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BIOCHEMISTRY 3 + 4 + 5

Alice Butterworth Vet Med 2 English 116 cards

Struvite crystals Magnesium ammonium phosphate

Cards in this deck (116)

  1. 1What are the major sources of glucose ?dDietary absorption
    Liver production :
    Glycogenolysis
    Gluconeogenesis
  2. 2What promotes glycogenolysis?Catecholamines
    Glucagon
  3. 3What promotes gluconeogenesis?Corticosteroids
    Glucagon
    Growth hormone
  4. 4What should blood be collected in if the sample can't be analysed in clinic?Fluoride oxalate
  5. 5What is the normal reference interval in monogastric animals?4-6mmol/L
  6. 6What may cause transient hyperglycaemia ?Adrenalin release due to fear/excitment?
  7. 7What may hypoglycaemia be caused by?Excessive use
    Reduced hepatic storage
    Insufficient dietro intake
    Excessive insulin or analogues
    Lack of corticosteroids
  8. 8What may cause excessive use of glucose?Sepsis
    Neoplasia
    Excessive physical exertion
  9. 9What may cause reduced hepatic storage of glucose?Advanced liver disease
    Sepsis
  10. 10When might animals have an insufficient dietary intake of glucose?Neonates and small dogs
    Starvation
    Malabsorption and malnutrition
  11. 11What may cause excessive insulin/ analogues?Insulinoma
    Iatrogenic insulin overdose
    Paraneoplastic
  12. 12What may cause a lack of corticosteroids ?Hypoadrenocorticism
  13. 13What may cause hyperglycaemia?After a meal (transient)
    Catehecholamines (usually transient)
    Iatrogenic (exogenous glucose administration )
    Insulin antagonism
    Diabetes mellitus
    Stress
  14. 14What may cause insulin antagonism ?Endogenous /exogenous steroids
  15. 15What serum glucose concentrations can cause glucosuria?10mmol/l -Digs
    16.6mmol/L cats
  16. 16Why might we want to test persistence of glucose alterations ?To confirm persistanent hyperglycaemia and diabetes mellitus
    To monitor response to treatment and tailor insulin
  17. 17What tests can we do to test persistence of glucose alterations?Glucose curve
    Glycated proteins
  18. 18What creates glaciated proteins?Glucose reacts non-enzymicatically and irreversibly with amino groups on all proteins in a slow process to give glaciated proteins
  19. 19What is fructosamine?Irreversibly glycated albumin
    It is high when glucose concentration is high and has been for the previous 1-3wks
  20. 20What affects fructosamine ? What causes altered turnover of fructosamine ?Affected by albumin / protein concentration
    Hyper/Hypothyroidism cause altered rate of protein turnover
  21. 21What controls sodium concentration?Thirst
    RAAS
    ADH release
  22. 22What alters sodium concentrationLoss of water
    Loss of sodium and water (volume depletion)
  23. 23What may cause hyponatraemia?Loss of Na
    Water retention or fluid overload
  24. 24How may Na be lost ?GI- vomiting, diarrhoea
    Kidneys - reduced tubular function, lack of aldosterone, increased diuresis
    Skin - burns, sweat
    3rd space
  25. 25What may cause water retention or fluid overload?Oedematous disorders
    Innapropriate ADH secretion
  26. 26What may cause hypernatraemia ?Water loss in excess of sodium
    -Free water loss
    -Hypotonic fluid loss
  27. 27How may free water loss occur?Inadequate water intake
    Lack of ADH
    Fever, panting
  28. 28How may Hypotonic fluid loss occur?GI
    Kidney - osmotic diuresis
  29. 29How does Na concentration affect Cl concentration?Na and Cl concentrations tend to follow each other i.e. if Na is high Cl is also high
    If this is not the case something is very wrong!
  30. 30When is hypochloridaemia seen without hyponatraemia?Vomiting of pure stomach contents
  31. 31What causes hyperkalaemia?Increased intake
    Reduced renal excretion
    Movement out of cells
  32. 32What causes hypokalaemia ?Reduced intake
    Renal losses
    GI losses
    Movement into cells
  33. 33What regulates calcium and phosphorous levels?Parathyroid hormone (PTH)
    Calcitonin
    Vitamin D3 (calictriol)
  34. 34How does PTH affect Ca and Phosphate?Increased PTH causes Hypercalcaemia and Hypophosphataemia
  35. 35How does vitamin D affect Ca and P?Hypevraminosis D causes hypecalcaemia and hyperphosphateaemia
  36. 36Is all calcium affected by PTH?No
    Only the free Ca
  37. 37What affects total calcium?Albumin
  38. 38What do we use urea and creatinine levels to asses?Renal function
  39. 39What is azotemia ?Raised levels of creatinine and urea
  40. 40Are urea and creatine sensitive markers of renal function?No, they are insensitive markers
    Azotemia only becomes apparent when >75% of functional nephrons are lost
  41. 41What may cause and increase in urea ?Decreased GFR due to any cause (pre renal, renal, post renal)
    GI haemorrhage
    High protein diet (mild)
    Recent meal (mild)
    Catabolism - fever
  42. 42What may cause a decrease in Urea?Reduced production by the liver
    Low protein diet
    Aggressive fluid therapy
    Deficiency of enzymes of the urea cycle
  43. 43What may cause an increase of creatinine ?Decreased GFR due to any cause
    High muscle mass (breed)
  44. 44What may cause a decrease in creatinine ?Reduced muscle mass
    Usually not clinically significance
  45. 45Types of azotaemia Pre renalCaused by: Dehydration or decreased CO
    Increased production
    Detection: V concentrated urine
    Other clinical evidence
    Should respond to fluid therapy
  46. 46Types of azotaemia RenalCaused by: Decreased functional nephrons
    Detection: Inadequately concentrated urine
    Doesn't resolve with fluid therapy
  47. 47Types of azotaemia Post renalCaused by: Urine leakage (+reabsorption)
    Blockage resulting in decreased excretion
    Detection: Clinical evidence
    Often hyperkalaemia
  48. 48What else do we use to asses kidney function?USG
  49. 49What extra renal things may affect kidney function?ADH action and release- decreased sensitivity to ADH in hypercalcaemia + hypokalaemia, endotoxemia
    Medullary concentration gradient
    Osmotic forces (gucosuria)
    Therapies
    Behavioural or metabolic (PD)
  50. 50What does can urinalysis tell us?UTI
    Neoplasia
    UTD
    Hyperglycaemia - DM
    Hypoproteinema - PLN
  51. 51What tests do we need to do in urinalysis?Sample collection
    Gross examination
    USG
    Dipstick (biochemistry)
    Sediment examination
  52. 52Voided/free catch sampling Where in the urine stream should you sample? When is it useful?Should be midstream
    Useful if pigmenturia
  53. 53Cather sampling When do we use Cather samplingUse as a therapeutic procedure
    When you suspect bladder/urethral cancer to increase the chance of collecting cells to analyse at microscopy
  54. 54Cystocentesis sampling BenefitsMinimises risk of contamination
    Preferred method for urine culture
  55. 55Why do we need to analyse urine rapidly ?Cells disntegrate
    CO2 evaporates which raises pH
    Crystals form
    Bilirubin, urobilinogen and casts break down
    Bacteria grow or die
  56. 56What can colour of urine tell us?Pale yellow to amber = normal
    Red to red brown = haematuria, haemoglobinuria, myoglobinuria
    Dark yellow/brown/green = bilirubinuria
  57. 57How can we differentiate haematuria from pigmenturia?Haematuria (RBCs):
    Red, cloudy urine
    Clears on centrifugation
    Erythrocytes in sediment
    Pigmenturia (Hgb/Mgb):
    Red to brown urine
    Doesn't clear on centrifugation of urine
    No erythrocytes in sediment
  58. 58What is myoglobin?Haemeprotein which transports and stores oxygen within muscles
    Released from muscle when theres membrane damage
    Readily passes into urine
  59. 59How does the dipstick distinguish between myoglobin, free haemoglobin and RBCRBC?It can't!
  60. 60Myoglobinuria v Hemoglobinuria MyoglobinuriaUrine red-brown
    After centrifugation ->clear plasma
    Doesn't stay in circulation
    Urine red but plasma clear
    Elevated CK and/or AST
  61. 61Myoglobinuria v Hemoglobinuria HaemoglobinuriaUrine red-brown
    After centrifugation ->pink/red plasma
    Stays in circulation
    Urine red and plasma red
    Decreased PCV/HCT
  62. 62What could cloudiness of urine suggest?Increased cellular elements
    Crystalluria
    Bacteria
    Lipids
    Mucus
    Casts
    Sperm
    Precipitation of salts
  63. 63What may cause an overestimation in USG?USG?Marked glycosuria and marked proteinuria
  64. 64What does USG tell us ?Concentrating ability
  65. 65What is more sensitive in measuring concentrating ability of the bladder, USG or azotaemia?USG (only slightly)
  66. 66Appropriate USGConcentrated
    >1.030 (dogs)
    >1.035 (cats)
    Some concentrating ability
    1.015-1.030 (dogs)
    1.015-1.035 (cats)
  67. 67What is isothenuria ?Urine has the same osmolarity as plasma
    1.008-1.012
  68. 68What is Hyposthenuira?Very low USG, suggests active effort by the kidney
    <1.008
  69. 69What do we need to disregard for dipstick analysis?Leucocytes
    Nitrite
    USG
  70. 70What may acidic urine suggest ?Meat diet
    Protein catabolic state
    Acidifying agents
    Metabolic / respiratory acidosis
    Bacterial contamination
  71. 71What is normal pH for dogs and cats?5-7.5
  72. 72Alkaline urineCereal diet
    UTI w urease +ve organisms
    Old samples /exposed to air
    Metabolic or respiratory alkalosis
    Post-prandial alkaline tide
  73. 73How much protein is normal in the urine?Small amounts of urine (up to 1+)
    However must be interpreted light of USG
  74. 74When might you get a false positive with protein dipstick?With alkaline urine
  75. 75When is protein increased in the urine?Inflammation or haemorrhage of LUT
    If there is significant haematuria
    Protein loss from kidney
  76. 76When is glucose found in the urine?When serum glucose is above 10mmol/l (dogs) and 16.6 (cats)
    Fanconi's syndrome (when serum glucose is normal- failure of resorption by tubules)
  77. 77Are ketones normally found in the urine ?Nope
  78. 78When are ketones found in the urine?Result of exaggerated, incomplete oxidation of fatty acids
    Diabetes mellitus
    Negative energy balance
  79. 79How good are dipsticks at detecting blood in urine?Very sensitive but don't differentiate well
    Erythrocytes (Spotting)
    Haemoglobin (Diffuse colour change)
    Myoglobin
  80. 80How is bilirubin conjugated in urine?Only conjugated bilirubin in urine
  81. 81What are the causes of bilirubinurea ?Haemolysis
    Liver disease
    Biliary obstruction
  82. 82What is a normal amount of bilirubin in the urine ?Up to +2 may be normal in a dog (male esp) in concentrated urine
  83. 83Describe how you would perform a sediment analysisCentrifuge 1ml of urine (1000-1500 rpm for 3 mins)
    Decant and re-suspend pellet
    Place a drop on top of a glass slide and coverslip
  84. 84Is RBC normal in urine sediment analysis?Occasional RBC normal - depends on method of selection
    <5 per hpf
  85. 85Is WBC normal in urine sediment analysis ?Occasional WBC normal
    <5 per hpf
    Increased WBC indicate inflammation in the urinary tract
  86. 86Are epithelial cells normal in urine sediment analysis?Small numbers of squamous and transitional epithelial cells are normal
    Increased in UTI, Irritation, Neoplasia
  87. 87What are casts ? Are they a normal finding?Cyndrical moulds of tubules composed of mucoproteins +/- cells
    Occasional hyaline and granular casts may be normal
    Granular, cellular and waxy indicate tubular damage
  88. 88Are crystals a normal finding in urine?Crystals detected in fresh urine likely formed in vitro
    Crystals can precipitate in stored urine after collection
    Crystalluria should be interpreted w USG
  89. 89—Struvite crystals
    Magnesium ammonium phosphate
    Struvite crystals Magnesium ammonium phosphate
  90. 90Significance of struvite crystals ??UTI
    Urolithiasis
    Could be normal
  91. 91—Amorphous
    Urate - acidic pH
    Phosphate - alkaline pH
    No clin significance
    Amorphous Urate - acidic pH Phosphate - alkaline pH No clin significance
  92. 92—Calcium oxalate dihydrate
    Can be normal
    Calcium oxalate dihydrate Can be normal
  93. 93—Calcium oxalate monohydrateCalcium oxalate monohydrate
  94. 94Clinical significance of calcium oxalate monohydrateHyperoxaluric disorders or Hypercalciuria due to ethylene glycol toxicoxis
    Ingestion of oxalate rich foods
  95. 95—Ammonium birurate / uric acidAmmonium birurate / uric acid
  96. 96Ammonium birurate / uric acid significancePortosystemic shunts
    Liver disease
  97. 97—CystineCystine
  98. 98Cystine clinical significanceAssociated w metabolic defect in tubular reabsorption of cystine
  99. 99—CholesterolCholesterol
  100. 100—BilirubinBilirubin
  101. 101—Drug metabolitesDrug metabolites
  102. 102Significance of increased activity of enzymesCell damage
    Impairment of enzyme clearance
    Physiological
    Induction
    Artefactual
  103. 103What do we measure when assessing enzymes ?Enzyme activity
  104. 104Properties of diagnostically useful enzymesHigh sensitivity
    Specific for one tissue
    Be readily assayed in the lab and stable in the sample
    Be cleared from plasma at a rate appropriate to the diagnostic test
    Show clear separation between normal and pathological values
  105. 105What enzymes suggest muscle damageCK - Creatine Kinase
    AST - Asparate aminotransferase
    LDH - Lactate dehydrogenase
    Leak from muscles cells due to : degeneration, necrosis, inflammation
  106. 106What is CK?Makes ATP available for muscle contraction
    Catalyses the production of high energy ATP via transfer of a phosphate bond from creatine phosphate to ADP
  107. 107What is creatinine?A waste product made from spontaneous breakdown of creatine at a constant rate at a constant rate and eliminated via the kidneys
  108. 108When is creatinine increased after awn injury ? When does it return to normalIncreases rapidly post injury (6-12h)
    Returns to normal (1-2d with single injury)
    NB if there it is increased persistently there is ongoing damage
  109. 109What can increased CK suggest ?Muscle injury :
    Degenerative
    Metabolic
    Neoplasia that damages the membrane
    Nutritional
    Inflammatory / infectious -Myostisis
    Toxic
    Trauma
  110. 110Degeneratice muscle injuryHypoxia:
    Seizure
    Saddle thrombus
    Exertional rhabdomyolysis
    Prolonged recumbancy
  111. 111Metabolic muscle injuryHypothyroidism
  112. 112Nutritional muscle injuryAnorexia
    Decrease in vit E/selenium
  113. 113Toxic muscle injuryMonensin
    Castor bean
  114. 114Traumatic muscle injurySeizures
    Exertion
    IM injections
    Restraint
    Post surgery
  115. 115What may cause a false increased CK?Haemolysis
    Hyperbilirubinaemia
    Lipemia
  116. 116—

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Vet Med 2 Flashcards on BIOCHEMISTRY 3 + 4 + 5, created by Alice Butterworth on 20/05/2019.
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