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Lab D > 1. Homeostasis-changes of isovolaemia, isoionia and isoosmosis > Flashcards

1. Homeostasis-changes of isovolaemia, isoionia and isoosmosis Flashcards

1
Q

Samples used for haematology and why

A

Na2, K2, or NaK-EDTA(EthyleneDiamineTetraacetic Acid)-solution as an anticoagulant. This inhibits coagulation by irreversibly binding calcium ions in the sample.

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2
Q

What is important with heamatology samples?

A

It is important to fill the blood collection vial only up to its mark and then gently turn it 8-10 times for mixing.
If the sample with EDTA is stored for over 12 hours, blood cells swell.

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3
Q

Samples used for blood biochemistry parameters?

A

Mostly evaluated in serum, without adding any anticoagulant to the sample. Sometimes blood plasma is used, where coagulation is blocked by heparin.

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4
Q

Function of heparin

A
  • Heparin enhances the binding of coagulation factors to antithrombin III, which in turn blocks the conversion of fibrinogen to fibrin.
  • Heparin is a protein produced by the body (mast cells), but in laboratory diagnostics and treatment protocols we use synthetic heparin.
  • Heparin often has a necrotizing effect on white blood cells in vitro.
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5
Q

Samples used for the testing of blood clotting parameters?

A

Na2-citrate (3.8% solution) is used as an anticoagulant.

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6
Q

Function of Na2-citrate as anticoagulant?

A
  • Similarly to EDTA the mode of action involves Ca2+ binding, but this bond is not irreversible.
  • Citrate causes the least damage in blood cell metabolism, therefore it is also suitable for preparing blood smears.
  • Also for this reason citrate is the anticoagulant of choice in blood transfusion transport bags to maximize cell life. -3,8%-os Na2-citrate is also used for RBC sedimentation test, but in this case citrate:blood ratio is 1:4.
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7
Q

Samples used for coagulation measurements?

A

Na2-citrate as anticoagulant, but Ca2+ is always included in the reagents to restart the coagulation cascade.

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8
Q

ISOVOLAEMIA

A

The physiological and pathological alterations of fluid volume

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9
Q

Water compartments in the organism of animals are?

A

The extracellular space (EC), intracellular space (IC), and the transcellular or interstitial space.

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10
Q

The fluid (water) volume in each compartment is influenced by?

A

The lungs, kidneys, skin and the gastrointestinal tract.

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11
Q

The total water content of the body?

A

Approx. 600-650 ml/BWkg

  • EC: 250-300 ml/BWkg
  • IC: 350-400 ml/BWkg.
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12
Q

What kinds of volume disturbances can be distinguished?

A

Perfusion and hydration disorders.

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13
Q

What is a decrease of tissue perfusion, and what are the causes?

A

It is a volume deficit in the intravascular space.
Can be caused by objective volume-loss e.g. blood loss or a relative decrease in circulating volume e.g. in heart insufficiency.

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14
Q

What is evaluation of volume-disturbances based on?

A
  1. Based on clinical signs:
    –Evaluation of perfusion
    -Evaluation of hydration
  2. Based on packed cell volume (PCV, haematocrit - Ht)
  3. Based on haemoglobin (Hb) concentration
  4. Based on plasma total protein (TP) or albumin (Alb) concentration
  5. Based on change in Mean Corpuscular Volume of the RBCs (MCV), influenced by osmotic
    state
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15
Q

Evaluation of perfusion

A

=Intravascular deficit or circulation problems
• capillary refill time (CRT) (decr. hypovolaemia, incr. hypervolaemia)
• colour of mucous membranes (e.g. pale, livid)
• strength of pulse
• heart rate (e.g. elevation)
• blood pressure (central venous pressure)

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16
Q

Evaluation of hydration

A

=interstitial or intracellular water supply
• skin turgor (elasticity) – pulling up to form a wrinkle
• mucous membranes – e.g. shiny, wet or dry
• sunken eyes (enophthalmos), prolapse of the third eyelid, especially in cats
• turgor (elasticity) of the eye
• skin around the oral cavity or anus – signs of water loss
• changes of body weight
• volume of urine prod, specific gravity of urine

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17
Q

Clinical and laboratory signs of volume changes:

a) DEHYDRATION b) HYPERHYDRATION
1. Capillary refill time (CRT)
2. Strength of pulse
3. Body weight
4. Mucous membranes
5. Elasticity of the skin
6. Placement of eyeballs
7. Turgor of the eyes
8. Heart rate (HR)
9. Central venous blood pressure
10. Hb concentration
11. PCV (Ht)
12. TP and/or Alb
13. MCV
14. Osmolality (serum, urine)
15. Urine output
16. Urine specific gravity

A

a) DEHYDRATION b) HYPERHYDRATION
1. Capillary refill time (CRT): increased / no change/decrease
2. Strength of pulse: decreased / increased
3. Body weight: decreased / increase/no change
4. Mucous membranes: dry / no change/oedema
5. Elasticity of the skin: decreased / no change/oedema
6. Placement of eyeballs: enophthalmos / no change/exophthalmos
7. Turgor of the eyes: decreased / no change/increased
8. HR: increased / no change/increased
9. Central venous BP: decreased / normal/increased
10. Hb conc.: increased / decreased
11. PCV (Ht): increased / decreased
12. TP and/or Alb: increased / decreased
13. MCV: decr. (hyperosmosis) / incr. (hypoosmosis)
14. Osmolality: incr. (hyperosmosis) / decr. (hypoosmosis)
15. Urine output: decreased / increased
16. Urine specific gravity: increased / decreased

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18
Q

Typical total volume loss in acute bleeding

A
  • 5-15%: loss of TBV (total blood volume) - no change in BP
  • 15-25% loss of TBV – tachycardia (incr heart rate), vasoconstriction, initially incr in BP
  • 35-45%: loss of TBV - severe decr in BP, oliguria/anuria and then vasodilatation - shock
  • 50%: loss of TBV – death (exitus letalis)
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19
Q

Packed cell volume (PCV)

  1. What is it?
  2. Expressed as?
  3. Indication/goal
  4. Sample type
A
  1. PCV is a ratio number. It informs us about the ratio of whole blood volume to the volume of RBCs.
  2. Can be expressed as a number without unit, l/l or %
  3. PCV is evaluated routinely; fluid volume changes and quantitative changes of RBCs (e.g. anaemia) can be detected.
  4. Anticoag. blood is necessary (mostly EDTA, sometimes heparin). Some ready-to-use Ht capillaries are coated with heparin.
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20
Q

Methods to measure PCV

A
  1. Mikrohematokrit or microcapillary method
  2. Establishing PCV using automated cell counter
  3. Handheld HCT Meter
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21
Q

Calculation of PCV

A

PCV = (MCV (fl) x RBC (10^12/l)) / 1000 = … l/l / %

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22
Q

The physiological range of PCV

A

in most species: 0.35-0.45 l/l or 35-45 %.

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23
Q
  1. What is oligocythaemia/anaemia?

2. What is polycythaemia?

A
  1. The decrease of the PCV
  2. The increase of the PCV
    Both can be physiological or pathological, absolute or relative.
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24
Q

Normal PCV result - normocythaemia

  1. In case of normovolaemia
  2. In case of hypovolaemia
  3. In case of hypervolaemia
A

Normocythaemia and…

  1. Normovolaemia: the fluid homeostasis and the number of RBC is normal
  2. Hypovolaemia: during acute blood loss or immediately afterwards – Ht does not change: Shock
  3. Hypervolaemia: overdosing of full blood transfusion, chronic stress (usually with high BP)
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25
Q

Causes of increased PCV (polycytaemia)

A

• False: long sample storage with EDTA – corpuscular volume of RBCs incr
• Physiological: (=absolute normovolaemic polycythaemias)
o Congenital
o Changes related to age: new borne animals
o Physiological long-term hypoxia: living in high altitude, regular intensive long training or work e.g. sled dogs (normovolaemic polycythaemia)
• Relative polycytaemia: decr plasma volume (dehydration – hypovolaemic polycythaemia) e.g. lack of drinking water, vomiting, diarrhoea
• Absolute polycythaemia (normovolaemic): incr RBC prod (primary and secondary)
• Complex problem: hypervolaemic polycythaemia – life threatening acute stress or extreme physical exercise

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26
Q

Physiological congenital increased PCV species and breed characteristics

A

lama, yak, greyhound, whippet, borzoi dogs, hot blooded horses

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27
Q

Absolute polycythaemia types

A
  • PRIMARY: without incr erythropoietin (EPO) (bone marrow neoplasia - polycythaemia absoluta vera i.e. chronic leukaemia of RBCs)
  • SECONDARY: due to incr EPO
    a) TRUE: caused by long term hypoxia (can be physiological - low atmospheric O2, training) due to chronic respiratory or circulatory disorders e.g. brachycephal syndrome in dogs, ROA – recurrent airway obstruction in horses, right-left shunt in the heart
    b) NOT TRUE: without hypoxia: autonomous incr of EPO (EPO producing tumour of the kidney, liver)
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28
Q

Causes of decreased PCV (oligocythaemia = anaemia)

A
  • False: microcytosis (decr RBC volume), inappropriate sample homogenization etc.
  • Physiological: incr. plasma volume in the 3rd trimester of pregnancy
  • Relative: pathological incr in plasma volume (hyperhydration – hypervolaemic oligocythaemia) i.e. overdose of fluid therapy, terminal phase of chronic kidney insufficiency
  • Absolute: these are normovolaemic oligocythaemias
  • Complex problem: the absolute oligocythaemias listed above frequently cause refusal of water, vomiting or diarrhoea leading to hypovolaemic oligocythaemia
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29
Q

Absolute oligocythaemia types

A
  • several hours after acute bleeding
  • decr RBC prod.
    a) suppression of bone marrow e.g. heavy metal poisoning, mycotoxins, drug side effects, viral infections (e.g. parvovirus)
    b) lack of some nutrients e.g. iron, copper, B6, B12 vitamins, folic acid
  • decr life-span in circulation e.g. immune-mediated haemolytic anaemia (IHA), ectoparasitosis e.g. extensive flea invasion
  • sequestration of RBCs in the spleen due to hypersplenismus
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30
Q

Additional information gained by examining blood in Ht tubes after centrifuging

A
  1. Colour change of plasma
  2. Buffy coat.
  3. Microfilaria larvae (Dirofilaria immitis or repens): on top of the buffy coat layer
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31
Q

Colour change of plasma

A

-Physiologically plasma: transparent; depending on sp. Colour can be yellowish or colourless like water.
• Reddish tint is seen in haemolysis. Can be intravascular haemolysis or due to error in sampling or sample handling/storage.
• White, opaque colour: indicates alimentary hyperlipidaemia or other lipid-metabolic disorder (e.g. diabetes mellitus, pancreatitis).
• Strong or dark yellow colour: sign of hyperbilirubinaemia (>30 µmol/l). In horses normal plasma is yellowish, since physiological blood bilirubin level is high (about 45
µmol/l). In ruminants yellowish plasma is seen if there is high carotenoid (especially Beta-carotene) content in feedstuff. In these species colourless or very pale plasma may be a sign of carotene-deficiency.
• Chocolate brown colour is suggestive for methaemoglobinaemia.

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32
Q

Buffy coat

  1. What is it?
  2. Physiological width
  3. When does the width increase/decrease?
A
  1. On the top of the RBC layer the WBCs form a white(ish)
    layer, the buffy-coat layer.
  2. The physiological width of this layer is 1-2 mm in a tube of 10 cm, 1-2 units on the Ht scale.
  3. In case of substantial increase (leukocytosis, leukaemia) of decrease of the WBC count.
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33
Q

Estimation of dehydration based on clinical symptoms

A

-Mild:
<5% - clinically hardly detectable (somewhat decreased skin elasticity, dryer mucosa)
5-6% - decrease of skin turgor
6-8% - decrease of skin turgor, enophthalmos and/or dry mucosa
-Moderate: 8-10% - longer CRT, dry mucosa, enophthalmos, tachycardia, strongly decr skin elasticity
-Advanced:
10-12% - signs of shock may occur (weak pulse, tachycardia, cold extremities, low BP), skin remains in the pulled up fold, disturbed consciousness
12-15% - Shock, life threatening

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34
Q

Normovolaemia

  1. Normocythaemic
  2. Oligocythaemic
  3. Polycythaemic
A
  1. Normocythaemic - normal status
  2. Oligocythaemic – also called anaemia: may occur some hours after acute blood loss, absolute anaemias e.g. decr prod. (e.g. suppression of BM in heavy metal toxicities, mycotoxins, drug side effects), shorter life-span e.g. IHA, hypersplenismus
  3. Polycythaemic – can be false, physiological (species, breed, age characteristics) or pathological. These are absolute polycythaemias e.g. non-EPO or EPO-dependent, true or false
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35
Q

Hypovolaemia:

  1. Normocythaemic
  2. Oligocythaemic
  3. Polycythaemic
A
  1. Normocythaemic – immediately after acute bleeding, shock (in hypovolaemic shock, and relative hypovolaemia in anaphylactic and cardiogen shock)
  2. Oligocythaemic – concurrent dehydration and anaemia (e.g. chronic renal failure or suppression of bone marrow + vomiting, diarrhoea)
  3. Polycythaemic – most frequent form of polycythaemia: relative polycythaemias: e.g. vomiting, diarrhoea, polyuria, loss of plasma e.g. burns)
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36
Q

Hypervolaemia:

  1. Normocythaemic
  2. Oligocythaemic
  3. Polycythaemic
A
  1. Normocythaemic – acute stress e.g. strenuous exercise, hyperthermia, fever. Relative volume increase is due to vasoconstriction. Absolute volume
    increase: full blood transfusion overdose.
  2. Oligocythaemic – relative oligocythaemia: in 3rd trimester of pregnancy(physiological), infusion overdose, acute renal failure (subterminal phase of oliguria, anuria)
  3. Polycythaemic – acute stress, where vasoconstriction occurs together with spleen contraction (strenuous exercise, hyperthermia, fever etc.)
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37
Q

Serum osmolality

  1. What is it?
  2. Expressed in?
A
  1. Osmolality expresses the osmotic pressure of the (body) fluids.
  2. Expressed in different units than osmolality:
    osmolality – kg, osmolarity – l.
    The unit of osmolality is osmol/kg, but in practice 10-3rd of this unit is used: miliosmol per kilogram (mOsmol/kg or
    mOsm/kg)
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38
Q

Methods for measure serum osmolality

A
  1. Mathematical method: in plasma or serum
  2. Measurement of osmolality using osmometer: measures the freezing point of the sample compared to the freezing point of water
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39
Q

Mathematical method for serum osmolality

A

Osmolality (mOsm/kg) = 2 (Na+ + K+) + urea + glucose

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40
Q

Osmolar gap

  1. What is it?
  2. Reference range
A
  1. The difference between calculated and measured osmolality
  2. Reference range: 270-310 mOsm/kg. In 97% of cases the osmolar gap fits in the range from
    - 10 to +10; an osmolar gap above 15 is regarded to be pathologic.
41
Q

Interpretation of osmolality

1. Causes of decrease or increase?

A

The decrease or increase in especially Na+ cc. causes the decrease or increase in osmolality.

  • Other factors are the change in plasma glucose cc. in diabetes mellitus, or urea in renal failure.
  • This causes the swelling or shrinking of cells, because water flows from the space with lower osmolality (diluted) to the space with higher osmolality (concentrated).
42
Q

Values of hyperosmolality/hypoosmolality, and what does it mean?

A
  • Hyperosmolality: >310 mOsm/kg - shows that the fluids of the EC space became more concentrated
  • Hypoosmolality: <270 mOsm/kg - show that the fluids of the EC space became more diluted
43
Q

Rapid change in osmolality

  1. Causes?
  2. Effects?
A
  1. Can be caused by incorrect therapeutic interventions, e.g. in hyperglycaemia of advanced diabetes mellitus (DM) if we try to decr blood glucose cc. too quickly by exogenous insulin administration.
  2. Can lead to hypophosphataemia and hypokalaemia,
    also cellular oedema.
    -Iv. administration of hyperosmotic fluids with too big speed or in too large amount, also salt poisoning may cause “cellular” exsiccosis i.e. dehydration
44
Q

Causes of the increase of osmolar gap

A

By the presence of ethanol, ethylene-glikol, methyl-alcohol or isopropyl-alcohol in the blood.

45
Q

Dehydration - effects during:

  1. Isotonic
  2. Hypertonic
  3. Hypotonic
A
  1. Isotonic: blood-, plasma loss, vomiting, diarrhoea –
    may turn to hypotonic, chronic renal failure, primer cellular water loss (in old age)
  2. Hypertonic: primary water loss e.g. diarrhoea,
    hyperventilation, fever, ADH- function loss (central and peripheral/nephrogenic diabetes insipidus); Henle-loop diuretics; beginning of osmotic diuresis
  3. Hypotonic: enhanced sweating in horses; advanced
    osmotic diuresis, hypotonic infusion overdose, aldosterone antagonist diuretics overdose; hypoadrenocorticism, chronic kidney disease, diarrhoea
46
Q

Hyperhydration - effects during:

  1. Isotonic
  2. Hypertonic
  3. Hypotonic
A
  1. Isotonic: concurrent enhanced water and salt intake;
    Na+ and water retention, overdose of iv. plasma or
    isotonic inf.; cardiac or hepatic disorders
  2. Hypertonic: salt poisoning; primary and secondary
    hyperaldosteronism, enhanced glucocorticosteroid effect
  3. Hypotonic: water poisoning; hypotonic infusion
    overdose; increased ADH function (neoplasia of neurohypophysis); hypothyreosis
47
Q

Concentration of electrolytes

  1. Indication
  2. Sampling type
  3. Not recommended sample types
  4. Method of measurement
A
  1. Indication: conc of electrolytes so called “ionogram” is measured in variable conditions, because the basic life-processes can occur only in the appropriate osmotic
    environment: enzymes’ activity, forwarding of nerve impulses.
  2. Sampling type:
    - Heparinised full blood: for acid-base/blood gas analyzer
    - Many biochemistry blood analyzers are capable of performing ionogram - usually serum of heparinised plasma.
    - Before sampling we need to carefully consider the anticoagulant agent.
  3. Na- or K-EDTA incr Na+ or K+ conc and decr Ca2+ conc, Ca-heparin incr Ca2+ conc; non electrolyte equilibrated Na- or Li-heparinate decr Ca2+ conc.
  4. Method: Plasma or serum electrolyte measurements are mostly performed using ion selective electrodes, similarly to pH measurements. Measurement of Cl can be performed by spectrophotometry.
48
Q

Anticoagulant for Ca2+

A

Equilibrated Na- or Liheparinate should be used

49
Q

Na+ Reference range

A

140-150(-160) mmol/l

50
Q

Role of Na+

A

Plays an important role in maintaining plasma
osmolality, because water molecules move freely through biological membranes, but sodium ions can only be transported from the IC to the EC space only through Na+/K+ ion pumps.

51
Q

What is Na+ conc dependent on?

A

-Intake – too high intake per os occurs mostly in pigs and
poultry, but in any species iatrogen iv overdosing can occur.
-Na+ conc in plasma is also influenced by its degree of excretion
-Plasma Na+ conc may be influenced by the degree
of plasma dilution.

52
Q

What is excretion of Na+ in the kidneys is dependent on?

A
  • The condition of the proximal tubules, where 60% of the Na+ is reabs, on the effect of aldosterone and on the condition of the distal tubules.
  • Excretion is also dependent on the excretion of other osmotically active substances in the kidneys, sweating in horses and also excretion/loss via GI-tract.
53
Q

What is plasma dilution of Na+ dependent on?

A

Fluid intake (drinking water, fluid therapy) and the effect of antidiuretic hormone (ADH)

54
Q

Causes of hypernatraemia (↑ Na)

A
  • Incr water loss or decr water intake (dehydration):
  • decr intake (lack of thirst or no drinking water available)
  • polyuria e.g. diabetes insipidus (loss of water via the kidneys)
  • vomiting or acute diarrhoea (water loss via GI system)
  • hyperthermia / enhanced panting (water loss via the resp. system)
  • Increased Na+ retention in the kidneys:
  • primary hyperaldosteronia (Conn’s syndrome)
  • secondary hyperaldosteronism
  • Other:
  • overdose of hypertonic salt solution
  • increased intake of salt (“salt poisoning”)
55
Q

Causes of hyponatraemia (↓ Na)

A
  • excessive fluid intake - “water poisoning”
  • per os possible in ruminants
  • overdose of hypotonic fluid e.g. iv
  • Retenstion of water
  • cardiac insufficiency
  • advanced renal or hepatic insufficiency
  • Enhanced Na+ loss
  • gastrointestinal (diarrhoea)
  • renal loss – also hypoadrenocorticism (Addison’s disease)
  • sweating (in horses mainly)
  • sequestration in body cavities (e.g. ascites)
  • Water outflux from the IC to the EC space
  • Hyperosmolality
56
Q

K+ reference range

A

3.5-5.5 mmol/l

57
Q

What is plasma K+ conc influenced by?

A

Intake, excretion and transport mechanisms bw the EC and IC space.

  • Intake: happens via food, water and sc/iv fluid therapy.
  • Normally in the kidneys 90% of K+ is reabsorbed from the glomerular filtrate.
  • K+ excretion can be substantial through the intestinal walls.
58
Q

How does excretion of K+ increase?

A

Under aldosterone effect in the epithelial cells of the distal tubules via regulation of Na+/K+-ATPase.

59
Q

What does secretion and reabsorption of K+ depend on in the distal tubules?

A

Blood pH and the eventual use of diuretic drugs.

60
Q

What does the transport mechanisms bw IC (high conc.) and EC (low conc.) space include?

A

Blood pH, integrity of cells and the effect of insulin.

61
Q

Effect of insulin on K+

A

Insulin induces the co-transport of K+ with glucose into

the cells, which has a lowering effect on plasma K+

62
Q

Causes of hypokalaemia

A

Decr intake (anorexia), long term polyuria (e.g. chronic kidney insufficiency), administration of loop-diuretic drugs (e.g. furosemide), enteral potassium loss (e.g. diarrhoea, enteral bleeding), primary or secondary hyperaldosteronism, alkalosis and insulin

63
Q

Causes of hyperkalaemia

A

Incr per os intake, overdose of potassium containing fluids, acute kidney failure, rupture of urinary bladder, hypoaldosteronism and acidosis.

64
Q

Pseudohyperkalaemia occurance

A

May occur in damage of tissue cells or RBCs (e.g. necrosis, haemolysis). Can occur as laboratory error. In dogs haemolysis induced pseudohyperkalaemia is very rare, because RBCs’ K+ content is not much higher than plasma conc (exception: Akita inu).

65
Q

Consequences of K+ changes

A

The normal range for plasma K+ conc is very narrow, because substantial change in either direction influences the conduction of neural stimuli.
Both increase and decrease causes similar muscle weakness.
-In hyperkalaemia muscle spasm may also occur, which is related to secondary hypocalcaemia. This can be seen in hyperkalaemia >7 mmol/l.

66
Q

Consequences of hypokalaemia

A

Decreased neuromuscular irritability, muscular weakness, paresis, glucose intolerance, decr insulin secretion, decr conductance of electrical stimuli in heart (bradycardia), polyuria, polydypsia, Na+ -retention, alkalosis.

67
Q

Cl- reference range

A

100-125 mmol/l

68
Q

Most important anions of the plasma

A

Cl- HCO3-

69
Q

Symptoms of Cl- - systemic diseases

A

Vomiting, diarrhoea, polyuria/polydypsia

70
Q

Occurance of hyperchloraemia

A

Mostly after excessive per os intake (salt poisoning), iv overdose in fluid therapy, decreased excretion (hyperaldosteronism) and other processes with hypernatraemia

71
Q

Typical causes of decreased Cl-cc

A

Abomasal displacement, vomiting, diarrhoea, sweating (horse) and other processes with hyponatraemia

72
Q

Roles of calcium

A
  • Maintenance of neuromuscular irritability
  • Initiation of muscle contraction
  • Regulation of cell membrane permeability and irritability
  • Blood clotting processes (e.g. IV. factor)
  • The building and stabilizing of bones and teeth (calcium is also stored in bones)
73
Q

Forms of calcium in blood plasma

A

Three forms:

  • 47% is bound to proteins (albumin)
  • 40% is free ionised form
  • 13% is chelated form (with organic acids)
74
Q

Indications of calcium imbalance

A

Lethargy, weakness, vomiting, constipation, PU/PD (suspect incr of tCa and/or Ca2+); restlessness, muscle tremor, seizures (suspect decr ionized fraction); pathologic fractures of bones (suspected decr tCa).

75
Q

Calsium reference range

A
  1. 1-3.0 mmol/l (Ca2+ is 45-50% of this)

- In poultry laying eggs tCa may be even double (~5.8 mmol/l)

76
Q

Calcium:

  1. Sampling
  2. Method
A
  1. Sampling:
    - tCa: serum (preferred) or heparinised plasma.
    - Ionized Ca: mostly heparinised plasma.
  2. Method:
    - in laboratory testing ionized Ca is measured mostly using ion-selective electrodes and tCa is measured using spectrophotometry.
77
Q

What is spectrophotometric measurement of Ca based on?

A

Based on the fact that Ca in higher pH can form violet purple complex with ortocresolphtalein, which shows maximum absorbance at the length wave of 570 nm.

78
Q

What can influence the conc. of Ca?

A

Dietary, enteral, hormonal, paraneoplastic effects and excretion via the kidney can influence the conc of both forms of Ca in the bloodstream. For this reason
mostly the measurement of tCa is recommended.

79
Q

Causes of hypocalcaemia

A

-Insufficient intake or absorption (vit D deficiency or its decr activation)
-Hypofunction of parathyroid gland (e.g. caused by
deficiency of Mg)
-Cats: after surgical thyroidectomy (transient)
-Lactating animals: due to incr loss of Ca with milk and toxicosis due to the above mentioned Ca binding substances.
-Mild hypocalcaemia can be caused by alkalosis

80
Q

Symptoms of decrease of the ionized fraction of Ca

A

Acute symptoms of muscular rigidity, muscle tremor or seizures.

81
Q

Causes of hypercalcaemia

A
  • Excessive Ca or vit.D intake
  • Cats: Hyper A vitaminosis
  • Hyperfunction of parathormone (but it can also occur in some inflammatory or neoplastic diseases as so called paraneoplastic syndrome)
82
Q

Causes of paraneoplastic syndrome

A

By ectopic parathormone activity or prod of parathormone-like substances by neoplastic cells.

83
Q

Effects of hypercalcaemia

A

Causes damage in bones (ectopic bone formation), soft tissue calcification.

84
Q

Role of Magnesium (tMg, Mg2+)

A
  • Plays an important role in ATP metabolism, since ATP is bound to Mg2+ within the cells forming a complex.
  • It is an actin-myosin activator (maintains neuromuscular irritability).
  • It is a catalysator for more than 300 enzymes
  • Facilitates the synthesis and breakdown of acetylcholine.
85
Q

Indications of Magnesium

A
  • Hypocalcaemia of unknown origin (deficiency of Mg2+ blocks PTH production and activity)
  • Hypokalaemia (which is resistant to supplementation)
  • DKA (diabetic keto-acidosis)
  • Muscle weakness of unknown origin, tremor, seizure, dysphagia, dyspnea and arrhythmia.
86
Q

Magnesium reference range

A

0.8-1.5 mmol/l

87
Q

Magnesium

  1. Sample
  2. Method
A
  1. Sample: tMg – serum or heparinised plasma, ionised – heparinised plasma
  2. Method: Ionselective electrodes (ISE), which is 70%
    of the total Mg. TMg by spectrophotometry: the method is based on xylidineblue reagent with which Mg forms purple complex (max abs at 520 nm wave length).
88
Q

Causes of hypomagnesaemia

A
  • Decreased intake e.g. grass tetany in cattle and sheep. —May be a precipitating factor to transport tetany
  • Absorption disturbance e.g. in lymphangiectasia
  • Due to increased excretion (renal, enteral) e.g. in chronic diarrhoea
  • Due to hyperthyroidism: in addition to incr excretion, intracellular Mg storing also incr.
89
Q

Causes of hypermagnesaemia and consequences

A
  • Increased intake: iatrogenic e.g. increased absorption after laxative agents or overdose of Mg containing infusion.
  • Decr excretion, in chronic insufficiency, milk fever, hypothyreosis or Addison’s disease
  • Its conc may incr as a consequence of dehydration.
  • Consequences: muscular weakness, paralysis, until Mg-narcosis develops.
90
Q

Grass tetany in cattle and sheep

A

Complex metabolic disturbance characterized by hypomagnesaemia (plasma tMg <0.65 mmol/L) and reduced conc of tMg in the CSF (0.4 mmol/L), which lead to hyperexcitability, muscular spasms, convulsions, respiratory distress, collapse,
and death.

91
Q

Inorganic phosphate (Pi): roles

A

Phosphate is a product, reaction partner and source of several synthetic, transitional and breakdown processes. Phosphate is one of the plasma buffer-systems, and it is also an important constituent of the energy household of the RBCs.

92
Q

Inorganic phosphate (Pi): Indications/goals

A

See all the indications for calcium measurement, additionally haemolysis of unknown origin, anorexia, weakness, ataxia, seizures and to check kidney glomerular function.

93
Q

Inorganic phosphate reference range

A
  • dog, horse: 0,8-1,8 mmol/l
  • cat, cattle, sheep: 1-2,4 mmol/l
  • swine, goat: 1-3 mmol/l.
94
Q

Inorganic phosphate

  1. Sample
  2. Method
A
  1. Sample: serum or heparinised plasma
  2. Method: Spectrophotometry. In acidic environment P reacts with ammonium-molybdate and forms a yellow phosphate-molybdic acid complex.
95
Q

Interpretation of inorganic phosphate - When does it increase/decrease?

A

-Intake: incr when meat or grains are fed.
-Rate of abs: incr under vit.D effect and decr in exocrine pancreatic insufficiency, intestinal inflammation and vit.D deficiency.
-Metabolic utilisation of phosphorus has great impact on plasma Pi conc, the highest utilisation occurring in quick growth of young animals, high pregnancy and egg
production in poultry.
-Liver function: in case of liver dysfunction Pi decr.
-Kidney function: in case of decr kidney function the excretion of Pi is decr, so the Pi in plasma incr.
-Both in primary and secondary hyperparathyroidism the excretion of Pi is enhanced, which causes the
plasma Pi to decr
-Hyperthyroidism: the PTH excretion is decr so Pi excretion also decr.
The amount of phosphorus mobilized from the bones can be substantial e.g. in bone tumours extensive osteolysis occurs, which incr plasma Pi.

96
Q 
Parathyroid hormone (PTH) does what?
What happens during physiologic conditions?
A

Induces phosphate and calcium mobilization from the bones and increases the Pi-excretion and Ca-reabs through the kidneys.
-In physiologic condition: the net effect is decr Pi and incr Ca-conc in the plasma.

97
Q

Effect of calcitonin

A

Increases calcium, and phosphate abs from the intestines and their incorporation into the bones. The net effect is decr Ca and Pi values.

98
Q

Decrease of plasma pH effects Pi and Ca how?

A

Causes a decrease in Pi-conc and an increase in Ca2+ level (tCa does not change).

99
Q

The effect of the parathyroid gland on plasma calcium and phosphorus:

a) plasma / b) urine
1. Primary hyperparathyroidism:
- adrenal tumour
- Ectopic PTH secretion
2. Secondary hyperparathyroidism:
- renal failure
- increased phosphate intake
- (long term high meat intake)
3. Hypoparathyroidism
4. D-hypervitaminosis

A

a) plasma / b) urine
1. Primary hyperparathyroidism:
- adrenal tumour: Ca incr / Ca incr
- Ectopic PTH secretion Pi decr / Pi incr
2. Secondary hyperparathyroidism:
- renal failure: Ca incr / Ca incr/same, Pi incr/same / P same
- Incr phosphate intake: Ca decr / Ca decr
-(long term high meat intake): Pi incr / Pi incr
In both last cases bones become demineralised.
3. Hypoparathyroidism Ca decr Ca decr, Pi incr Pi incr
4. D-hypervitaminosis Ca incr Ca incr, Pi incr Pi incr

Lab D (18 decks)

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