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
Decreased renal excretion of Na due to aldosterone
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
26
Dehydration with net loss of isotonic fluids
Normonatremia - alimentary: vomit, diarrhea, sequestration - renal: polyuric renal dz with defective tubular functions, osmotic diuresis, increased diuresis - cutaneous: profuse sweating in horses
27
Edema or transudation with net retention of isotonic fluids
Creates normonatremia or hyponatremia
28
Congestive heart failure
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
29
Hepatic cirrhosis with abdominal transudation
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
30
Hepatic cirrhosis - Peripheral arterial vasodilation theory
Decreased effective blood volume --> RAS --> increases hydraulic pressure in the hepatic sinusoids --> transudation
31
Nephrotic syndrome
Protein losing nephropathy (leads to abdominal transudation) - H2O and Na retention mechanism is not understood - involves several processes
32
Hyponatremia occurs due to decreased _____
Na/water ratio, or IC to EC water shifting
33
Na deficit
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
34
Hypoadrenocorticism
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)
35
Renal loss of Na
Prolonged diuresis by diuretics - osmotic or by furosemide: Na poor - thiazide: Na, K, and Cl loss
36
Ketonuria
Ketone bodies in tubular lumen --> obligate excretion of cations, thus increased excretion of Na
37
Na wasting nephropathies
Especially tubular diseases or pyelonephritis | - mostly seen in horses
38
Sweating
Cutaneous loss in horses | - Na, K, Cl rich = hyponatremia
39
Third space loss
Repeated drainage of chylous throacic effusions - acute internal hemorrhage or acute exudation - hyponatremia
40
H2O excess
Water retention > Na retention - edematous disorders: CHF, hepatic cirrhosis, nephrotic syndrome = hyponatremia
41
Water ICF --> ECF
Marked or persistent osmolality by hyperglycemia or mannitol infusion --> osmotic draw of water into the blood --> dilute Na
42
Na ECF --> ICF
- 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
43
Na IV --> EV
Uroperitoneum | - urine is Na and Cl poor --> diffusion of Na and Cl to peritoneal cavity
44
K depletion
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
45
Potassium concentration is dependent on
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
46
[K] should be interpreted with consideration of ____
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
47
____ and ____ promote K uptake
Epinephrine and insulin - Na/K ATPase pump - hyperkalemia --> cellular uptake of K
48
Renal excretion of K
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
49
Shifting of K ICF --> ECF
- 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)
50
Increased total body K
- 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
51
Hypoaldosteronism
Decreased activity of Na/K ATPase pumps | - decreased resorption of Na and decreased movement of K
52
Repeated chylous effusion drainage
May be related to hyponatremia + hypovolemia --> less Na resorbed in the distal nephron, less K excretion
53
Acidotic
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
Alkalotic
Expected to decrease concentration, thus it suggests concurrent hyperkalemia (usually causes normokalemia)
55
Hypokalemia due to metabolic alkalosis
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
Decreased total body K due to increased excretion
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
Hyperaldosteronism
Promote renal K secretion by stimulation of Na/K ATPase pump
58
Hypokalemia is also caused by
- increased excretion via increased alimentary loss - increased excretion via increased cutaneous loss - hypokalemic renal failure in cats
59
Na:K ______ may be diagnostic of hypoadrenocorticism
<27, 25, or 22
60
Decreased Na:K due to hypoadrenocortisim
Decreased aldosterone - hyponatremia by increased renal excretion - hyperkalemia by decreased renal secretion
61
Decreased Na:K due to diarrhea
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
Decreased Na:K due to renal failure
Decreased ability of tubules to resorb Na and secrete K (oliguria)
63
Decreased Na:K due to urinary tract obstruction or uroperitoneum
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
Decreased Na:K due to diabetes mellitus with ketonuria
Hyponatremia due to osmotic diuresis --> increased Na excretion and plasma dilution - hyperkalemia not expected
65
Decreased Na:K due to third space loss
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
Chloride concentration
- serum [Cl} = ECF [Cl} --> influenced by Na and HCO3 | - controlled by renal resorption and secretion, and alimentary tract functions
67
Hyperchloremia typically occurs with _____
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
Hyperchloremia due to water deficit
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
Excess Cl
- increased intake of Cl with restricted water (salt poisoning) - decreased renal excretion of Na: hyperaldosteronism (rare)
70
Hyperchloremic metabolic acidosis - alimentary
- vomiting, diarrhea with loss of intestinal secretions | - cattle with esophageal obstruction (cannot ingest saliva) --> loss of Na and HCO3 (Cl poor solution)
71
Hyperchloremic metabolic acidosis - renal
- 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
Respiratory alkalosis (chronic)
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
Hypochloremia typically occurs with
Hyponatremia or increased serum bicarb | - also metabolic acidosis with increased anion gap
74
Hyponatremic dehydration
Alimentary, renal, cutaneous or third space loss | - leads to hypochloremia
75
Hypochloremia due to acid base disturbances
Low [Cl] is present in the absence of hyponatremia --> electrical neutrality must be maintained - increased bicarb - increased anion gap
76
Metabolic alkalosis - hypochloremia
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
Bovine renal failure
Causes alkalosis - changes result from abomasal atony --> functional obstruction and sequestration of Cl - more excretion of K in saliva --> limit absorption of Cl
78
Metabolic acidosis with increased anion gap
Ketoacidosis and lactic acidosis: obligate excretion of Na --> less resorption of Cl - foreign substances that generates anions also lead to obligate Na loss
79
_____ is a major buffer that helps maintain the blood pH
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
Bicarb measurements
- 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
Increased [HCO3[ or [tCO2] due to gastric loss
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
Metabolic alkalosis in cattle renal failure
Abomasal atony --> HCl sequestration generating alkalosis | - increased [HCO3] or [tCO2]
83
Renal loss of H due to loop of Henle diuretics
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
Renal loss of H due to thiazide diuretics
Inhibits Na/Cl cotransporter --> hypovolemia and hypochloremia - increased [HCO3]
85
Increased [HCO3] secondary to respiratory _____
Acidosis | - renal compensation
86
Increased [HCO3] due to hypokalemia
Stimulates H/K ATPase in distal nephron --> K retention, H secretion and HCO3 generation
87
Increased [HCO3] due to renal loss of H
``` Endurance races (sweating) and intestinal disorders in horses - lead to hypovolemia and hypochloremia --> secretion of H ```
88
Shift of H from ECF to ICF due to hypokalemia
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
Contraction alkalosis
- 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
Decreased [HCO3] or [tCO2] due to metabolic ____
Acidosis (primary or compensating)
91
Generation of excess H
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
Decreaed renal excretion of H
- renal failure --> decreased acid excretion - urinary tract obstruction and uroperitoneum - distal renal tubular acidosis: tubular disease --> decreased secretion of H - hypoaldosteronism in hypoadrenocoricism
93
Increased HCO3 loss
- 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
Dilutional acidosis
Rapid saline infusion (minor changes) | - decreased [HCO3] or [tCO2]
95
Cation
Atom or molecule with positive charge - monovalents - divalents
96
Measured cation charge (mC)
Na and K | - monovalents and measured as free ions: [ion] = [charge]
97
Unmeasured cation charge (uC)
[charge] of all other cations of blood - fCa, fMg, and cationic globulins - [charge] > [ion]
98
Anion
Atom or molecule with negative charge - monovalent - divalent - trivalent
99
Measured anion charge
Cl and HCO3 | - monovalents, are measured as free ions [ion] = [charge]
100
Unmeasured anion charge
[charge] of all other anions of blood - PO4, albumin, anions of organic acids, and SO4 - [charge] >[ion]
101
Total cation or anion charges
Total [charge] | - measured + unmeasured
102
Anion gap
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
Serum is always ______
Electrically neutral - [+charges] = [-charges] - cations: Na and K (95%) - anions: Cl and HCO3 (85%)
104
What is the major purpose of calculating the anion gap
Identify increased uA, thus defect increased circulating anionic molecules (L-lactate and ketone bodies)
105
Healthy anion gap
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
Anion gap - normochloremic and hypochloremic metabolic acidosis
Increase AG due to increased uA - organic acids (lactic) - inorganic acids (renal failure)
107
Anion gap - hypochloremic metabolic alkalosis
- 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
Anion gap - hyponatremia and hypochloremia
- 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
Anion gap - hypoproteinemia
- lower concentrations of proteins - increased sum of [Cl] and {HCO3] - no change in sum of [Na] and [K] - decreased AG
110
Increased anion gap - metabolic acidosis
- 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
Hyperchloremic metabolic acidossi will typically not
Increase
112
False increase/decreased anion gap
- pseudo-hyponatremia and pseudo-hypochloremia: unreliable AG valvue - falsely increased if [HCO3] is falsely decreased due to escape of CO2 from sample
113
Decreased anion gap
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
Skeletal muscle is the major source of ______
Lactate - diffuses from myocyte to plasma - taken up by hepatocytes
115
D-lactate
Produced by bacteria (some produce L lactate) | - very small concentrations in plasma in mammals
116
Hyperlactatemia
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
Hyperlactatemia due to stagnant hypoxia
- shock - equine colic: poor perfusion of tissues, absorbed endotoxin, production of L and D-lactate by intestinal bacteria (higher hyperlactatemia = worse prognosis)
118
Hyperlactatemia due to demand hypoxia
Strenuous exercise
119
Hyperlactatemia due to increased production by metabolic pathways
- grain overload --> increases formation of lactate by bacteria - defective glycolyic pathways: hyperammonemia, pyruvate dehydrogenase deficiency
120
Other unknown causes of hyperlactatemia
- sepsis - canine babesiosis - liver disease - transfusion of stored RBCs: L-lactate rich
121
Both, _____ and _____ will contribute to an anion gap
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
Ketogenesis in hepatocytes
AcCoA into ketone bodies - BHB and AcAc - acetone - promoted by glucagon and inhibited by insulin
123
Ketosis
- 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
Ketonemia
- 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
Osmolality
Concentration of a solute in moles/kg
126
Osmolarity
Concentration of a solute in moles/L
127
Major components of osmolality
- 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
_____ detect increases and decreases in effective plasma osmolality
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
Increased osmolality
- increased Na, urea, glucose - increased concentration of a nonanionic compound - mannitol infusion, radiograph contrast media, ethanol, methanol, ethylene glycol
130
Decreased osmolality
Hyponatremia