Clinical Biochemistry Flashcards
1
Q
Why are diagnostic tests perfromed?
A
- Investigate the disease processes underlying clinical signs
- To investigate the risk of disease/presence of positive traits in healthy animals.
- To minimise the risk of adverse events during/following treatment or diagnostic procedure.
- To provide baseline parameters for future monitoring.
2
Q
How can samples be processed?
A
- Machine vs manual
- As submitted vs concentrated/enriched
- With/without processing, additives, fixatives, stains
3
Q
What information can laboratory tests give us?
A
- Organ/tissue damage – often chemical that are released due to damage or stress, but do not always relate to function.
- Organ function
- Susceptibility to disease – such as genetic tests
- Cell pathology – metabolic derangements, inflammation, neoplasia
- Presence or historic evidence of infectious agents
- Host response to disease
4
Q
How must a sample be submitted?
A
- Appropriate sample collection
- Correct tube
- Accurately filled
- Well mixed
- Stores/transported correctly
5
Q
Why should a sample not be shaken or put near a window?
A
Releases haemoglobin, these are a bright colour and interferes with results
6
Q
What are the uses and colours of different sample tube?
A
EDTA - haematology (cytology) = pink
Serum - biochemistry = red/orange
Heparin - rapid biochemistry = orange
Oxalate fluoride - glucose = yellow
Citrate - clotting function = green/white
7
Q
Compare protein in plasma and serum.
A
Plasma proteins greater in plasma than serum, due to loss in clot
8
Q
Compare potassium in plasma and serum.
A
Potassium is greater in serum than plasma, released from platelets during clot formation
9
Q
What tests is serum used for?
A
Bile acids and haptoglobin concentration measurement and serum protein electrophoresis.
10
Q
What tests is plasma used for?
A
Plasma better in emergency setting by rapid processing, serum takes 30 mins to clot and be spun down. Required for some parameters such as PTH and ammonia.
11
Q
How does PCV have result variation?
A
Puppies and kittens expected to be low. Cats have a quarter and 50%, dogs are a third to 2 thirds. Greyhounds will have 2 thirds. There may be breed variations and machine may only give normal values.
12
Q
How does cell morphology have result variability?
A
Mammalian vs camelids vs birds vs reptiles. Camelids have oval shaped cells without nuclei, so will not fit through haematology machines so must be done manually. Some reptiles have green plasma and they have a lot of haem.
13
Q
How does age cause result variability?
A
PCV, indicators of bone growth (ALP, calcium), starts to become normal at around 6 months
14
Q
What is biological result variation?
A
Intra-individual variation: diet, reproductive status, drugs/therapy, stress/excitement/fear
15
Q
What is the impact of stressful sampling on white blood cells?
A
Neutrophilia and/or lymphotcytosis: marginating becomes circulating due to adrenaline and cortisol
16
Q
What is the impact of stressful sampling on red blood cells?
A
Increased red cell mass and increases reticulocytes due to splenic contraction. Decreased red cell mass if haemolysis
17
Q
What is the effect of stressful sampling on glucose?
A
Increases glucose > increases cortisol > insulin resistance – cats more susceptible
18
Q
What is the effect of stressful sampling on creatine kinase activity?
A
Increased creatine kinase activity – stressful/repeated restraint
19
Q
What is the impact of stressful sampling on clotting?
A
Activation of clotting cascade – can speed up the rate of clotting of the sample
20
Q
What are the pre-analytical errors that cause analytic variability?
A
- Incorrect blood tube
- Contamination (EDTA > increased K+ and decreased Ca2+)
- Incorrectly filled tube
- Incorrect storage
- Haemolysis, lipaemia (decrease serum per ml of blood sample, so have them fasted), icterus will all alter testing parameters
21
Q
How does haemolysis interfere with spectrometric assays?
A
Pink/red, due to lysed red blood cells. False increase in RBC constituents. In vivo, sampling, post-sampling. Mimicked by synthetic oxygen carrying solutions.
22
Q
How does lipaemia interfere with spectrometric assays?
A
Visible turbidity. Physiological vs. pathological. False decrease in other substances in serum. May want to cool sample and then spin it so as to separate out fat.
23
Q
How does icterus interfere with spectrometric assays?
A
Plant eating herbivores have carotene-rich plasma = slight yellow discolouration (this is not jaundice). Herbivore species with high carotene may appear yellow, fat can be quite yellow and is not jaundice but is anoterh colour that can impact testing.
24
Q
How can analytical error occur during analysis?
A
- Laboratory environment – temperature/humidity outside range, affecting enzyme activity of stored reagents
- Incorrect use of machine/inaccurate pipetting
- Equipment – lack of appropriate maintenance, expired reagents, lack of calibration
- Analytical procedure – technique not validated for species/sample used, working in plasma doesn’t mean it will work in serum, vice versa
25
What do enzymatic assays include?
Include liver (ALT, ALP) and muscle (CK) enzymes
26
What are the disadvantages of pattern recognition?
The normal reference range is devised from 95% of the target population: 5% of ‘normal’ animals will fall outside the reference range.
Individuals have their own ‘normal’. The target population for the assay, may not match the patient population
27
What does haematology assess?
RBC, WBC, platelets
28
What does serum biochemistry assess?
Proteins, kidney parameters (urea, creatinine, phosphate, calcium), glucose, sodium, potassium, chloride, calcium, liver parameters, enzyme s(ALT, ALP, GGT, GLDH), bilirubin, bile acids, albumin, cholesterol, triglycerides
29
What are the markers of systemic inflammation that can be assessed?
APP, CRP, alpha1-AGP
30
What are the hormones we can assess?
T4, TSH, cortisol, insulin
31
What 2 types of protein are tested for?
Total protein comprises albumin and globulin fractions, the ratio of which can narrow the differential list.
Specific proteins, such as those that increase/decrease in inflammation and clotting factors
32
Define negative acute phase protein.
Produced at maximum rate by the liver in normal conditions, so only time we have increased albumin is if we have increased liver mass or reduced water in the blood.
33
What is serum albumin primarily responsible for?
Maintaining colloids oncotic pressure
34
What are some examples of analytes that are albumin bound?
- Calcium – changes in albumin affect total calcium readings, directly proportional
- Thyroid hormones
- Steroids and fatty acids
35
What are the 2 types of hyperalbuminaemia?
Absolute hyperalbuminaemia is uncommon, relative hyperalbuminaemia occurs due to haemoconcentration (also increased TP).
36
What are the 3 mechanisms of hypoalbuminaemia?
- Reduced absorption – malnutrition, GI disease
- Reduced production – hepatic dysfunction, mild APP response
- Increased loss
37
How can hypoalbuminaemia be caused by increased loss?
- Protein losing enteropathy (globulins and albumins)
- Protein losing neuropathy (just albumin as barrier of charge being lost to prevent loss)
- Haemorrhage
- Severe exudative disease
- 3rd spacing (fluid developing in body cavities) with/without losses via drainage
38
What is the effect of hypoalbuminaemia on the body?
Decreased oncotic pressure > effusions/oedema
39
What does hypoglobulinaemia cause?
- Immunological incompetencies, such as failure to passive transfer
- Protein loss, with concurrent hypoalbuminaemia
- Haemorrhage, exudative disease and PLE
40
What is the more common mild-moderate form of hyperglobulinaemia?
Accompanies inflammatory/infectious diseases – APP response, polyclonal gammopathy/diverse antigen stimulation (producing too many antibodies and blood becomes sludgy)
41
What is the less common form of hyperglobulinaemia?
Marked - secondary to B cell neoplasia
42
How can you differentiate the 2 forms of hyperglobulinaemia?
Use serum protein electrophoresis to differentiate
43
What are negative acute phase proteins?
With decreased inflammation – albumin and transferrin (iron sequestered > inhibits RBC production)
44
What are positive acute proteins?
With increased inflammation – C-reactive protein in dogs, serum amyloid A in horses, alpha1-acid glycoprotein in cats, haptoglobin in ruminants.
45
How is mild post prandial hyperglycaemia measured in cats and dogs?
Fasted samples in cats and dogs. Due to stress, cats will have high glucose in the blood so sent home for urine sample after a few days.
46
How is mild post prandial hyperglycaemia measured in equine and ruminants?
Avoid fasting in equine
Fasted samples not possible in ruminants – in lactating cows, mammary vein glucose is less than jugular vein glucose
47
What are the ways that inadequate synthesis causes hypoglycaemia?
- Hepatic dysfunction/portosystemic shunting
- Toy dog hypoglycaemia, inadequate glycogen stores
- Hypoadrenocorticism
48
How can excessive consumption cause hypoglycaemia?
Sepsis, indicated by brick red mmbs. Can have very low glucose levels as both body and bacteria are consuming glucose
49
How can paraneoplasia cause hypoglycaemia?
Insulinoma, hepatomas, IGF-2 producing tumours
50
How should you investigate hypoglycaemia?
- Consider age and signalment
- Liver dysfunction/portvascular anomaly - blood analysis, NH3 and bile acid stimulation tests
- Hyperadrenocorticism - SCTH stimulation test
- Sepsis - T-FAST, A-FAST tests
- Neoplasia - imaging
51
What is transient hyperglycaemia?
Stress-associated hyperglycaemia common in cats, post-prandial in monogastrics
52
What is persistent hyperglycaemia?
Diabetes mellitus = insulin insufficiency. Glucosuria with/without ketonaemia/ketonuria, usually increased serum fructosamine
53
What causes production of ketones?
Negative energy balance due to inadequate carbohydrate provision leading to lipolysis and ketone bodies
54
What are some examples of when ketones can be produced?
- Starvation/prolonged anorexia
- DM – glucose provision but cannot use in absence of insulin
- Ruminant ketosis in cattle
- Pregnancy toxaemia in sheep
55
Which ketone is not measured on urine dipsticks?
Beta-hydroxybutyric acid
Most common ketone body in cats, dogs cattle, sheep. Acetone and acetoacetate produced in lower concentrations and can be measured with dipsticks.
56
What is a marker of lipolysis?
Non-esterified fatty acids. Mostly used in assessment of energy balance in ruminants
57
When are non-esterified fatty acids increased?
Pre-prandial sample
Stress
Delayed sample analysis
Negative energy balance from food deprivation
Excess demands
Hepatic lipidosis
58
What is cholesterol used for in the body?
- Cell membrane formation
- Steroid/sex hormone pathways
- Vitamin D metabolism
- Bile acid metabolism
59
What is the serum level of cholesterol dependent on?
- Dietary uptake
- Hepatic synthesis
- Excretion in bile
60
What are the main sites of triglycerides in the body?
Enterocytes - from diet
Adipocytes - from fat
Hepatocytes
61
What alters the level of triglycerides in the blood?
Decreased by lipoprotein lipase
Increased by hormone sensitive lipase
62
When can altered metabolism cause hyperlipidaemia?
Increased cholesterol by exogenous steroids, endocrinopathy and nephrotic syndrome
Increased triglycerides by negative energy balance (especially horses and camelids) and hepatic lipidosis
63
How does hypocholesterolaemia develop?
- Artefact - severe icterus
- Decreased supply - fat restricted diet, malabsorption
- Reduced production - liver dysfunction
- Increased losses - blood loss, cancer
- Hypoadrenocorticism
64
What are the clinical signs of liver disease?
Inappetence, lethargy
Vomiting, diarrhoea
Weight loss
Polyuria, polydipsia
Icterus
Coagulopathy
Ascites
Hepatic encephalopathy
65
What are the markers of liver damage/stress?
Hepatocellular enzymes - ALT, AST
Cholestatic enzymes - ALP, GGT
66
What are the markers of reduced liver function?
Hepatic synthetic products reduced production - urea, albumin, cholesterol, clotting factors
Hepatic detoxification products - bilirubin, bile acids, ammonia
67
What marker is increased in cats and dogs with hepatocellular damage?
Increased hepatocellular enzymes - AST, ALT
68
Explain how alanine aminotransferase/ALT is a marker of liver damage.
Cytoplasmic enzyme in liver cells so released if these cells are damaged. Also released during hepatocellular repair, dog, cat, rabbit, not useful in horses, ruminants and pigs.
69
Explain how aspartate aminotransferase/AST is a marker for liver damage.
Mitochondrial so released in more severe hepatic cell damage, also significant muscle presence
70
Is ALT or AST a better marker of liver damage?
ALT is a more specific and sensitive marker of liver damage in dogs and cats than AST, as ALT is not always liver related
71
What is sorbitol dehydrogenase/SDH?
Enzyme of choice for measurement of hepatocellular damage in horses and cattle, assay not readily available. More stable so can be used for exotics too.
72
What is glutamate dehydrogenase/GLDH?
Found in tissues, primarily hepatocellular mitochondrial origin. More useful marker in large animals and exotics. Is more stable than SDH.
73
How does primary liver disease cause hepatocellular damage?
Hepatic inflammation, infections, trauma, neoplasia, vacuolar hepatopathy, toxins and some drugs
74
How does secondary/reactive liver disease cause hepatocellular damage?
Inflammatory/metabolic process elsewhere in the body. Commonly seen with dental disease, GI disease and endocrinopathies. Often mild unless concurrent vacuolar hepatopathy.
75
Define cholestasis.
Impaired bile flow.
76
What is alkaline phosphatase/ALP?
Cholestatic isoenzyme, steroid isoenzyme (dogs), bone isoenzyme
77
What is gamma glutamyl transferase/γGT?
Steroid isoenzyme (dogs). Cattle, sheep, dogs have high GGT levels in colostrum
78
What is GGT a marker of?
- Valuable marker of colostrum ingestion in calves
- More sensitive marker of cholestasis in equines/cattle than ALP
79
What causes cholestatic enzyme activity to increase?
- Cholestatic disease - primary biliary tree disease, diseased causing compressive lesions of the biliary tree
- Endocrinopathies or metabolic > vacuolar hepatopathy
- Steroid induced in dogs
- Bone induced (ALP)
80
Define cholestasis.
When mild, evidence of cholestatic enzyme activity increases. As it progresses, serum accumulation of other substances typically excreted in the bile: cholesterol, bile acids, bilirubin.
81
How does the half lives of hepatic enzymes influence significance?
SDH short (12-24 hours) in horses. All short (6 hours) in cats, dogs is nearer 3 days. Cats should bever have increase in liver enzyme activity due to half-life.
82
List the non-specific markers of liver dysfunction.
Decreased albumin, urea, cholesterol, glucose
83
List the specific markers of liver dysfunction.
Increased bilirubin, bile acids and ammonia (failure of detoxification)
84
What are the 3 stages of bilirubin metabolism?
1. Synthesis from haemoproteins
2. Breakdown for excretion – conjugation in the liver
3. Excretion – biliary export
85
Briefly give the process of bilirubin metabolism.
1. Haemoglobin
2. Reticuloendothelial cell
3. Bilirubin-albumin
4. Hepatocyte
5. Conjugated bilirubin
6. Biliary system
7. Intestine
8. Urobilinogen – can end up in urine, not normally seen incats
9. Stercobilin
86
What are the 3 causes of hyperbilirubinaemia?
Pre-hepatic – haemolysis
Hepatic – swelling or significant loss of liver function
Post-hepatic – obstruction
87
How are jaundice and liver dysfunction related?
There can be jaundice without primary liver dysfunction.
There can be severe liver dysfunction without jaundice.
88
What can cause hyperbilirubinaemia when PCV is low?
Regenerative (pre-hepatic) and non-regenerative anaemia
89
What can cause hyperbilirubinaemia when PCV is normal?
Hepatic: increased hepatocellular enzymes, decreased albumin/cholesterol/glucose, increased ammonia.
Post hepatic: increased cholestatic enzymes, cholestasis
Anorexia horses and cattle, feline infectious peritonitis, toxoplasmosis
90
What is the bile acid tolerance test?
Evaluates hepatic clearance of enterohepatically recycled bile acids. Overnight (>12 hour) fast > serum sample. Feed (> gall bladder contracts). 2 hours post-prandial > serum sample
91
What does increased serum bile acids cause?
- Cholestasis – exclude based on biochemistry, enzyme increases and/or
- Liver dysfunction and/or
- Portosystemic shunts – differentiate with imaging
92
What can hyperammonaemia be caused by?
Liver dysfunction vs portosystemic shunts. Ruminants have urea toxicosis from contaminated feed, horses from strenuous exercise
93
When is creatine kinase released?
Released from muscle cells into blood during muscle damage
94
What causes creatine kinase to be released?
- Muscle trauma – overly form handling, intramuscular injections, traumatic accidents
- Muscle belly hypoxia
- Myopathies – inflammatory/infectious, degenerative/hereditary, toxic, recumbency in large animals, equine rhabdomyolysis
95
Which pancreatic diseases affect endocrine function?
- Diabetes mellitus – hyperglycaemia, with glucosuria, fructosamine
- Insulinoma
96
Which pancreatic disease affect exocrine function?
Exocrine pancreatic insufficiency – cTLI/fTLI (trypsin-like immunoreactivity) – sensitive/specific measure of functional pancreatic mass
Pancreatitis – routine biochemistry, non-specific lipase/amylase assays are inadequate and no longer used, cPLI/fPLI or DGGR lipase
97
Where are vitamin B9 and B12 absorbed?
Folate/vitamin B9 absorbed in proximal small intestine (jejunum)
Cobalamin/vitamin B12 absorbed in distal small intestine (ileum)
98
What are the clinical signs of hypocobalaminaemia/low B12?
- Chronic diarrhoea
- Weight loss and failure to thrive
- Hyperammonaemia > encephalopathy
- Blood cell changes – neutropenia, increased MCV, hypersegmented neutrophils
99
What are the possible differentials for hypocobalaminaemia?
- EPI – exclude with TLI
- Ileal malabsorption – gastrointestinal ultrasound, biopsy
- Dysbiosis
100
When is hypofolataemia seen?
Often seen alongside hypocobalaminaemia, limited clinical significance, easy to supplement, jejunal malabsorption
100
What is hypercobalaminaemia caused by?
Limited clinical significance, seen with supplementation, hepatopathy, neoplasia, others
100
What is hyperfolataemia caused by?
Dysbiosis, especially following antimicrobials, no clinical significance.
101
Name 3 indicators of kidney injury.
Nephron loss
Glomerular disease - proteinuria
tubular disease - glucosuria, proteinuria
102
What can be caused as a result of nephron loss?
- Loss of electrolyte/water regulation > polyuria/polydipsia and electrolyte derangements
- Loss of acid-base regulation > metabolic acidosis > lethargy, inappetence and nausea
- Accumulation of organic solutes > uraemia > lethargy, inappetence, vomiting/diarrhoea
- Hyperphosphataemia/renal secondary hyperparathyroidism
- Impaired hormone synthesis > decreased calcitriol, decreased erythropoietin > anaemia
- Hypertension
103
What is azotaemia indicated by?
Increased urea and/or creatinine
104
What is the clinical syndrome arising from azotaemia and how?
Uraemia
Inadequate excretory, regulatory and endocrine function. .
105
What are the clinical signs of uraemia?
Lethargy, inappetence, nausea and vomiting causing stomatitis, encephalopathy and bone pain
106
How does pre-renal azotaemia arise?
Decreased blood flow to kidneys or increased protein catabolism or GI haemorrhage
107
What is the body's response to pre-renal azotaemia?
Kidneys do everything possible to conserve water. Azotaemia with concentrated urine (not all cases if electrolyte disturbances).
108
What is renal azotaemia?
Fewer functional nephrons, at 67-75% loss of nephrons
109
What is the body's response to renal azotaemia?
The kidneys are unable to conserve water in the face of reduced blood flow so has dilute urine.
110
What is post-renal azotaemia caused by?
- Urinary tract obstruction causes back pressure
- Urinary tract rupture > urine leakage > reabsorption of waste products.
111
In the event of urinary tract rupture, where can urine leak?
Typically uroabdomen, creatine concentration will be higher in fluid than in serum. Less commonly leakage into retroperitoneal space or pelvic/hindlimb tissues. Usually traumatic or iatrogenic.
112
How is increased urea a surrogate marker for GFR?
- Breakdown of ammonia from the GIT in the urea cycle.
- Production and excretion are not constant. So try to make constant by fasting.
113
How is increased creatinine a surrogate marker for GFR?
Breakdown product of muscles (physiologically increased in foals)
114
How is increased SDMA a surrogate marker fr GFR?
Independent on muscle mass
115
What are some important consideration of GFR of ruminants and equids?
- Urea may be normal in severe kidney disease, as most urea is excreted via the gut.
- Urea also influenced by diet – grass fed will be lower than pellet diet
- Creatinine much more reliable marker
116
How is phosphate changed with reduced GFR?
Hyperphosphataemia – as phosphate primarily renally excreted
117
How is calcium changed with reduced GFR?
Variable – typically, normal to hypercalcaemia in chronic kidney disease. Typically normal to low in acute kidney injury
118
How is potassium affected by GFR?
Dependent on GFR and urine output.
119
What at the kidney can cause hyperkalaemia?
- Anuria or oliguria, indicative of acute kidney injury or end stage chronic kidney disease.
- Aldosterone deficiency/hypoadrenocorticism/Adison’s disease
120
What at the kidney can cause hypokalaemia?
Polyuria
121
What does sodium levels reflect?
Volume status – hypernatraemia with dehydration and hyponatraemia with overhydration
Aldosterone deficiency/hypoadrenocorticism/Adison’s disease causing hyponatraemia
122
When and what is glycosuria from urinalysis indicative of?
With hyperglycaemia = diabetes mellitus or stress response
With euglycaemia = tubulopathy. Fanconi syndrome, leptospirosis, toxicity
123
When is bilirubin from urinalysis normal and abnormal?
Can be normal in dogs
Abnormal in other species and reflects hyperbilirubinaemia
124
When is ketonuria from urinalysis observed?
Diabetes mellitus – diabetic ketosis or ketoacidosis
(Rarely starvation)
125
List the causes of decreased urine concentration.
Hypercalcaemia
Hypokalaemia
Hyponatraemia
Hyperadrenocorticism
Hypoadrenocorticism
Hyperthyroidism
Liver disease (low urea)
Glucosuria – diabetes mellitus, Fanconi
Endotoxins – pyometra
Drugs – mannitol, phenobarbital, prednisolone
Kidney disease
Young age (short loop of Henle)
High salt diet
Intravenous fluid therapy
Oral fluid intake > requirements
126
What are the possible mechanisms of decreased urine concentration?
Central diabetes insipidus
Nephrogenic DI
Osmotic diuresis
Medullary washout - chronic water excess
Excess water intake - not always pathological
127
What is blood in urinalysis indicative of?
Haematuria – primary urinary tract disease, coagulopathy
Haemoglobinuria or myoglobinuria – haemolysis, severe myopathy, aged sample with haematuria
128
What is the usefulness of pH from urinalysis?
Not very accurate but useful when evaluating crystalluria.
129
What is the usefulness of protein on urinalysis?
inaccurate as it does not take into account how concentrated urine is.
Assess for post-renal causes then measure UPC/urine protein : creatinine ratio
130
What is pre-renal proteinuria indicative of?
Increased blood proteins – hyperglobulinaemia, haemoglobinuria/myoglobinuria
Functional – pyrexia, post-exercise, seizure
131
What is renal proteinuria indicative of?
Intrinsic kidney disease - glomerular or tubular
132
What is post-renal proteinuria indicative of?
Urinary tract – inflammatory, neoplastic disease, haemorrhage into urinary tract
Reproductive tract
133
What is the role of sodium in the body?
Responsible for preservation of electroneutrality. Primarily responsible for water retention and loss via the kidneys. For maintenance for osmolarity
134
How is sodium gained?
Reduced renal perfusion
Hypovolaemia
Increased osmolarity
135
How is sodium lost?
Increased blood volume
136
What are the clinical signs of hyponatraemia dependent on?
Typically localised to central nervous system, primarily forebrain. Depends on whether acute or chronic
137
How does loss of sodium lead to hyponatraemia?
V/D, renal disease, Addison's, 3rd spacing, osmotic diuresis, diuretics, sweating
138
How does gain of free water cause hyponatraemia?
Drinking water
IVFT
Congestive heart failure, liver failure, nephrotic syndrome
ADH secretion
139
How do endogenous shifts caused hyponatraemia?
Diabetes mellitus
Acute muscle damage
140
What are the clinical signs of hypernatraemia?
Typically CNS, depending on whether acute or chronic: anorexia, lethargy, vomiting, diarrhoea as non-specific signs
141
How can sodium be gained to cause hypernatraemia?
Sodium containing fluids
Salt poisoning
Hyperaldosteronism
142
How can water be lost to cause hypernatraemia?
Impaired intake
GI losses
Urinary losses
Diabetes mellitus
Diuretics
Evaporation
Burns
143
What is a risk of correction of sodium disturbance?
Brain shrinking and swelling causes myelinosis
144
What is the role of chloride in the body?
Mainly follows sodium to preserve electroneutrality, except in hypercholaraemic metabolic acidosis
145
When is chloride artefactually increased?
Lipaemia, hyperbilirubinaemia, haemoglobinemia, bromide inadvertently measured as chloride
146
What is caused when hyperchloraemia is present with hypernatraemia?
Troubleshoots the hypernatraemia
147
What is caused when hyperchloraemia is present without hypernatraemia?
Interference from bromide or true due to compensatory
Loss of the ions causes retention of chloride to compensate for electroneutrality, causing hyperchloraemic metabolic acidosis
148
What is caused when hypochloraemia is present with hyponatraemia?
Troubleshoots the hyponatraemia
149
What is caused when hypochloraemia is present without hyponatraemia?
Gain of other anions causes loss of chloride and HCO3- to compensate = high anion gap metabolic acidosis. Lactic acidosis, ketosis, azotaemia, ethylene glycol toxicity, diuretics
150
How does derangement regulation of potassium have profound cardiac implications?
Hyperkalaemia > bradycardia > ultimately arrest
Hypokalaemia > tachydysrhythmias
151
How can hyperkalaemia be caused by iatrogenic or lab error?
Potassium adminstration
Potassium sparing drugs
Thrombocytosis/post-clot
EDTA contamination
Failure to separate serum in horses and ruminants
152
How is hyperkalaemia caused by failed excretion?
Hypoaldosteronism
Acute kidney injury
Chronic kidney disease
Post-renal disease
153
How is hyperkalaemia caused by shifts from ICF to ECT?
Cell lysis - tumour, reperfusion injury, marked haemolysis
154
What is the reference interval for sodium potassium ratio?
27-40
Below 20 is highly suspicious of hypoadrenocorticism
155
What are the clinical signs of hypokalaemia?
Tachydysrhythmias
Muscular and generalised weakness, lethargy and inappetence
156
How is hyokalaemia caused by inadequate intake?
Nutritional or iatrogenic
157
How can hypokalaemia be caused by excessive losses?
Urinary - kidney disease, diuresis, hyperaldosteronism, diuretics
V/D
Diabetic ketoacidosis
158
How do endogenous shifts cause hyperkalaemia?
Alkalaemia
Insulin therapy
Glucose infusion
159
What is the role of calcium in the body?
Muscle contraction and nerve conduction
160
What are the 3 fractions of calcium within plasma?
Ionised = 50% – biologically active, measure anaerobically/refrigerated
Protein bound = 40% complexed to albumin (so hypoalbuminaemia can decrease calcium)
Complexed = 10%
161
Why are calcium and phosphate physiologically linked?
Hormonal regulation
162
What is the effect of hhypercalcaemia on calcitonin?
Increased calcitonin > storage and renal excretion of calcium > decreased calcium
163
What causes parathyroid hormone to decrease and increase?
Hypercalcaemia decreases PTH release
Hypocalcaemia and hyperphosphataemia increase PTH release
164
What is the effect of PTH?
Calcium and phosphate mobilisation from bone > increase calcium
Renal calcium reabsorption and phosphate excretion > increased calcium
Activation of Vitamin D > renal and GU calcium and phosphate reabsorption and mobilisation > increased calcium
165
What is the net effect of PTHrp?
increased calcium and decreased phosphate
166
What is the net effect of vitamin D?
Increased calcium and increased phosphate
167
What are the clinical signs of hypercalcaemia?
Inappetence
Lethargy
Vomiting
Diarrhoea
Related to primary disease process
168
Which ketones are not measured by urine test strips?
Acetone and beta-hydroxybutyric acid (aceto-acetic acid is measured on dipsticks)
169
What are the species differences in the main hepatocellular enzymes?
Cats and dog = ALT, AST
Horses = GLDH, SDH
170
What are the main cholestatic enzymes in cats, dogs and horses?
ALP and GGT
171
What is a defining feature of cholestatic horses?
Hyperbilirubinaemic
172
What are the possible causes of ALP increase?
Cholestasis
Steroids
Barbituates
173
What are the main diseases causing post-hepatic jaundice?
Primary biliary disease
Hepatocyte swelling causing intrahepatic disease
Pancreatic disease
174
What parameters indicate liver disease?
Albumin, cholesterol and urea
