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MT 1 Flashcards

1
Q

What different kinds of polycythaemia do we have?

A
  1. Normovolaemic polycythaemia: can be false, physiological (species, breed, age characteristics) or pathological. These are absolute polycythaemias e.g.
    non-EPO or EPO dependent, true or false
  2. Hypovolaemic polycythaemia: most frequent form of polycythaemia: relative polycythaemias: e.g. vomiting, diarrhoea, polyuria, loss of plasma e.g. burns)
  3. Hypervolaemic polycythaemia: acute stress, where vasoconstriction occurs together with spleen contraction (strenuous exercise, hyperthermia, fever etc.)
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2
Q

How do we examine the acute phase proteins and why is it important?

A
  • Glutaric aldehyde test: fibrinogen (APP) and globulin
  • ESR: APP attach to surface of RBCs - sediment quicker
  • CRP: C-reactive protein (APP)
  • Important because: The very first laboratory sign of inflammation is the increase of APPs in the blood and the decrease of negative APPs.
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3
Q

Causes of metabolic and respiratory alkalosis?

A

METABOLIC alkalosis causes:
- Incr alkaline intake: overdose of bicarbonates, feeding rotten food
- Incr ruminal alkaline prod: high protein intake, low carb intake, anorexia, hypomotility
- Decr hepatic ammonia catabolism (liver failure)
- Incr acid loss: vomiting, gastric dilatation volvulus syndrome, abomasal displacement
- Ion exchange: hypokalaemia: due to Henle loop diuretics
RESPIRATORY alkalosis causes:
-Increased loss of CO2: hyperventilation
*excitation
* forced ventilation (anaesthesia)
* epileptiform seizures
* fever, hyperthermia
* interstitial lung disease

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4
Q

Pathological RBC types

A
  • RETICULOCYTE: appearance; incr prod, chronic Fe def anaemia, haemolysis, acute/chronic blood loss
  • SPHEROCYTE: appearance; sensitive RBC membrane, IHA
  • STOMATOCYTE: appearance; incr RBC prod
  • ACANTOCYTE: (w. spikes) appearance: RBC membr failure – lipid metabolism disorder, hepatopathies
  • SCHYSOCYTE: (RBC fragment) appearance: traumatic or toxic damage
  • ANULOCYTE: appearance: iron def anaemia
  • CODOCYTE: (Target cell) appearance: regenerative process
  • ECHYNOCYTE: (Burr cell, spikes) appearance: lab error
  • SICKLE CELL: appearance: RBC damage, Hb globin chain malformation in humans
  • INCLUSION BODIES in RBCs:
  • HEINZ BODY: (denaturated Hgb) appearance: O2 effect, oxidative damage to RBCs
  • HOWELL-JOLLY BODY : (nuclear membr remnants), appearance: vit.B12 def, incr prod of red cells, splenectomy
  • BASOPHILIC PUNCTUATES: (nuclear remnants) appearance: regenerative process, young RBCs of cat, physio. in Ru, lead poisoning
  • HB INCLUSIONS: appearance: Hb damage, incr RBC prod, regenerative anaemia
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5
Q

Protein determination methods

A
  • Total protein conc in blood (TP)
  • Biuret test (usually photometrically)
  • Ultrasensitive total protein analysis
  • Refractometry
  • Electrophoresis: examines globulins
  • TT - Thrombin time: fibrinogen conc.
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6
Q

Laboratory evaluations for acute stress

A

-Physiological leukocytosis: on the effect of adrenalin, noradrenalin (epinephrine, norepinephrine), neutrophilia and/or lympocytosis, without left shift

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7
Q

Laboratory evaluations for chronic inflammation

A
  • Right shift: many segmented and hypersegmented, old neutrophils are seen in the smear. Incr. WBC count.
  • Haematology of Addison’s disease
  • Pelger-Huet anomaly: Normocytaemia, and left shift
  • Cyclic neutropenia: inhertitable disease of Grey Collies. Due to cyclic BM activity, neutropenia occurs in weekly, monthly intervals.
  • Bone marrow damage: Leukopenia, and neutropenia occurs. Thrombocytopenia and aplastic anemia is often accompanied.
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8
Q

Addison’s disease

A

(hypoadrenocorticism)

  • There is no inhibitory effect of glucocorticoids, as there is hypoplasia or necrosis of adrenal gland.
  • The typical changes are increase in WBC (due to the polyuria caused increased PCV), increase in young neutrophils, left shift (no inhibition of cell proliferation), lymphocytosis and eosinophilia.
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9
Q

Lipid fractions and their transport

A

Lipid fractions : apolipoproteins :

  • triacil-glycerols - VLDL
  • phospholipids - HDL
  • cholesterol - LDL/HDL
  • cholesterol-ester - (HDL)
  • free fatty acid - albumin
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10
Q

Lipid changes during starvation

A

-Decreased lipid content
-Increased FFA content
Total lipid (TL) conc decr because liver can not produce enough apolipoproteins for transporting lipids, however FFA conc is incr, because it is transported by albumin.

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11
Q

What are the methods for clotting time?

A

-Appearance of the first fibrin strand
-CT on watch glass
-CT in plastic syringe
-CT in glass tube
.CT in ACT (activated clotting time) tube

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12
Q

Thrombocytopenia

  • Definition
  • Tests
  • Causes
A
  • Decreased amount of thrombocytes in the blood
  • Test: BT, BMBT
  • Major causes:
    1. decr prod in bone marrow
    2. incr utilisation: DIC
    3. incr destruction: autoimmune thrombocytopenia (AITP)
    4. incr sequestration: in case of (chronic) splenomegaly
    5. incr loss: subacute/chronic bleeding
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13
Q

Gammopathies

  • Defintion
  • Their graf
  • Their causes
A

POLYCLONAL gammopathy: beta and gamma globulins derived from different clones
-Broad-based peak in beta and/or gamma region
-Causes:
*various chronic inflam. dis. (infectious, immune-mediated)
*liver disease
*FIP
*occult heartworm disease
*Ehrlichiosis.
*Beta-gamma bridging occurs in disorders with incr IgA and IgM such as lymphoma, heartworm disease and chronic active hepatitis.
MONOCLONAL gammopathy: one protein fraction derived from one clone
*Sharp spike in beta or gamma region
-Causes:
*during immune mediated or neoplastic conditions
*both neoplastic and non-neoplastic disorders

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14
Q

Ketone bodies

  • Appearance
  • Causes
  • Test
A
  • Appearance is due to energy deficiency in liver cells.
  • Causes:
  • Decr intake of carbohydrates
  • Decr insulin prod. (diabetes ketoacidosis; incr. hepatic prod. of KBs)
  • Ross reaction: estimate conc. of acetone, and acetoacetic acid: colour from white(grey) to purple. The depth of colour depends on ketone conc.
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15
Q

Hyperglycaemia – list the causes

A

(incr glucose conc)
-Transient increase:
o laboratory errors (haemolysis, lipaemia, icterus)
o stress (cats)
o food intake (dogs and humans)
o xylazin effect
o cranial trauma or inflam. (Rabies, Aujeszky disease)
o after/during adm. of glu-containing fluid therapy
-Constant hyperglycaemia:
o diabetes mellitus
o hyperadrenocorticism and glucocorticosteroid therapy
o progesterone effect (iatrogen or endogenous-insulin resistance)
o enterotoxaemia (sheep)

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16
Q

Hypoglycaemia - list the causes

A

(Decreased glucose concentration)

  • lab error (incorrect storage/transport of sample)
  • decr energy status (ketosis of Ru, growing pigs, etc.)
  • insulin overdose
  • insulinoma
  • anabolic steroid effect
  • liver failure, terminal stage
  • acute liver failure
  • hypoadrenocorticism
  • septicaemia
  • hyperthyroidism
  • paraneoplastic syndrome
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17
Q

Reticulocytes

  • Defintion
  • Appearance
  • How to count them
A

-Young, immature RBC w/ø nucleus
-Same functional properties as mature RBCs, so they are able to carry oxygen.
-Appearance: incr. prod. (regenerative anaemia) - chronic Fe def anaemia, haemolysis, acute or chronic blood loss
- No reticulocytes appear in horses and Ru (only in BM, not in the peripheral blood)
-Appearance is a sign of regenerative function of BM
-How to count reticulocytes:
*CRC-Corrected reticulocyte count:
CRC = reticulocyte % x RBC count
normal: <0,06 x 1012/l (w/ø anaemia)
-CRP-Corrected reticulocyte percentage:
CRP = (Htpatient / Htaverage (0,45 dog, 0,37 cat)) x reticulocyte %
normal: <1-2 % (w/ø anaemia)

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18
Q

List reasons for increased PCV

A

• False: long sample storage w. EDTA
• Physiological:
o Congenital
o Age: new borne animals
o Phys. long-term hypoxia: living in high altitude, regular intensive long training/work…
• Relative polycytaemia: decr plasma volume, e.g. lack of drinking water, vomiting, diarrhoea
• Absolute polycythaemia (normovolaemic): incr RBC prod
o Primary: without incr EPO
o Secondary: incr EPO
a) true: caused by long term hypoxia, due to chronic resp./circ. disorders
b) not true: without hypoxia: autonomous incr of EPO
• Complex problem: hypervolaemic polycythaemia – life threatening acute stress or extreme physical exercise

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19
Q

List reasons for decreased PCV

A

• False: microcytosis, inappropriate sample homogenization etc.
• Physiological: incr. plasma volume in the 3rd trimester of pregnancy
• Relative: pathological incr in plasma volume i.e. overdose of fluid therapy, terminal phase of chronic kidney insufficiency
• Absolute: normovolaemic oligocythaemias
o several hours after acute bleeding
o decr life-span in circulation e.g. IHA, ectoparasitosis
o sequestration of RBCs in spleen due to hypersplenismus
o decr RBC prod:
a) suppression of BM e.g. heavy metal poisoning, mycotoxins, drug side effect, viral infections
b) lack of nutrients e.g. iron, copper, B6, B12 vit, folic acid
• Complex problem: the abs. oligocyt. listed above frequently cause refusal of water, vomiting or diarrhoea leading to hypovolaemic oligocythaemia

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20
Q

Acid base evaluation

A
  • Routine test in emergency patients.
  • Gives info about acid-base status, and function of vital buffer systems.
  • Acid-base analyzers are complex devices; measure also blood-gas parameters, electrolytes and eventually Hgb, Ht, lactate, glucose etc.
  • Ionselective electrodes (ISE): measure pH and CO2
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21
Q

List methods for primary haemostasis tests

A
  • Tests performed by side of the animals:
  • Signs of incr bleeding tendency
  • Capillary resistance (humans)
  • Bleeding time BT, buccal mucosal bleeding time test, BMBT
  • Appearance of the first fibrin strand (clotting time)
  • Appearance of the clot
  • Clot retraction time
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22
Q 
Erythrocyte sedimentation rate (ESR)
-Theory
-Causes of increase
-Samples
-Phys.ESR value
-
A
  • Theory: there is incr sedimentation of RBCs due to inflam processes, as the APPs and other globulins tend to attach onto the surface of RBCs.
  • Cause of incr. ESR:
  • Incr globulin conc, due to inflam or neoplastic processes.
  • Decr albumin conc and as a consequence relatively incr globulin conc causes incr ESR, too.
  • Samples: Westergreen tubes (glass) - contains Na-citrate, and there is mm scale on it, and holes on the bottom and top
  • Sedimentation rate of RBCs should be checked after 1h, horses every 20m (very fast in horses)
  • Physiologically ESR: 0,5-3 cm/hour
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23
Q

pH of rumen

A
  • Normal pH: bw 6.3–7 (slightly acidic)
  • cows fed grain can have slightly lower, those fed hay or green slightly higher pH
  • Abnormal pH:
  • Elevated pH (Rumen alkalosis): Simple indigestion or reduced feed intake for greater than 2 days, urea indigestion, putrefaction of ruminal content from prolonged rumen stasis, saliva contamination
  • Lowered pH 5.5.-6 (Rumen acidosis): Grain overfeeding, chronic ruminal acidosis
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24
Q

Left shift

A
  • More young WBCs appaear in the circulating blood.
  • Young metamyelocytes and band forms are visible in greater proportion and abs. nu. in blood smear.
  • Two different types of left shift:
    1. Regenerative left shift: Incr WBC count, neutrophilia, and left shift (younger neutrophils). Mature neutrophils outnumber the immature neutrophils. Sign of favourable prognosis, because BM have time to respond to the inflam. stimulus.
    2. Degenerative left shift: Low, or normal WBC, neutrophil count and left shift (younger forms). Abs. nu. of band- or immature neutrophils are greater than the abs. nu. of mature/segmented neutrophils. Sign of poor prognosis; the disease is very serious and needs immediate treatment.
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25
Q

Thrombocytopathies

  • Definition
  • Causes
A

-Decreased ability of platelets to aggregate and adhere to the site of injury, and formation of the primary thrombocyte-thrombus, the second step of haemostasis
Major causes:
-improper development of platelets, for example because of hereditary glucoprotein deficiencies, etc.
-von Willebrand’s disease
-uraemia
-liver failure
-myelo-, and/or lymphoproliferative diseases
-NSAIDs
-etc.

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26
Q

Types of anaemia

A

=Oligocythaemia (decr RBCs or heamoglobin)

  1. REGENERATIVE a.: Incr. reticulocytes, macrocytic, hypohromic: MCV incr, MCHC decr, appearance of young RBCs, stomatocytes and Hb inclusions
    - Hemorrhage, hemolysis
    - Usually diseases with favourable prognosis, because enough new RBCs are prod in the BM to regenerate the anaemia and to reach normal RBC count quickly.
  2. NON REGENERATIVE a.: normocytic, normochromic; MCV same , MCHC same, normal or decreased MCH
    - Chronic anaemia diseases, chronic kidney dis., primary BM dis.
  3. IRON DEF. a.: high TIBC, decr MCHC, appearance of anulocytes,
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27
Q

Normal range of electrocytes

A
  • Sodium (Na+): 140-150(-160) mmol/l
  • Potassium (K+): 3.5-5.5 mmol/l
  • Chloride (Cl-): 100-125 mmol/l
  • Calcium: 2.1- 3.0 mmol/l (Ca2+ is 45-50% of this), in poultry laying eggs tCa may be even double (~5.8 mmol/l)
  • Magnesium: 0.8-1.5 mmol/l
  • Inorganic phosphate (Pi): dog, horse: 0,8-1,8 mmol/l, cat, cattle, sheep: 1-2,4 mmol/l, swine, goat: 1-3 mmol/l.
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28
Q

Routinely used acid-base parameters

A

-pH: Actual pH of the blood: 7.35-7.45
-pCO2 - partial CO2 pressure (mmHg, kPa)
*respiratory parameter
* 40 mmHg
-HCO3 - standard bicarbonate (HCO3-) conc (mmol/l)
*In plasma, if the blood is equilibrated to 40 mmHg pCO2 on 37 °C - it`s value depends on pCO2
*metabolic parameter
* 21-24 mmol/l
-ABE - actual base excess/demand/residue (mmol/l)
*Titratable acidity or basicity; the amount of acid or base
needed to equilibrate blood to pH: 7.4
*metabolic parameter
* ±3.5 mmol/l
-TCO2 - total CO2 conc in plasma (mmol/l)
*i.e. CO2 content of blood liberated by strong acid.
*TCO2 is 5% higher than plasma HCO3-.
*gives no direct info about resp function.
*may be ignored, when HCO3- result is presented
* 23-30 mmol/l
-SBE standard or in vivo base excess/demand, residue in
the whole extracellular space
*metabolic parameter
* ±3 mmol/l

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29
Q

Hypokalaemia: causes and effects

A

Causes:
-decreased intake (anorexia)
-long term polyuria (e.g. chronic kidney insufficiency)
-adm of loop-diuretic drugs (e.g. furosemide)
-enteral potassium loss (e.g. diarrhoea, enteral bleeding)
-primary or secondary hyperaldosteronism, alkalosis and insulin
Effects:
-decreased neuromuscular irritability
-muscular weakness
-paresis
-glucose intolerance
-decreased insulin secretion
-decreased conductance of electrical stimuli in heart (bradycardia, arrhythmia)
-polyuria
-polydypsia
-Na+-retention
-alkalosis

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30
Q

Spectrophotometric Method (Drabkin-method)

  1. Usage
  2. Sample
  3. Reagent and it´s method
  4. Colour
  5. Wave length
  6. Calculation
  7. Normal value
A
  1. Haemoglobin (Hgb) Measurement
  2. Whole blood sample
  3. Reagent: K3Fe(SCN)6: hemolyses RBCs and forms
    Fe3+, from Fe2+ in the haemoglobin molecule
  4. Orange coloured end product
  5. 540 nm wave length.
  6. (Esample/Estandard) x standard conc = result (E=extinction)
  7. Normal: 18-20 mmol/l or 12-18 g/dl (g%)
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31
Q

Red Blood Cell Count methods + normal range

A
  • Bürker-chamber method
  • Estimated RBC-count
  • RBC count measured by automatic cell counter
  • Normal range: 4.5-8 x 1012/lT/l
32
Q

How to determine BT, BMBT, what causes prolongation of bleeding time?

A
  • Use a sharp, sterile blade and make an 0,1-0,2 mm deep, 0,5 cm long incision on the skin on inner part of external ear or on buccal mucosal surface. Vipe the blood drop flowing under the wound with a cotton wool tissue in 20-30 sec intervals. (avoid touching the wound itself). Measure the time from appearance of first blood drop till the ceasing of bleeding. Normal BMBT : 3-5 min.
  • Prolongation of bleeding time is caused by thrombocytopenias, thrombocytopathies and vasopathies. So dependent on thrombocytic function, platelet count and capillary function.
33
Q

Lab signs of DIC

A

Disseminated Intravascular Coagulopathy

  • Common acute disorder, requires accurate, quick lab. d.
  • Usually a secondary problem, caused by primary diseases eg: septicaemia, pancreatitis, widespread burn injuries, or necrosis of big tumors, shock, polytraumatisation, etc.
  • Microthrombus formation and fibrinolysis are present at many different places in the body simultaneously, because of severe tissue damage or necrosis and blood vessel injury, so coagulation factors and platelets are consumpted very quickly during this process.
  • Can be a life threatening complication of the aforementioned diseases. Early diagnosis is very important in management of this condition.
  • Incr. utilization of thrombocytes
  • First lab. sign can be a pos. FDP or D-dimer test.
  • Incr: CT, BT, PT, APTT, TT, FDP and D-dimer
  • Decr: platelet count
  • Appearance of schysocytes and/or burr cells in blood smear
34
Q

Glutaric aldehyde test

A

-Examines incr. of fibrinogen and globulin conc in plasma.
-As fibrinogen is an APP, it can show a marked increase during acute inflam. processes.
-Used in clinical practice to indicate inflam. proc. in adult cattle (more than one year old).
-The solution causes a rapid coagulation of fibrinogen and labile globulins, so blood mixed with this solution can show coagulation within seconds in case of acute
inflam proc (high fibrinogen and globulin level in the blood), even if the blood sample contains heparin or EDTA.
-Generally use heparinised blood
-Tubes should be checked for coagulation every 30s by turning them upside down.

35
Q

Causes of hyperlipidaemia & decreased lipid content

A
  • Hyperlipidaemia
    1. Increased fat content in diet
    2. Diabetes mellitus
    3. Hypothyroidism
    4. Hyperadrenocorticism
    5. Nephrotic syndrome
    6. Septicaemia
    7. Pancreatitis
  • Decreased lipid content
    1. Starvation
    2. Chronic liver failure
36
Q

Causes of metabolic and respiratory acidosis

A

METABOLIC acidosis causes:
- incr acid intake: i.e. fruits, too acidic silage…
- incr acid prod e.g. incr lactic acid prod
- in cattle: grain overdose
- incr. ketogenesis, leading to ketosis
- decr acid excretion: renal failure
- ion exchange: hyperkalaemia
- some xenobiotic: ethylene-glycol toxicosis
RESPIRATORY acidosis causes:
-Upper airway obstruction
-Pleural cavity disease: pleural effusion, pneumothorax
-Pulmonary disease
-Depression of central control of respiration: drugs, toxins, brainstem disease
-Neuromuscular depression of resp.mm.
-Muscle weakness e.g. in hypokalaemia
-Cardiopulmonary arrest

37
Q

Causes of hyper/hypo – cholesterolaemia

A
  • Hypercholesterolaemia
    1. Increased dietary fat content
    2. Hypothyroidism
    3. Hyperadrenocorticism
    4. Nephrotic syndrome
    5. Diabetes mellitus
    6. Cholestatic diseases
    7. Primary dyslipidosis
  • Hypocholesterolaemia
    1. Protein loosing enetropathy
    2. Liver failure
    3. Malnutrition
    4. Neoplastic disease
    5. Decreased apolipoprotein synthesis
38
Q

Causes of increased/decreased Hgb

A
  • Increased Hgb: Usually associated with different types of relative (dehydration) or absolute polycytaemia.
  • Decreased Hgb: usually associated with relative (hyperhydration) or absolute (anaemia) oligocytaemia
39
Q

Regenerative anaemia, RBC parameter affected

A

Diseases with favourable prognosis, because enough new RBC’s are produced in the bone marrow to regenerate the anaemia, to replace the RBC loss and to reach normal RBC count quick.
→ Corrected reticulocyte count, CRC = reticulocyte % x RBC count
→ Corrected reticulocyte percentage, CRP = Ht(patient)/Ht(average) x reticulocyte %

40
Q

Non-regenerative anaemia, RBC parameter affected

A

Bone marrow is not producing new RBC. Not able to regenerate the anaemia.
→ MCV: indicates the average size of RBC’s
MCV(fl) = (PCV/RBC count) x 1000

41
Q

MCV

  1. Definition
  2. Calculation
  3. Normal value
  4. Causes of increased/decreased MCV
A
  1. Mean Corpuscular Volume: indicates the avg size of RBC’s (macro-, normo- or microcytic)
  2. PCV/RBC count x 1000 = MCV (fl)
  3. Normal: 60 – 70fl
  4. Caues of INCREASED (macrocytic):
    * regenerative anaemias
    * FeLV infection
    * vit. B12, Co or folic acid deficiency
    * erythroleukamia
    * In poodles
    - Causes of DECREASED (microcytic):
    * chronic blood loss
    * iron, copper, pyridoxine (vitamine B6) deficieny
    * portosystemic shunt
42
Q

MCHC

  1. Definition
  2. Calculation
  3. Normal value
  4. Causes of increased/decreased MCHC
A
  1. Mean Corpuscular Haemoglobin Concentration: indicates the avg conc. of Hgb in erythrocytes (normo-, hypo- or hyperchromasia)
  2. Hgb (g/l) / PCV = MCH (pg) / (MCV (fl) x 1000) = MCHC (g/l)
  3. Normochrom: 300-350 g/l (30-35%)
  4. Causes of INCREASED (hyperchromasia):
    *erythroleukemia (polycythaemia absoluta vera)
    *Vit B12, folic acid, cobalt deficiency
    *immunhemolytic anaemia (spherocytosis)
    *lead poisoning
    *splenectomy
    Causes of DECREASED (hypochromasia):
    *newborns
    *regenerative anaemia
    *iron deficiency anaemia.
43
Q

MCH

  1. Definition
  2. Calculation
  3. Normal value
  4. Causes of increased/decreased MCH
A
  1. Mean Corpuscular Haemoglobin: indicates average Hb content of RBCs.
  2. MCH (pg) = (Hgb(g/l)/RBC count) x 10^12/l
  3. Normal: 12-30 pg. In young animals it (and MCV) can be incr, to 28-32 pg
  4. (same as MCHC)
    Causes of INCREASED (hyperchromasia):
    *erythroleukaemia
    *vitamin B12, folic acid, cobalt deficiency
    *immunohemolytic anaemia
    *lead poisoning
    Causes of DECREASED (hypochromasia):
    *newborn animals
    *regenerative anaemias
    *iron deficiency
44
Q

Causes of hypo-/hyper -chloraemia

Why is Cl-, and HCO3- important

A

-Decreased Cl- causes:
*abomasal displacement
*vomiting, diarrhea
*sweating (horses)
*other proc. w. hyponatraemia
-Increase Cl- causes:
*Excessive intake - “salt poisoning”
*Decr. excretion - Conn`s disease
*infusion overdose
other proc. w. hypernatraemia
-Cl-, and HCO3- = most important anion of plasma (buffer)

45
Q

Hypoproteinemia causes

A
  • Decr. intake, decr. absorption (maldigestion, malabsorption)
  • Decr synthesis - liver failure, acute inflam.
  • Incr utilisation – physiologic conditions, chronic dis´s
  • Increased loss;
  • PLN-Protein loosing nephropathy (via kidneys)
  • PLE-Protein loosing enteropathy (via GI-tract)
  • Skin (burns, inflam.)
  • Whole blood loss (bleeding)
  • Sequestration after bleeding into body cavity
  • Other: Hyperhydration
  • Fibrinogen: liver function impairment, advanced protein def., DIC, inherited afibrionogenaemia (St. Bernard)
46
Q

Hyperproteinemia causes

A
  • Dehydration

- Fibrinogen: acute inflam (especially ruminants),

47
Q

Method: PCV or Ht

  • Def.
  • Indication
  • Sample
  • Method(s)
  • Interpretation
A

Packed cell colume / Hematocrit
-Indication: evaluated routinely; fluid volume changes and quantitative changes of RBCs (e.g. anaemia) can be detected.
-Sample: anticoag. blood (mostly EDTA, or heparin)
-Method:
1. Mikrohematokrit or microcapillary method
2. Establishing PCV using automated cell counter: measures the MCV and nu. of RBCs -> calculation for PCV
PCV = (MCV (fl) x RBC (10-12/l)) / 1000
3. Handheld HCT Meter: measures Ht and total Hgb in whole blood, in %.
-Interpretation:
*decr. PCV=oligocythaemia/anaemia
*incr. PCV=polycythaemia

48
Q

Method: serum osmolality

  • Indication
  • Sample
  • Method(s)
  • Interpretation
A

-Indications/goals: The ion changes of the body are reflected by the serum (plasma) osmolality. This is dependent on the conc. of osmotically active substances: the main electrolytes (Na+, K+, Cl-) and some small molecular weight molecules (urea, glucose, keton bodies).
-Sample: plasma (heparinised), serum.
-Method: calculated mathematically or measured.
1. Mathematical method:
Osmolality (mOsm/kg) = 2 (Na+ + K+) + urea + glucose
(the parameters used are in mmol/l)
2. Measurement of osmolality: using osmometer, which measures the freezing point of the sample compared to the freezing point of water.
-Interpretation: Dec/incr in especially Na+ cc. causes decr/incr in osmolality. This causes swelling/shrinking of cells.
-Hyperosmolality (>310 mOsm/kg) shows that the fluids of the EC space became more conc., hypoosmolality (<270 mOsm/kg) the EC space is more diluted.
-Incr of osmolar gap can be caused by ethanol, ethylene-glycol, methyl-alcohol or isopropyl-alcohol in the blood.

49
Q

Method: Concentration of electrolytes

  • Indication
  • Sample
  • Method(s)
  • Interpretation
A
  • Indication/goal: conc of electrolytes-“ionogram” is measured in variable conditions, because the basic life-processes can occur only in the appropriate osmotic
    environment. In bad/critical general condition the ionogram evaluation is most important, for choosing appropriate fluid therapy.
  • Sample: heparinised full blood; acid-base/blood gas analyzer. Serum of heparinised plasma; biochemistry blood analyzers. Specific anticoagulants for each electrolyte.
  • 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.
  • Interpretation: depending on each electrolyte
50
Q

Causes of hyper-/hyponatraemia

A

HYPERnatraemia (↑ Na)
• Incr water loss or decr water intake (dehydration, eg. polyuria, vomiting or acute diarrhoea, hyperthermia)
• Incr Na+ retention in the kidneys (prim (Conn’s syndrome) or secondary hyperaldosteronism)
• Other: overdose of hypertonic salt solution, incr intake of salt
HYPOnatraemia (↓ Na)
• Excessive fluid intake - “water poisoning”
• Retenstion of water: cardiac, renal or hepatic insuffic.
• Enhanced Na+ loss: GI; diarrhoea, renal loss (hypoadrenocorticism), sweating (horses), sequestration in body cavities
• Water outflux from IC to the EC space: hyperosmolality

51
Q

Hyperkalaemia causes

A
  • Incr. per os intake
  • Overdose of K+-containing fluids
  • Acute kidney failure
  • Rupture of urinary bladder
  • Hypoaldosteronism
  • Acidosis
  • (pesudohyperkalaemia)
52
Q

Method: calcium

  • Indication
  • Sample
  • Method(s)
  • Interpretation
A

-Indications: lethargy, weakness, vomiting, constipation, PU/PD; restlessness, muscle tremor, seizures; pathologic fractures of bones
-Sample: TCa; serum or heparinised plasma. Ionized calcium; mostly heparinised plasma
-Method: ionized calcium; mostly ion-selective electrodes, TCa; spectrophotometry; calcium in higher pH can form violet purple complex with ortocresolphtalein, at 570 nm.
-Interpretation:
HYPOcalcaemia;
*insufficient intake or absorption
*hypofunction of parathyroid gland
*in cats after surgical thyroidectomy
*in lactating animals due to incr loss of Ca w. milk *toxicosis due to the above mentioned Ca binding substances
*mild hypocalcaemia can be caused by alkalosis.
HYPERcalcaemia;
*excessive Ca or vit.D intake
*hyper A vitaminosis in cats
*hyperfunction of parathormone
*some inflammatory or neoplastic diseases

53
Q

Method: Magnesium

  • Indication
  • Sample
  • Method(s)
  • Interpretation
A

(tMg, Mg2+)
-Indications: hypocalcaemia of unknown origin, hypokalaemia, DKA, muscle weakness of unknown origin, tremor, seizure, dysphagia, dyspnea and arrhythmia.
-Sample: tMg; serum or heparinised plasma, ionised; heparinised plasma
-Method: Mg2+; ionselective electrodes, tMg; spectrophotometry: xylidineblue reagent w. Mg forms purple complex
-Interpretation:
HYPOmagnesaemia:
*decr intake e.g. grass tetany in cattle and sheep
*precipitating factor to transport tetany
*absorption disturbance e.g. in lymphangiectasia
*incr excretion (renal, enteral) e.g. chronic diarrhoea or hyperthyroidism
HYPERmagnesaemia
*incr intake: iatrogenic e.g. increased absorption
after laxative agents or overdose of Mg containing infusion.
*decr excretion, eg chronic insufficiency, milk fever, hypothyreosis or Addison’s disease
*dehydration

54
Q

Method: inorganic phosphate

  • Indication
  • Sample
  • Method(s)
  • Interpretation
A

-Indications/goals: as calcium measurement, additionally haemolysis of unknown origin, anorexia, weakness, ataxia, seizures and to check kidney glomerular
function.
-Sample and method: spectrophotometry from serum or heparinised plasma. In acidic environment P reacts w. ammonium-molybdate and forms a yellow phosphate-molybdic acid complex.
-Interpretation: Rate of abs. is important – incr. under vit.D effect and decr. in EPI, intestinal inflam and vit.D def.
-Increased plasma Pi level - causes:
* Incr. intake of meat or grains
* Metabolic utilisation (in quick growth of young animals, high pregnancy and egg prod in poultry)
* Decr. kidney function (decr. excretion)
* Hyperthyroidism (decr. PTH excretion->decr. Pi excr.)
* Incr. P mobilized from bones, e.g. in bone tumours extensive osteolysis occurs
-Decreased plasma Pi level - causes:
* Liver dysfunction
* Primary and secondary hyperparathyroidism

55
Q

Lab diagnosis of von Willebrand disease

A
  • Found in humans, Dobermans and pinchers
  • Often accompanied with hypothyroidsm
  • Incr. BT, BMBT
  • Decr. clot retraction ability
  • Sometimes coagulation disorders
56
Q

Increased/decreaed oxigen binding capacity of Hgb

A 
INCREASED BY:
-decreased ↓ 2,3 DPG level in RBCs,
-decreased ↓ pCO2 level in the blood
-increased ↑ pH of the blood
-decreased ↓ temperature of blood
DECREASED BY:
-increased ↑ 2,3 DPG level in RBCs,
-increased ↑ pCO2 level in the blood
-decreased ↓ pH of the blood
-increased ↑ temperature of blood
57
Q

Normal values:

  1. Normal RBC count
  2. MCV
  3. MCH
  4. MCHC
  5. CRC
  6. CRP
  7. BMBT
A
  1. Normal RBC count: 4.5-8 x 10^12/lT/l
  2. MCV: 60-70 fl
  3. MCH: 12-30 pg. (young animals; 28-32 pg)
  4. MCHC-Normochrom: 300-350 g/l (30-35%)
  5. CRC: <0,06 x 1012/l (w/ø anaemia)
  6. CRP: <1-2 % (w/ø anaemia)
  7. Normal BMBT : 3-5 min
58
Q

Species with abnormal values of…

1. MCV

A
  1. MCV: 1. Cats, horses, adult animals and Japanese Aktia have smaller RBCs. New borns and poodles have bigger (Young RBCs are bigger).
59
Q

SeFe

  1. Interpretation
  2. Normal value
  3. Sample
  4. Method
  5. Causes of increased/decreased SeFe
A

Serum Iron
1. If we suspect iron deficiency, especially due to chronic blood loss.
2. 18-20 mmol/l
3. Serum samples, because fibrinogen content of the plasma may disturb the measurement.
4. Fe3+ is reduced to Fe2+ by ascorbic acid. Fe2+ reacts with ferrosin and forms a red coloured chelate which can be measured photometrically (560nm).
(should always be measured together w. TIBC)
5. INCREASED SeFe: iron toxicosis (overload)
DECREASED SeFe:
* chronic blood loss
* decreased intake (piglets, calves)
* impaired gastric, duodenal, jejunal function (reduction, transport, absorption)

60
Q

TIBC

  1. Interpretation
  2. Normal value
  3. Determination
  4. Causes of increased/decreased TIBC
A

Total iron binding capacity
1. Gives info about the transferrin content.
TIBC=serum iron level (saturated transferrin) + free transferrin (not saturated)
2. 50-68 mmol/l
3. Determination: measure seFe then, add Fe-solution to plasma, put absorbent to solution, and centrifuge the absorbent. Use the upper layer and check seFe again.
4. INCREASED TIBC: iron def. anaemia (not severe: normal iron level+high TIBC, severe: low iron level+high TIBC)
DECREASED TIBC:
* chronic inflammation (negative APP)
* chronic liver failure (decr transferring synt. in liver)
* neoplastic disease

61
Q

Iron Saturation:

  1. Calculation
  2. Normal values
A
  1. (SeFe / TIBC) x 100 = Iron saturation

2. normal: 20-55% (30%)

62
Q

Ways to count WBC´s

A
  • WBC counting by using Bürker-chamber
  • WBC counting by hematology analyser
  • Automatic cell counters can count WBC
  • Laser cell counters
63
Q

Causes and effects of neutropenia

A

Causes:
-During the first period of the inflam. process, or widespread severe inflammation.
-By the migrating factors (i.e. leukotriens, interleukins etc.) prod. by tissue cells, macrophages.
Effects: Neutrophils are migrating out of the blood vessels to the site of inflammation, and this can lead to a transient decrease in total WBC count.

64
Q

Causes and effects of neutrophilia

A

Causes:
-During later phases of inflammation
-Due to the granulocyte colony stimulating factor (G-CSF), or granulocyte macrophage colony stimulating factors GM-CSF prod. by the macrophages.
Effects: These factors stimulate WBC prod. in BM, which leads to increased total WBC count.

65
Q

Leukemoid reaction

  1. Occurance?
  2. Causes?
A
  1. When there is a great stimulus for prod. neutrophil granulocytes an enormous number of neutrophils can be present in the peripheral blood due to incr. effects of G-CSF, GM-CSF.
  2. Causes:
    * Big abscesses
    * Endometritis (pyometra)
    * Some neoplastic (but not leukaemia) diseases.
66
Q

CRP

  1. Interpretation
  2. Sample
  3. Method(s)
  4. General physiological value of CRP
A
  1. Interpretation: In the beginning of acute inflammatory process CRP values are incr, before the appearance of the clinical signs. Therefore it is a very useful diagnostic tool for the early detection of inflam. processes.
  2. Sample: Serum
  3. Immunological (ELISA or immunturbidimetric) method.
  4. 8 mg/l
67
Q

What is ruminal fluid properties influenced by?

A
  • The composition of the diet
  • The circumstances of the feeding and sampling
  • The time interval from feeding or drinking
68
Q

Nitrite reduction test

  1. Solution used?
  2. Interpretation?
A
  1. Potassium nitrate (KNO2) and Griess-Ilosvay reagent
  2. Interpretation: In the presence of nitrite the color will be pink. In a healthy ruminal fluid after 10 minutes normally there is no nitrite.
69
Q

Rumen fluid ammonia

  1. Normal level
  2. Cause of increased ammonia
A
  1. Normal level in rumen is low (6-20 mmol/l).
  2. Incr. ammonia:
    - High dietary protein intake
    - In energy deficiency
    - Liver disorders. After calving the liver function is reduced because of energy deficiency and fatty infiltration.
70
Q

Cause of increased rumen fluid chloride

A

INCREASED:

  • Gastric torsion or pylorus obstruction (hydrogen chloride will pass into rumen and can incr. Cl)
  • High salt intake
  • Abomasal displacement
  • Obstruction of intestinal flow (ileus), pyloric stenosis,
  • Abomasal disorders (inflam, ulcer, hyperacidity)
71
Q

Normal and abnormal odor, colour and consistency of rumen fluid

A

-Odor: Aromatic
Abnormal:
 Ammonia smell (urea poisoning)
 Moldy rotting (protein putrefaction)
 Acidic/sour odor (excess lactic acid/grain overfeeding)
-Color: Olive-brownish green (hay ration), deeper green (green ration), yellowish brown (grain or silage ration)
Abnormal:
 Milky grey (grain overfeeding, lactic acidosis)
 Darker greenish or brownish (ruminal stasis)
 Grey with clots of milk (calves with abomasal reflux)
Consistency: Slightly viscous
Abnormal:
 Increased viscosity (saliva contamination)
 Decreased viscosity, watery with few feed particles (inactive bacteria or protozoa)
 Excess frothy, stable bubbles (frothy bloat/ vagus indigestion)

72
Q

Causes of WBC increase

A
  • Acute stress
  • Acute inflammation - later phase
  • Chronic inflammation
  • Regenerative left shift
  • Leukemoid reaction
  • Stress leukogram (chronic stress)
  • Hypoadrenocorticism
  • Myeloid leukemia
  • Lympocytic leukemia
  • Cushings disease
73
Q

How can you obtain ruminal fluid?

A
  • By orogastric tube: down oesophagus (Placement of tube in rumen confirmed by auscultation of abdomen as air is simultaneously blown into the tube. ), w. stirrup pump
  • By ruminal puncture: on L side, by inserting needle into ventral rumen and aspirating a sample of rumen fluid.
74
Q

Cause of decreased WBC

A
  • Acute inflammation - first phase
  • Degenerative left shift
  • Cyclic neutropenia
  • Bone marrow damage
  • Immune deficiency disease
  • Incr. tissue damage
  • Atypical leukemia
75
Q

Characteristics of right shift

A
  • Appaearance of many segmented and hypersegmented, old neutrophils - seen in the blood smear.
  • Appearance of this and incr. WBC count is typical for chronic inflammatory process, and for the effects of glucocorticoid treatment.
  • Glucocorticoids inhibit cellular proliferation (disappearance of young cells), and have membrane stabilizing effect.
  • Common finding in case of macrocytosis in poodles.

Lab D (18 decks)

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