the alkalemia: increased retention of H and decreased conservation of HCO3
- decrease in HCO3 leads to increase in Cl and other anions

73
Q

Hypochloremia typically occurs with

A

Hyponatremia or increased serum bicarb

- also metabolic acidosis with increased anion gap

74
Q

Hyponatremic dehydration

A

Alimentary, renal, cutaneous or third space loss

- leads to hypochloremia

75
Q

Hypochloremia due to acid base disturbances

A

Low [Cl] is present in the absence of hyponatremia –> electrical neutrality must be maintained

  • increased bicarb
  • increased anion gap
76
Q

Metabolic alkalosis - hypochloremia

A

Loss or sequestration of Cl rich secretions (vomiting, displaced abomassum, bovine hemorrhagic bowel syndrome)

  • depletion of Cl
  • furosemide: inhibits Cl resorption in loop of Henle
  • thiazide diuretics
77
Q

Bovine renal failure

A

Causes alkalosis

  • changes result from abomasal atony –> functional obstruction and sequestration of Cl
  • more excretion of K in saliva –> limit absorption of Cl
78
Q

Metabolic acidosis with increased anion gap

A

Ketoacidosis and lactic acidosis: obligate excretion of Na –> less resorption of Cl
- foreign substances that generates anions also lead to obligate Na loss

79
Q

_____ is a major buffer that helps maintain the blood pH

A

Bicarbonate

  • produced from H2O and CO2 by carbonic anhydrase
  • RBCs, proximal renal tubular cells, parietal cells from gastric acid and abomasal epithelium, intercalated cells of collecting tubules, exocrine pancreatic epithelial cells
80
Q

Bicarb measurements

A
  • HCO3 is calculated in blood gas analysis
  • total CO2 reflects total amount of CO2 gas that can be liberated from serum
  • 95% of potential CO2 gas is in the form of HCO3 –> 5% is dissolved, so [tCO2] is equal to [HCO3]
81
Q

Increased [HCO3[ or [tCO2] due to gastric loss

A

Vomiting, pyloric obstruction

  • secretion of H by gastric mucosa generates HCO3
  • if H lost by vomiting or sequestration before intestines –> not absorbed –> bicarb not used for buffering –> accumulates in plasma
  • hypovolemia with concurrent hypochloremia –> resorption of Na in distal nephron with H secretion and generation of bicarb
82
Q

Metabolic alkalosis in cattle renal failure

A

Abomasal atony –> HCl sequestration generating alkalosis

- increased [HCO3] or [tCO2]

83
Q

Renal loss of H due to loop of Henle diuretics

A

Furosemide and other loop diuretics block resorption of Na, K, and Cl –> decreased water resorption and increased fluid flow –> increased secretion of H and bicarb generation
- hypovolemia and hypochloremia may contribute to the H secretion = increased [HCO3] or [tCO2]

84
Q

Renal loss of H due to thiazide diuretics

A

Inhibits Na/Cl cotransporter –> hypovolemia and hypochloremia
- increased [HCO3]

85
Q

Increased [HCO3] secondary to respiratory _____

A

Acidosis

- renal compensation

86
Q

Increased [HCO3] due to hypokalemia

A

Stimulates H/K ATPase in distal nephron –> K retention, H secretion and HCO3 generation

87
Q

Increased [HCO3] due to renal loss of H

A 
Endurance races (sweating) and intestinal disorders in horses
- lead to hypovolemia and hypochloremia --> secretion of H
88
Q

Shift of H from ECF to ICF due to hypokalemia

A

Alkalosis can lead to hypokalemia and hypokalemia can contribute to an alkalosis
- depletion of tbK –> K out of cell and H into = increased [HCO3]

89
Q

Contraction alkalosis

A
  • loss of Cl rich ECF: vomiting, sequestration, and loop diuretics –> ECV volume contraction and increased [HCO3] (minimal)
  • volume contraction –> aldosterone response –> promoting renal secretion of H and Cl
  • concurrent loss of H might happen
90
Q

Decreased [HCO3] or [tCO2] due to metabolic ____

A

Acidosis (primary or compensating)

91
Q

Generation of excess H

A

Depletion of HCO3

  • titrational acidosis
  • lactic acidosis: anaerobic glycolysis –> excess H
  • ketoacidosis: excessive B-oxidation of TGs in hepatocytes
  • ingestion of certain compounds (ethylene glycol, methanol): catabolism generates acid
92
Q

Decreaed renal excretion of H

A
  • renal failure –> decreased acid excretion
  • urinary tract obstruction and uroperitoneum
  • distal renal tubular acidosis: tubular disease –> decreased secretion of H
  • hypoaldosteronism in hypoadrenocoricism
93
Q

Increased HCO3 loss

A
  • alimentary: intestinal and pancreatic secretion are HCO rich –> vomiting, sequestraiton can cause bicarb depletion and loss of buffering capacity
  • renal: proximal renal tubular acidosis (Fanconi’s syndrome) –> defect in HCO3 conservation
94
Q

Dilutional acidosis

A

Rapid saline infusion (minor changes)

- decreased [HCO3] or [tCO2]

95
Q

Cation

A

Atom or molecule with positive charge

  • monovalents
  • divalents
96
Q

Measured cation charge (mC)

A

Na and K

- monovalents and measured as free ions: [ion] = [charge]

97
Q

Unmeasured cation charge (uC)

A

[charge] of all other cations of blood

  • fCa, fMg, and cationic globulins
  • [charge] > [ion]
98
Q

Anion

A

Atom or molecule with negative charge

  • monovalent
  • divalent
  • trivalent
99
Q

Measured anion charge

A

Cl and HCO3

- monovalents, are measured as free ions [ion] = [charge]

100
Q

Unmeasured anion charge

A

[charge] of all other anions of blood

  • PO4, albumin, anions of organic acids, and SO4
  • [charge] >[ion]
101
Q

Total cation or anion charges

A

Total [charge]

- measured + unmeasured

102
Q

Anion gap

A

Difference in the [charge] (not ion) between uA and uC

  • is also equal to the difference between measured C and A
  • measured cations and anions: charges concentrations are the same as ions concentrations
103
Q

Serum is always ______

A

Electrically neutral

  • [+charges] = [-charges]
  • cations: Na and K (95%)
  • anions: Cl and HCO3 (85%)
104
Q

What is the major purpose of calculating the anion gap

A

Identify increased uA, thus defect increased circulating anionic molecules (L-lactate and ketone bodies)

105
Q

Healthy anion gap

A

uA are greater than uC: charges from proteins, organic ions, PO4 and SO4 are greater than charges from fCa, fMg, and H
- anion gap is almost equivalent to the [anions] from organic acids and proteins, PO4, and SO4 since [uC] are small

106
Q

Anion gap - normochloremic and hypochloremic metabolic acidosis

A

Increase AG due to increased uA

  • organic acids (lactic)
  • inorganic acids (renal failure)
107
Q

Anion gap - hypochloremic metabolic alkalosis

A
  • decreased [Cl] and increased [HCO3]
  • no change in AG
  • sum of [Cl] and [HCO3] and sum of [Na] and [K] have not changed
  • occurs with vomiting and GI sequestration of H and Cl
108
Q

Anion gap - hyponatremia and hypochloremia

A
  • concurrent Na and Cl decrease
  • no changes in other concentrations
  • no change in AG
  • same proportion of Na and Cl loss
  • intestinal, via diarrhea or renal, in hypoadrenocorticism
109
Q

Anion gap - hypoproteinemia

A
  • lower concentrations of proteins
  • increased sum of [Cl] and {HCO3]
  • no change in sum of [Na] and [K]
  • decreased AG
110
Q

Increased anion gap - metabolic acidosis

A
  • increased lactate
  • increased ketone bodies
  • renal failure –> increased phosphate, sulfate, or citrate
  • massive rhabdomyolysis: probably increased lactate and PO4
  • ingestion of ethylene glycol, methanol, paraldehyde, metaldehyde, penicillin
111
Q

Hyperchloremic metabolic acidossi will typically not

A

Increase

112
Q

False increase/decreased anion gap

A
  • pseudo-hyponatremia and pseudo-hypochloremia: unreliable AG valvue
  • falsely increased if [HCO3] is falsely decreased due to escape of CO2 from sample
113
Q

Decreased anion gap

A

Minimal clinical significance

  • often due to hypoalbuminemia
  • important to know if animal has hypoalbuminemia, AG would be high if normal albumin
  • occasionally due to hypercalcemia, hypermagnesemia, or multiple myeloma (increased positively charged Igs)
114
Q

Skeletal muscle is the major source of ______

A

Lactate

  • diffuses from myocyte to plasma
  • taken up by hepatocytes
115
Q

D-lactate

A

Produced by bacteria (some produce L lactate)

- very small concentrations in plasma in mammals

116
Q

Hyperlactatemia

A

L-lactate concentration

  • formation exceeds removal by tissues
  • hypoxia is primary reason!! –> anaerobic conditions (pyruvate–>L-lactate) or accumulation of H and acidemia
  • may also be due to defective metabolic pathways
  • decreased removal potentially can contribute to increase concentration, but is not common
117
Q

Hyperlactatemia due to stagnant hypoxia

A
  • shock
  • equine colic: poor perfusion of tissues, absorbed endotoxin, production of L and D-lactate by intestinal bacteria (higher hyperlactatemia = worse prognosis)
118
Q

Hyperlactatemia due to demand hypoxia

A

Strenuous exercise

119
Q

Hyperlactatemia due to increased production by metabolic pathways

A
  • grain overload –> increases formation of lactate by bacteria
  • defective glycolyic pathways: hyperammonemia, pyruvate dehydrogenase deficiency
120
Q

Other unknown causes of hyperlactatemia

A
  • sepsis
  • canine babesiosis
  • liver disease
  • transfusion of stored RBCs: L-lactate rich
121
Q

Both, _____ and _____ will contribute to an anion gap

A

L-lactate and D-lactate
- if there is an increase anion gap and L-lactate is not increased sufficiently for the magnitude, it could be due to D-lactate or other unmeasured anions

122
Q

Ketogenesis in hepatocytes

A

AcCoA into ketone bodies

  • BHB and AcAc
  • acetone
  • promoted by glucagon and inhibited by insulin
123
Q

Ketosis

A
  • excess glucagon or insulin deficiency –> excessive B-oxidation of fatty acids –> excess of AcCoA –> ketogenic pathway (diabetes mellitus and starvation)
  • in negative energy status: oxidation of lipids with inadequate amount of oxaloacetate –> accumulation of AcCoA
124
Q

Ketonemia

A
  • all mammals: starvation, prolonged anorexia, diabetes mellitus
  • cattle: bovine ketosis in lactation, displaced abomasum, hepatic lipidosis
  • dogs: starvation, lactation, endurance racing
  • horses: endurance racing
125
Q

Osmolality

A

Concentration of a solute in moles/kg

126
Q

Osmolarity

A

Concentration of a solute in moles/L

127
Q

Major components of osmolality

A
  • Na is major solute in serum, Cl is the second
  • at physiological concentrations, urea and glucose are small contributors –> marked azotemia or hyperglycemia will cause hyperosmolality
  • protein contribute very little to osmolality
128
Q

_____ detect increases and decreases in effective plasma osmolality

A

Hypothalamic osmoreceptors

  • increased: ADH is released –> stimulate water resorption, thirst center stimulated –> dilutional correction of plasma solute concentration
  • decreased: diminished ADH secretion –> less water resorption
129
Q

Increased osmolality

A
  • increased Na, urea, glucose
  • increased concentration of a nonanionic compound
  • mannitol infusion, radiograph contrast media, ethanol, methanol, ethylene glycol
130
Q

Decreased osmolality

A

Hyponatremia

Clinical Pathology (9 decks)

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