Lab 1 Flashcards
Causes of increased PCV (polythaemia)
False: long sample storage with EDTA – corpuscular volume of RBCs increases
Physiological: (the physiological polycythaemias are also absolute normovolaemic polycythaemias)
o Congenital: species and breed characteristics: lama, yak, greyhound, whippet, borzoi dogs, hot blooded horses
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 polycythaemia: decreased plasma volume (dehydration – hypovolaemic polycythaemia) e.g. lack of drinking water, vomiting, diarrhoea
Absolute polycythaemia (normovolaemic): increased RBC production (physiological see above)
o Primary: without increased erythropoietin (EPO) (bone marrow neoplasia - polycythaemia absoluta vera i.e. chronic leukaemia of RBCs)
o Secondary: due to increased EPO
a. true: caused by long term hypoxia (can be physiological - see above: 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 (shunt: a hole or a small passage which moves, or allows movement of, fluid from one part of the body to another)
b. not true: without hypoxia: autonomous increase of EPO (EPO producing tumour of the kidney, liver)
Complex problem: hypervolaemic polycythaemia – life threatening acute stress or extreme physical exercise (concurrent constriction of blood vessels and the spleen)
Causes of decreased PCV (oligocythaemia = anemia):
False: microcytosis (decreased RBC volume), inappropriate sample homogenization etc.
Physiological: incr. plasma volume in the 3rd trimester of pregnancy (this is also relative hypervolaemic oligocythaemia!)
Relative: pathological increase in plasma volume (hyperhydration – hypervolaemic oligocythaemia) i.e. overdose of fluid therapy, terminal (oliguric/anuric) phase of chronic kidney insufficiency
Absolute: these are normovolaemic oligocythaemias
o several hours after acute bleeding (replacement of plasma is much quicker than replacement of cells)
o decreased red blood cell production
a. suppression of the bone marrow e.g. heavy metal poisoning, mycotoxins, drug side effect (e.g. chemotherapeutic agents), viral infections (e.g. parvovirus)
b. lack of some nutrients e.g. iron, copper, B6, B12 vitamins, folic acid o decreased life-span in circulation e.g. immune-mediated haemolytic anaemia (IHA), ectoparasitosis e.g. extensive flea invasion
o sequestration of RBCs in the spleen due to hypersplenismus
Complex problem: the absolute oligocythaemias listed above frequently cause refusal of water, vomiting or diarrhoea leading to hypovolaemic oligocythaemia
Changes of PCV in different volume conditions:
- Normovolemia
Normocythaemic - normal status
Oligocythaemic – also called anaemia: may occur some hours after acute blood loss, absolute anaemias see table 3. e.g. decreased production (e.g. suppression of the bone marrow in heavy metal toxicities, mycotoxins, drug side effects), shorter life-span e.g. IHA, hypersplenismus
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 - see Table 3!
Changes of PCV in different volume conditions:
- Hypovolaemia
Normocythaemic – immediately after acute bleeding, shock (in hypovolaemic shock, and relative hypovolaemia in anaphylactic and cardiogenic shock)
Oligocythaemic – concurrent dehydration and anaemia (e.g. chronic renal failure or suppression of bone marrow + vomiting, diarrhoea)
Polycythaemic – most frequent form of polycythaemia: relative polycythaemias: e.g. vomiting, diarrhoea, polyuria, loss of plasma e.g. burns)
Changes of PCV in different volume conditions
- Hypervolaemia
Normocythaemic – acute stress e.g. strenuous exercise, hyperthermia, fever. Relative volume increase is due to vasoconstriction. Absolute volume increase: full blood transfusion overdose.
Oligocythaemic – relative oligocythaemia: in 3rd trimester of pregnancy (physiological), infusion overdose, acute renal failure (subterminal phase of oliguria, anuria)
Polycythaemic – acute stress, where vasoconstriction occurs together with spleen contraction (strenuous exercise, hyperthermia, fever etc.)
Osmotic changes in different hydration (volume) status:
- Dehydration
Isotonic:
- blood-, plasma loss, vomiting, diarrhoea – may turn to hypotonic, chronic renal failure, (middle grade), primer cellular water loss (in old age)
Hypertonic:
- primary water loss e.g. diarrhoea, hyperventilation (typical dehydration of panting species), fever,
- ADH- function loss (central and peripheral/nephrogenic diabetes insipidus); Henle-loop diuretics; beginning of osmotic diuresis (e.g. DM – when excretion of Na+ is not yet enhanced but there is hyperglycaemia)
Hypotonic:
- enhanced sweating in horses; advanced osmotic diuresis (in advanced DM, when Na+ is lost together with water: Na+ wash out); hypotonic infusion overdose; after water and salt loss, drinking large amount of water (when isovolaemia is not yet re-established); aldosterone antagonist diuretics overdose; hypoadrenocorticism (Addison’s disease); chronic kidney disease (tubular damage); diarrhoea
Osmotic changes in different hydration (volume) status:
- Hyperhydration
Isotonic:
- concurrent enhanced water and salt intake; Na+ and water retention (e.g. acute kidney insufficiency); overdose of iv. plasma or isotonic inf.; cardiac or hepatic disorders (localized hyperhydration)
Hypertonic:
- salt poisoning; primary and secondary hyperaldosteronism (Conn’s syndrome), enhanced glucocorticosteroid effect (Cushing’s syndrome or iatrogen)
Hypotonic:
- water poisoning (excessive water intake – haematuria of calves); hypotonic infusion overdose; increased ADH function (neoplasia of neurohypophysis); hypothyreosis
Causes of Hypernatraemia:
Increased water loss or decreased water intake (dehydration):
o decreased intake (lack of thirst or no drinking water available)
o polyuria e.g. diabetes insipidus (loss of water via the kidneys)
o vomiting or acute diarrhoea (water loss via the GI system)
o hyperthermia / enhanced panting (water loss via the resp. system)
increased Na+ retention in the kidneys:
o primary hyperaldosteronizmus (Conn’s syndrome)
o secondary hyperaldosteronism (glucocorticosteroid therapy, liver disease, neoplasm)
Other:
o overdose of hypertonic salt solution o increased intake of salt (“salt poisoning”)
Causes of Hyponatraemia:
excessive fluid intake - “water poisoning” :
o per os possible in ruminants o overdose of hypotonic fluid e.g. iv
Retenstion of water o cardiac insufficiency:
o advanced renal or hepatic insufficiency
Enhanced Na+ loss o gastrointestinal (diarrhoea):
o renal loss – also hypoadrenocorticism (Addison’s disease)
o sweating (in horses mainly)
o sequestration in body cavities (e.g. ascites)
Water outflux from the IC to the EC space:
o Hyperosmolality
Causes of Hypokalaemia:
- decreased 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 15 hyperaldosteronism,
- alkalosis and insulin (especially 1st phase of insulin treatment, insulinoma, insulin overdose).
Causes of Hyperkalaemia:
- increased per os intake,
- overdose of potassium containing fluids,
- acute kidney failure,
- rupture of urinary bladder,
- hypoaldosteronism (hypoadrenocorticism /Addison’s disease/) and acidosis.
- Pseudohyperkalaemia may occur in damage of tissue cells or RBCs (e.g. necrosis, haemolysis).
- The latter can occur as laboratory error e.g. if during sampling of handling/storage haemolysis occurs.
- In dogs haemolysis induced pseudohyperkalaemia is very rare, because RBCs’ K+ content is not much higher than plasma concentration (exception: Akita inu).
Causes of Hyperchloraemia:
- occurs mostly after excessive per os intake (salt poisoning),
- iv overdose in fluid therapy,
- decreased excretion (hyperaldosteronism = Conn’s syndrome) and other processes with hypernatraemia
Causes of Hypochloraemia:
- abomasal displacement, vomiting, diarrhoea, sweating (horse) and other processes with hyponatraemia
Causes of Hypocalcaemia:
- insufficient intake or absorption (vitamin D deficiency or its decreased activation),
- hypofunction of parathyroid gland (e.g. caused by deficiency of Mg), in cats after surgical thyroidectomy (transient),
- in lactating animals due to increased loss of calcium with milk and toxicosis due to the above mentioned calcium binding substances.
- Frequently both the tCa and the Ca2+ are decreased.
- Acute symptoms of muscular rigidity, muscle tremor or seizures are caused by the decrease of the ionized fraction (puerperal eclampsia, parturient paresis, hypocalcaemic tetany, ethylene-glikol toxicosis).
- Mild hypocalcaemia can be caused by alkalosis (Ca2+ decreases due to increased bound to albumin).
Causes of Hypercalcaemia:
- excessive calcium or vitamin D intake,
- hyper A vitaminosis in cats,
- hyperfunction of parathormone can be mentioned in the first place but it can also occur in some inflammatory (systemic mycosis, granulomatosus diseases, osteomyelitis) or neoplastic (lymphoma, perianal gland adenocarcinoma, osteosarcoma, pulmonary carcinoma, primary hyperparathyroidismus) diseases as so called paraneoplastic syndrome.
- The latter is caused by ectopic parathormone activity or production of parathormone-like substances by neoplastic cells.
- Hypercalcaemia causes damage in bones (ectopic bone formation), soft tissue calcification (calcinosis - skin, intracavitary organs e.g. decrease of kidney tubular function).
