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Small animal (fourth year) > Clinical pathology > Flashcards

Clinical pathology Flashcards

1
Q

what are the four things that can be tested in regards to the liver?

A

hepatocellular injury
cholestasis
hepatocellular function
hepatic portal circulation

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2
Q

what is used to test for hepatocellular injury?

A

enzyme leakage

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3
Q

what can be used to test for cholestasis?

A

enzyme release due to retained bile

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4
Q

how do the tests for liver enzymes work?

A

testing the activity of the enzyme in question rather than the direct amount

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5
Q

what are the enzymes associated with liver damage?

A

ALT, AST, LDH, SDH, GLDH

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6
Q

what enzyme is specific to the liver in small animals?

A

ALT

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7
Q

where is AST and LDH found?

A

both liver and muscle (not liver specific)

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8
Q

what is the most common enzyme used to determine liver damage?

A

AST (aspirate aminotransferase)

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9
Q

what does the magnitude of AST increase correlate to?

A

the degree of liver damage (not the reversibility, prognosis or function)

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10
Q

what is a possible artifactual reason that ALT can be increased?

A

haemolysis (not liver disease)

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11
Q

what are the enzymes used to measure for cholestasis?

A

ALP and GGT

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12
Q

is the sensitivity of testing for ALP better for dogs or cats?

A

better sensitivity for dogs

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13
Q

what components of bile can be tested for?

A

bilirubin, bile acids, cholesterol

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14
Q

where is ALP found normally?

A

on the membrane of cells (when pressed on due to cholestasis they fall off)

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15
Q

other than cholestasis what can cause increase in ALP?

A

drugs - corticosteroids and phenobarbital (also diseases that increase corticosteroids)

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16
Q

what bile components may increase in cholestasis cases?

A

bilirubin, bile acids, cholesterol

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17
Q

what are the two isoenzymes of ALP?

A

intestinal and non-tissue specific

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18
Q

what are the three types of hyperbilirubinaemia?

A

pre-hepatic
hepatic
post-hepatic

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19
Q

what is pre-hepatic hyperbilirubinaemia?

A

secondary to haemolysis so too much bilirubin is being produced (check for anaemia)

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20
Q

what is hepatic hyperbilirubinaemia?

A

decreased bilirubin uptake, excretion and conjugation - disfunctional/diseased liver

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21
Q

what is post-hepatic hyperbilirubinaemia?

A

occurs secondary to an obstructed bile duct

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22
Q

what are the ways bilirubin can be measured?

A

total bilirubin
conjugated bilirubin (direct)

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23
Q

what is the main clinical signs of hyperbilirubinaemia?

A

jaundice (icterus)

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24
Q

when will jaundice be seen without a bilirubinaemia?

A

if jaundice is due to delta-bilirubin (bilirubin bound to albumin) - cause of jaundice is resolved but jaundice persists for a little while

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25
Q

what are some of the functions of the liver?

A

store glycogen, iron, copper, vitamins
detoxification
synthesis of cholesterol and bile acids
synthesis of plasma proteins
RBC breakdown
produce clotting factor
metabolisation

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26
Q

what ways can hepatocellular function be tested?

A

uptake/excretion of bilirubin and bile acids
conversion of ammonia to urea
synthesis of metabolites (albumin, cholesterol…)
synthesis of coagulation proteins
immunologic function

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27
Q

how can decreases in hepatic blood supply be tested for?

A

increased bile acids (decreased uptake)
increased ammonia (decreased conversion)
decreased antigens (immune function) - infection

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28
Q

how is ammonia metabolised?

A

uptake by hepatocytes and synthesised to urea, amino acids and proteins then diffuse into sinusoidal blood or bile canaliculi

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29
Q

what happens to the majority of bile acids secreted into the intestine?

A

reabsorbed from the oleum and enter the portal vein to return to the liver (small amount lost in faeces)

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30
Q

what can cause an increase in bile acids in blood?

A

reduced uptake/excretion by hepatocytes
disruption to enterohepatic circulation - portosystemic shunts, cholestasis…

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31
Q

do bile acids need taking if bilirubin is already raised?

A

no - bilirubin a much more sensitive test

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32
Q

what value of fasting bile acids would be a cause for concern?

A

> 25-30 mmol/L

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33
Q

how can you stimulate bile acid release?

A

give food (post prandial serum bile acids)

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34
Q

how is a post prandial serum bile acid test carried out?

A

take resting sample and then feed a fatty meal
measure bile acids 2 hours after feeding

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35
Q

what are possible abnormalities that can be seen on haematology of animals with liver disease?

A

microcytosis (altered iron transport/metabolism)
ovalcytes (cats with hepatic lipidosis)
acanthocytes

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36
Q

what can be seen on urinalysis of liver disease?

A

often unremarkable
isosthenuria or low USG
bilirubinuria
uroliths

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37
Q

what are the three functions of the pancreas?

A

digestive enzymes (exocrine)
regulate glucose (endocrine)
bicarbonate secretion
(main source of intrinsic factor in dog)

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38
Q

what are the three main diseases that involve the pancreas?

A

diabetes
pancreatitis
exocrine pancreatic insufficiency

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39
Q

what are the exocrine cells of the pancreas called?

A

acinar cells

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40
Q

what are the endocrine cells of the pancreas called?

A

islets of langerhan

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41
Q

what are the exocrine functions of the pancreas?

A

enzymes
bicarbonate secretion
B12 and zinc absorption
antibacterial
intestinal mucosal modulation

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42
Q

what tests is used to identify injury to the exocrine pancreas?

A

specific enzymes assays for amylase and lipase

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43
Q

what does amylase do?

A

catalyst for hydrolysis of complex starch

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44
Q

what does lipase do?

A

catalyst for hydrolysis of triglycerides

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45
Q

how long is the half life of amylase and lipase?

A

short (about 2 hours)

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46
Q

what species is amylase a more useful test for exocrine pancreas integrity?

A

dogs

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47
Q

what (relating to the kidney) can cause an increase in amylase and lipase?

A

decreased GFR (dehydration)

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48
Q

what enzyme test is a more specific test for pancreatitis?

A

DGGR lipase

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49
Q

how is pancreatitis diagnosed?

A

elevated DGGR lipase
clinical signs
ultrasound

50
Q

what can often be seen on haematology in pancreatitis cases?

A

leucocytosis, neutrophilia and left shift (due to inflammation)

51
Q

what abnormalities can possibly be seen on biochemistry in cases of pancreatitis?

A

hyperglycaemia (diabetes)
hyperlipidaemia
hypocalcaemia

52
Q

what can cause hypocalcaemia in pancreatitis cases?

A

saponification of fat causes increased calcitonin release

53
Q

what can be used to test for pancreatic function?

A

trypsin like immunoreactivity (TLI)

54
Q

how useful is the TLI test?

A

very good for diagnosing exocrine pancreas function

55
Q

what TLI cutoff is used to determine if a patient has exocrine pancreatic insufficiency?

A

<2.5 ug/L in dogs

56
Q

what are the functions of the kidney?

A

excretion of waste
control of body fluid balance (volume and composition)
production of hormone

57
Q

what hormones do the kidneys produce?

A

erythropoietin
calcitriol
renin

58
Q

what does the nephron conserve?

A

water
amino acids/proteins
glucose
bicarbonate
sodium and chloride
magnesium and calcium

59
Q

what does the nephron excrete?

A

urea
creatinine
potassium
hydrogen
phosphate
ketones/lactate

60
Q

how is glomerular filtration rate measured?

A

using indirect markers - urea and creatinine

61
Q

what produces creatinine?

A

muscle (constant steady rate)

62
Q

is urea or creatinine a better marker of GFR?

A

creatinine (urea can be reabsorbed and isn’t produced at a steady rate)

63
Q

what can cause an increase in urea in blood?

A

decreased GFR
upper GI haemorrhage
recent meal
catabolic state (fever, corticosteroids…)

64
Q

what can cause a decreases blood urea concentration?

A

severe liver disease/portosystemic shunt
low protein diet
aggressive fluid therapy
PUPD
young animals

65
Q

what can cause increased creatinine in blood?

A

decreased GFR
high muscle mass
high dietary protein

66
Q

what can cause a decreased concentration of creatinine in blood?

A

reduced muscle mass

67
Q

what is azotaemia?

A

increase in urea and creatinine in blood

68
Q

what could cause post-renal azotaemia?

A

urethral obstruction
urinary tract rupture

69
Q

how can you differentiate if an animal has pre-renal azotaemia?

A

evidence of dehydration/hypovolaemia
very concentrated urine (>1.030 in dogs and >1.035 in cats)
they respond to fluid therapy

70
Q

how can you differentiate if an animal has renal azotaemia?

A

inadequately concentrated urine

71
Q

how much kidney function has to be lost to see a change in creatinine?

A

75% of functioning nephrons

72
Q

what is SDMA used for?

A

marker of GFR

73
Q

what is SDMA?

A

symmetrical dimethyl arginine (GFR marker)

74
Q

what does hyperphosphataemia in species with high dietary phosphorus suggest?

A

decreased GFR

75
Q

what is the cut off for adequately concentrated urine in dogs/cats?

A

dogs - >1.030
cats - >1.035

76
Q

is it normal to have a dehydrated patient with a USG of 1.020?

A

no - should be well concentrated if dehydrated (could be normal)

77
Q

what does isosthenuric mean?

A

urine has the same specific gravity at plasma

78
Q

what is the range on USG for isosthenuria?

A

1.008 - 1.012

79
Q

what does hyposthenuria indicate about kidney function?

A

they are working because otherwise urine wouldn’t be this dilute (would be isosthenuric)

80
Q

what figure can be used to quantify proteinuria?

A

urine protein to creatinine ration

81
Q

what are some possible causes of pre-renal proteinuria?

A

fever
systemic inflammation
haemoglobinuria
myoglobinuria

82
Q

what are some possible causes of a post-renal proteinuria?

A

UTI
nephrolithiasis
urinary tract tumour

83
Q

if the UPCR is above 2 where is the problem probably localised to?

A

glomerular

84
Q

what figures aren’t accurate and should be disregarded on a dipstick test?

A

nitrites
leucocytes

85
Q

where do casts come from in urine?

A

kidney tubules (inside of the kidney tubule)

86
Q

where can disease be localised to if you see casts in the urine?

A

kidney

87
Q

what are struvite crystals made of?

A

magnesium ammonium phosphate

88
Q

what pH urine do struvite crystals form in?

A

alkaline

89
Q

what pH urine do urate crystals form in?

A

acidic

90
Q

what urianry crystals are seen with ethylene glycol poisoning?

A

calcium oxalate monohydrate (picket fence appearance)

91
Q

what electrolytes are mainly found within cells?

A

potassium
magnesium
phosphorous
sulfure

92
Q

what electrolytes are mainly found outside cells?

A

sodium
chloride

93
Q

what anions are responsible for balancing sodium?

A

chloride and bicarbonate

94
Q

what systems regulate sodium in the body?

A

RAAS
ADH

95
Q

what is the rough outline of the RAAS system?

A

decrease BP/perfusion to kidney causes renin release, which acts on angiotensinogen to form angiotensin 1, this is converted to angiotensin 2 by ACE. This then causes vasoconstriction and aldosterone release from adrenal gland

96
Q

what dies ADH act on?

A

collecting duct

97
Q

what is the function of ADH?

A

prevent water excretion from kidney

98
Q

what are some possible causes of hyponatraemia?

A

sodium loss - GI, kidney, drugs, Addisons
water gain - CHF, iatrogenic

99
Q

what are some possible causes of hypernatraemia?

A

hypotonic fluid loss - GI, kidney, post-obstructive diuresis
free water loss - heat stroke, pyrexia, no water access, adipsia
gain salt - excessive intake, iatrogenic

100
Q

what controls potassium concentration in plasma?

A

aldosterone (and insulin)

101
Q

how does aldosterone control potassium levels in plasma?

A

causes excretion if too high

102
Q

what are clinical signs of hypokalaemia?

A

muscle weakness
PUPD
anorexia
ileus/constipation

103
Q

what are some possible causes of hypokalaemia?

A

decreased intake - anorexia, low potassium fluid therapy
translocation (from ECF to ICF) - insulin, catecholamines
potassium loss - GI, renal, excess aldosterone, drugs

104
Q

what are some clinical signs of hyperkalaemia?

A

muscle weakness
cardiac abnormalities
bradycardia (can be tachy)

105
Q

what are some possible causes of hyperkalaemia?

A

artefactual - EDTA contamination, aged samples
decreased urinary excretion - obstruction, bladder rupture, Addisons, drugs
translocation (ICF to ECF) - tumour lysis syndrome, repercussion injuries
increased intake - excessive supplement, iatrogenic

106
Q

what is a potassium sparing diuretic?

A

spironolactone (aldosterone antagonist)

107
Q

how is hyperkalaemia managed?

A

IVFT - saline/hartmans
calcium gluconate

108
Q

what hormone is most important for controlling plasma osmolarity?

A

ADH

109
Q

what are the three forms of calcium?

A

protein bound
complexed (bound to other anions)
ionised

110
Q

what is most of protein bound calcium bound to?

A

albumin

111
Q

what is ionised calcium regulated by?

A

PTH and vitamin D

112
Q

what are the possible causes of hypercalcaemia?

A

malignancy (lymphoma…)
renal failure
primary hyperparathyroidism
Addisons

113
Q

what is the main clinical sign of hypercalcaemia?

A

extreme PUPD

114
Q

what are the clinical signs of hypocalcaemia?

A

muscle tremors, twitch, cramps
seizures
restless, behavioural change

115
Q

what should be checked first if the animal has hypocalcaemia?

A

if they have hypoalbuminaemia - this could be the cause of low calcium

116
Q

what are some possible causes of hypocalcaemia?

A

eclampsia
renal disease
hypoparathyroidism
nutritional
ethylene glycol

117
Q

what is the main regulator of phosphate?

A

parathyroid hormone

118
Q

what effect does parathyroid hormone have on phosphate?

A

causes excretion

119
Q

what are some possible causes of hyperphosphataemia?

A

failure of excretion (decreased GFR, obstruction)
release from bones (young animals)
increased intake
hypoparathyroidism
tumour lysis

120
Q

what are some possible causes of hypophosphataemia?

A

(rare)
anorexic cats

121
Q

how will EDTA effect calcium levels?

A

cause an artifactual decrease

Small animal (fourth year) (26 decks)

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