Exam 3 Flashcards
(170 cards)
1
Q
What is FIBRINOGEN increased with?
A
- inflammation
- physiologic stress
2
Q
What is FIBRINOGEN decreased with?
A
- DIC
- snake bites
(less sensitive in detecting decreases)
3
Q
Where are most plasma proteins synthesize?
A
liver
4
Q
Where are immunoglobulins synthesized?
A
lymphoid organs
5
Q
How are plasma proteins removed/lost?
A
- catabolism
- GI loss (protein losing enteropathy
- renal loss (protein losing nephropathy)
6
Q
How are plasma proteins replaced?
A
- synthesis
- dietary intake
7
Q
How does age affect plasma protein concentration?
A
- albumins low at birth
- globulins low until colostrum ingested/absorbed
- geriatric generally lower
8
Q
How does diet affect plasma protein concentration?
A
- hypoalbuminemia can result when intake is less than need (NEB, malnutrition, malabsorption)
9
Q
How does dehydration affect plasma protein concentration?
A
- relative hyperproteinemia and erythrocytosis
10
Q
How does external hemorrhage affect plasma protein concentration?
A
- hypoproteinemia and anemia (all components lost equally, fluid replaced first)
11
Q
How does inflammation affect plasma protein concentration?
A
- increased loss of some proteins
- increased synthesis of positive acute phase proteins
- decreased synthesis of negative acute phase proteins
12
Q
Albumin: low
Globulins: variable to normal
Cholesterol: low
A
liver failure
13
Q
Albumin: low
Globulins: normal to high
Cholesterol: high
A
glomerular disease
14
Q
`Albumin: low
Globulins: low
Cholesterol: low
A
GI disease
15
Q
What are acute phase proteins?
A
proteins that change their serum concentration by > 25% in response to inflammatory cytokines and are considered part of the innate immune system
16
Q
What are positive acute phase proteins?
A
increased synthesis in response to inflammation
17
Q
Examples positive acute phase proteins?
A
C-reaction protein (CRP) - complement activation
Serum amyloid A (SAA)
Fibrinogen
18
Q
What are negative acute phase proteins?
A
decreased synthesis in response to inflammation
19
Q
Examples negative acute phase proteins?
A
Albumin
Transferrin
20
Q
Total protein: high
A:G ratio: normal
A
dehydration
21
Q
Total protein: high
A:G ratio: low
A
hyperglobulinemia
22
Q
Total protein: low
A:G ratio: normal
A
non-selective protein loss
23
Q
Total protein: low
A:G ratio: low
A
selective - hypoalbuminemia
24
Q
Four reasons for hypoproteinemia
A
- decreased production
- increased loss
- sequestration
- iatrogenic dilution
25
Hypoproteinemia d/t decreased production
- chronic hepatic failure (usually only albumin)
- inadequate protein intake/digestion (only albumin)
- hypergammaglobulinemia (if high IG, body will downreg albumin)
26
Hypoproteinemia d/t increased loss
- protein losing enteropathy (both albumin + globulins, cholesterol)
- protein losing nephropathy/kidney disease (only albumin)
- whole blood loss (albumin + globulins)
- severe exudative skin wound (albumin + globulins)
27
Hypoproteinemia d/t sequestration
- body cavity effusion (only albumin)
| - vasculopathy (only albumin)
28
Hypoproteinemia d/t iatrogenic dilution
- IV fluid administration (albumin + globulins)
29
Two reasons for hypoglobulinemia
- decreased production
| - increased loss
30
Hypoglobulinemia d/t decreased production
- severe, chronic hepatic failure
- neonate before colostrum
- humoral immunodeficiency (rare)
31
Hypoglobulinemia d/t increased loss
- protein losing enteropathy
| - whole blood loss
32
Four reasons for panhypoproteinemia
- hemorrhage
- protein losing enteropathy
- severe exudative skin lesion
- iatrogenic dilution
33
Hyperalbuminemia
Not clinically significant
| ONLY occurs with hemoconentration (dehydration: albumin + globulins)
34
Hyperglobulinemia d/t increased immunoglobulins
- inflammatory disease + antigenic stimulation = polyclonal
| - neoplasia = monoclonal
35
PTH
- increased Ca
| - decreased P
36
Calcitriol/Vitamin
- increased Ca
| - increased P
37
Calcitonin
- decreased Ca
| - decreased P
38
Affect of hypoalbuminemia on calcium
- decreases total calcium
- no change in ionized calcium
- decreases albumin bound calcium
39
Affect acidosis on calcium
- no change in total calcium
- increases ionized calcium
- decreases albumin bound calcium
40
Affect of alkalosis on calcium
- no change in total calcium
- decreases ionized calcium
- increases albumin bound calcium
41
Calcium changes with renal disease
- most animals normocalcemic
- hypocalcemia d/t decreased production of calcitriol by kidney (decreased ionized, increased P)
- hypercalcemia in equines (kidney major route of Ca excretion), uncommon in SA (but renal dz can cause hypercalcemia)
42
Causes of hypocalcemia (acronym)
```
"HARP IS ALE"
- hypoparathyroidism
- hypoalbuminemia
- renal disease (not horses)
- pancreatitis
- intestinal malabsorption
- spurious/artifact
- alkalosis
- lactation (eclampsia/milk fever)
- ethylene glycol
Others:
- phosphate containing enemas
-citrate toxicity (blood transfusions)
- hypovitaminosis D
- inadequate Ca intake
- excess P
```
43
Signs of hypocalcemia
- OCCURS WHEN IONIZED LOW
- increased neuron excitability: nervousness, trembling, muscle fasciculations/twitching, muscle cramping, tetanic paralysis
- excessive panting
- seizures
- intense licking at paws
- stiff pelvic limb gait
44
CLASSIC signs of hypocalcemia in cats and cows
cats: intense facial rubbing
cows: flaccid paralysis with S shaped neck
45
Causes of hypercalcemia (acronym)
"GOSH DARNIT"
- granulomatous
- osteolysis
- spurious/iatrogenic
- hyperparathyroidism
- vitamin D toxicosis
- addison's disease
- renal disease in horses
- neoplasia
- idopathic in cats (seen with Ca Oxalate uroliths)
- hypothermia
46
Signs of hypercalcemia
- PU/PD: high Ca blocks ADH
- lethargy, weakness
- constipation
- mineralization of soft tissue
- calcium containing uroliths
47
Hypercalcemia d/t primary hyperparathyroidism
- hormone secreted by functional adenoma (most common), hyperplastic gland, functional carcinoma
- MUST INTERPRET IN LIGHT OF CA (PTH should normally be low with high Ca, bad: normal PTH + high Ca)
LOOK FOR:
- increased total Ca, ionized Ca, PTH
- decreased to normal P
- increased to normal calcitriol
- undetectable PTHrP
48
Hypercalcemia d/t hypervitaminosis D
- vitamin D toxicity from dietary, medications, rodenticides, plants, granulomatous disease
- increased vit D = Ca release from bone/intestinal absorption
- increased Ca + P
49
Hypercalcemia d/t hypoadrenocorticism (addison's disease)
- SECOND MOST COMMON CAUSE IN DOGS
- increased total Ca +/- ionized
- tx with corticosteroids and/or volume replacement
50
Hypercalcemia of malignancy
- MOST COMMON CAUSE
- lymphoma = most common, usually T cell
- apocrine gland adenocarcinoma of anal sac
- multiple myeloma
- associated with PTHrP
51
Causes of hyperphosphatemia (7)
- decreased renal excretion/decreased GFR = MOST COMON, can be pre-renal, renal or post-renal
- disorders of Ca homeostasis
- growing animals
- vitamin D toxicity
- hypoparathyroidism
- shifts from ICF to EFC with metabolic acidosis, rhabdomyolysis, acute tumor lysis syndrome
- iatrogenic/spurious (fluids, enemas, diet)
52
Concerns with hyperphosphatemia
- soft tissue mineralization when Ca x P > 70
| - bone resorption, fibrous osteodystrophy
53
Causes of hypophosphatemia (9)
- primary hyperparathyroidism
- hypercalcemia of malignancy (PTHrP)
- hypovitaminosis D
- decreased intestinal absorption
- Fanconi syndrome (renal tubules)
- chronic kidney disease in horses
- lactation
- iatrogenic (antacids binding P)
- shifts from ECF to ICF with DKA, starvation-reseeding syndrome, respiratory alkalosis
54
Concerns with hypophosphatemia
- intravascular hemolysis (decreased ATP)
- intestinal ileus
- weakness, ataxia, seizures
55
How does insulin affect phosphorus shifting?
shifts P into cells, decreasing serum P concentrations
56
How does alkalosis affect phosphorus shifting?
shifts P into cells, decreasing serum P concentrations
57
How does acidosis affect phosphorus shifting?
shifts P out of cells in order to shift excess H + into cells, increasing serum P concentrations
58
Two causes of hypomagnesemia
- increased loss
| - decreased intake
59
Hypomagnesemia d/t increased loss
- MOST COMMON CAUSE SA
- renal: diuresis, disease (#1)
- GI: malabsorption, diarrhea
60
Hypomagnesemia d/t decreased intake
- MOST COMMON CAUSE IN RUMINANTS
- lush gren pasture = high K, low Mg (K block normal Mg absorption)
- milk-only diets in older calves
- prolonged anorexia/poor diet
- prolonged IV fluid therapy or parenteral nutrition WITHOUT Mg supplementation
61
Signs of hypomagnesemia
- NM + cardiac abnormalities
- hyperexcitability, tremors
- fasciculations, ataxia
- tetany
- cardiac arrhythmias, possible arrest
62
Concerns with hypomagnesemia
- secondary hypocalcemia d/t impaired PTH release + calcitriol resistance
- secondary hypokalemia d/t renal wasting of K when Mg is low
63
Causes of hypermagnesemia
Less clinically significant
- iatrogenic
- decreased renal excretion (AKI/urethral obstruction)
Patients can develop CV, near, GI problems
64
Causes of hypernatremia
- increased sodium (salt poisoning, sea water, fluids)
| - decreased water (inadequate intake, loss of sodium poor fluid - effusion)
65
Signs of hypernatremia
- depression, dementia, seizures, coma
- MUST REHYDRATE SLOWLY to prevent cerebral edema (idiogenic osmoles)
- dehydration (mild hypernatremia only)
66
Diseases associated with hypernatremia
- lack of ADH or ADH resistance (diabetes insipidus)
- hypotonic diarrhea/vomiting
- inappropriate mixed milk-replacement in calves
67
Causes of hyponatremia
- decreased sodium (loss or deficient intake in herbivores)
- increased water (mannitol, ethylene glycol, edema, psychologic PD, near drowning in fresh water, sodium poor IV fluids, ADH secretion)
68
Signs of hyponatremia
- usually d/t underlying disease: GI, renal
| - rarely severe enough for signs for hypoosmolality
69
Diseases associated with hyponatremia
- addison's (hypoadrenocorticism)
- lack of aldosterone and glucocorticoids
- may present in hypovolemic shock
70
What is pseudohyponatremia?
hyperosmolality not due to high sodium; draws water into ECF + dilutes measured sodium (though whole body Na normal)
71
Causes of pseudohyponatremia
- hyperglycemia (diabetic)
- lipemia
- hyperproteinemia
- ethylene glycol
- mannitol
- methodology + artifact (affected when Na reported as #/total vol of serum, but not when #/total vol of serum water)
72
True hyponatremia vs pseudohyponatremia
True: Na LOW <290
Pseudo: Na normal or HIGH >290
73
Causes of hyperkalemia
- altered external balance
- altered internal balance
- spurious
74
Hyperkalemia d/t altered EXTERNAL balance
- failure of renal excretion (anuric/oliguric RF, urinary tract rupture, urethral obstruction)
- addison's disease
- chylothorax with repeated drainage
- iatrogenic (excessive IV fluids with K)
75
Hyperkalemia d/t altered INTERNAL balance
- leakage from cell with damaged membranes
| - shifting from ICF to ECF: hyperchloremic metabolic acidosis, diabetes mellitus
76
Signs of hyperkalemia
- abnormal membrane electrical potential
- decreased muscle electrical conduction
- weakness, bradycardia, ECG changes, cardiac arrest
77
Causes of hypokalemia
- altered external balance
- altered internal balance
- spurious
78
Hypokalemia d/t altered EXTERNAL balance
- GI loss
- increased renal excretion
- decreased intake in LA
- iatrogenic
79
Hypokalemia d/t altered INTERNAL balance
- shifts from ECF to ICF: metabolic alkalosis
| - iatrogenic: bicarbonate admin, glucose + insulin
80
Signs of hypokalemia
- PU/PD (d/t medullar washout)
- skeletal muscle weakness, respiratory arrest
- ECG changes, arrhythmias
- CAT: neck ventroflexion, nephropathy, polymyopathy
81
When can hypokalemia be associated treatment of diseases?
- treatment of male cat obstruction - post diuresis
| - treatment of DKA (shifts into cells)
82
Causes of hypochloremia
- Na related decreases
- loss of Cl rich secretions or sequestration (ruminants: abomasum disease; monogastrics: GI obstruction, NGtube suctioning)
- sweating in horses (excess Na)
- renal disease in cattle
- iatrogenic (diuretics)
- spurious
83
Causes of hyperchloremia
- Na related increases (dehydration)
- compensation for decreased bicarbonate (from GI or kidneys)
- iatrogenic (hypertonic saline IV fluids)
- spurious ( PBr admin)
84
USG of canine
>1.030
85
USG of felines
>1.040
86
USG of large animals
>1.025
87
Hyposthenuria
USG <1.008
kidney activity diluting urine (PT + LOH), but can't concentrate
- tubules unresponsive to ADH or decreased production of ADH
- NOT associated with primary renal disease
88
Isosthenuria
USG 1.008-1.012 (same as plasma)
| Kidney doing nothing to urine, likely primary renal disease
89
Normal results for urine sediment
EVERYTHING LESS THAN 5 PER FIELD
- epithelial cells: 0-5/LPF
- hyaline/granular casts: 0-1/LPF
- WBCs: 0-3/HPF
- RBCs: 0-5/HPF
90
Dysuria
clinical sign of LOWER urinary tract disease; usually d/t inflammation, partial/complete urethral obstruction or neurological
91
UMN dysuria vs LMN dysuria
UMN: tight distended bladder, difficult to express
LMN: large flaccid blades, easy to express
92
Causes of PU/PD
- loss of medullary gradient
- decreased ADH secretion
- ADH resistance
- iatrogenic
- psychogenic
93
PU/PD d/t loss of medullary gradient
- osmotic diuresis: CKD, diabetes mellitus, Fanconi syndrome, post-obstructive diuresis
- medullary washout: any chronic PU/PD, liver failure
94
PU/PD d/t decreased ADH secretion
- central diabetes insipidus (rare - lack of increased BG, usually hyposthenuric)
- congenital, sx, infection, inflammation, tumor, brain injury
95
PU/PD d/t ADH resistance
COMMON CAUSE
- primary nephrogenic diabetes insipidus (rare - USG isothenuric)
- secondary nephrogenic diabetes insipidus (common - USG hyposthenuric -- pyometra, pyelonephritis, cystitis, hyperCa, hypoK, cushion's, addisons)
96
PU/PD d/t iatrogenic causes
- diuretics
- corticosteroids
- anticonvulsants
- excessive thyroid supplements
- fluids
97
Normal renal solute handling: net conservation
Na, Cl, H2O, HCO3, Ca, Mg
glucose
proteins
AA
98
Normal renal solute handling: net excretion
urea
creatinine
K, H, NH4, PO4
99
Function of the glomerulus
major route for solute/water excretion, plasma is filtered
100
Function of renal tubules
- regulate solute/water balance
- ion exchange
- mineral balance
- acid-base balance
- glucose/protein reabsorption
101
Manifestations of glomerular disease
CAN STILL CONCENTRATE URINE
- leak albumin: significant proteinuria
- leak antithrombin 3: coagulopathies
102
Manifestations of tubular disease
LOST ABILITY TO CONCENTRATE/DILUTE - PU/PD, dehydration
- loss of electrolytes
- acid/base abnormalities
- inadequate USG
- glucosuria without hyperglycemia
- mild proteinuria
103
Function of ADH
- acts on kidney tubules + arterioles
- decrease urine output
- increases water reabsorption
- constricts vessels to increase BP
- decreases sweating
104
Function of aldosterone
- promotes Na reabsorption in exchange for K + H ions
| - increases NaK ATPase activity
105
Diseases associated with hormones of acting on the kidney
- hyperCa interferes with ADH action at distal tubules
| - Cushing's, Addison's, hyperthyroidism inhibit ADH effects
106
Clinical findings with AKD
- dehydrated, vomiting, depressed
- initially anuric or oliguric, later polyuric
- typically good BCS
107
Lab findings with AKD
- anuric/oliguric
- hyperkalemia
- metabolic acidosis with high anion gap
- Na, Cl normal/high d/t dehydration
- NOT anemic - maybe relative erythrocytosis d/t dehydration
- P can be elevated
108
Clinical findings with CKD
- dehydrated, vomiting, depressed
- usually present with PU/PD
- will become oliguric/anuric in end-stage
- usually anemic d/t lack of EPO production
109
Lab findings with CKD
- polyuric
- Na, K more likely to be low d/t loss
- CL may be elevated d/t loss of HCO3
- metabolic acidosis with normal anion gap
- Non-regenerative anemia of CRF
- P can be elevated
110
Azotemia d/t uroabdomen
- high BUN/creatinine (C 2x serum)
- low Na
- high K
111
Azotemia d/t ethylene glycol intoxication
- BUN/creatinine
- low Ca
- high anion gap
- seizures
- crystalluria: Ca oxalate monohydrate
- anuria/oliguria 1-4 days post ingestion
112
Azotemia vs uremia
azotemia: elevated BUN/creatinine
uremia: azotemia + clinical signs
113
Azotemia characterized by decreased blood flow to kidney and high USG
Other findings: increased PCV, RBC, Na, CL, plasma proteins
pre-renal azotemia
114
Pre-renal azotemia disease states
- dehydration/hypovolemia
- high protein diet (creatinine normal)
- GI hemorrhage
115
Azotemia characterized by decreased GFR and an inadequate USG (>1.008, NOT HYPOSTHENURIC)
Other findings: increased K + P, high anion gap, polyuric/oliguric/anuric
renal azotemia - can be masked by dehydration (clinically dehydrated should have max concentrated urine)
116
Azotemia characterized by decreased GFR
| Other findings: increased K + Mg, decreased Na, possible uroabdomen
post-renal azotemia d/t obstructed outflow/rupture in outflow tract
117
Renal disease without azotemia
>25% functional nephrons
- need U/A with USG: reduced ability to concentrate in dehydrated animal
- proteinuria
- glucosuria without hyperglycemia
- casts
118
Causes of decreased BUN
- hepatic failure
- low protein diets
- overhydration
NOT indicator of renal disease
119
Causes of creatinine increases
- decreased GFR
- pre-renal, renal, or post-renal causes that also increase BUN
- severe muscle damage (myoglobin release)
120
Causes of creatinine decreases
- GFR increased
- severe muscle atrophy/wasting
- artifact of increased serum bilirubin (icterus)
- pregnancy (via increased GFR)
121
Is BUN or creatinine reabsorbed by the renal tubules?
BUN only
122
decreased pH
increased PaCO2
increased HCO3
respiratory acidemia
123
increased pH
decreased PaCO2
decreased HCO3
respiratory alkalemia
124
decreased pH
decreased PaCO2
decreased HCO3
metabolic acidemia
125
increased pH
increased PaCO2
increased HCO3
metabolic alkalemia
126
Elevated anion gap physiology
- build up of H+ (HCO3 not lost, Cl not conserved
| - decreased HCO3, normal Cl (excess other acids)
127
Causes of elevated anion gap (acronym)
```
"P SKULE"
- phosphates
- sulfates
- ketones
- uremic acid
- lactic acid
- ethylene glycol metabolites
(titrational acidosis = where acids neutralize HCO3)
```
128
Normal anion gap physiology
- loss of HCO3 and compensation with increased Cl
129
Causes of normal anion gap
"secretional acidosis"
- loss/sequestration of HCO3 rich fluids or secretion diarrhea
- proximal renal tubular acidosis
- distal renal tubular acidosis
- loss of saliva in ruminants
130
Low anion gap physiology
Not clinically significant, normally d/t hypoalbuminemia
131
Mixed acidosis/alkalosis physiology
- decreased Cl and normal to increased HCO3
132
Causes of mixed acidosis/alkalosis
- combined alkalosis + high AG acidosis
- high GI obstruction and lactic acidosis from shock
- renal failure and vomiting that increases HCO3
133
Two types of metabolic acidosis and associated anion gap
- loss of HCO3 (conserve Cl) = normal anion gap
| - build up of acids (HCO3 normal, Cl not conserved) = elevated anion gap
134
Renal failure is an example of what type of acid/base disturbance?
metabolic acidemia
135
Renal causes for increased potassium
- anuric/oliguric RF
- CKD in horses
- uroabdomen
- addison's
- hypoaldosteronism
136
Renal causes for decreased potassium
- increased aldosterone
- increased distal tubular flow rate
- renal tubular disease
- polyuric RF
137
Renal causes for increased sodium
- osmotic/chemical diuresis
| - RF
138
Renal causes for decreased sodium
- hypervolemic states: nephrotic syndrome, advanced RF
- hypovolemic states: addison's, proximal renal tubule dysfunction, hypoaldosteronism, osmotic diuresis/diabetes mellitus, CKD
- obstructed/ruptured urinary tract
139
Urine dipstick: + bilirubin
NEVER NORMAL IN CATS
- liver disease
- hemolysis
- pigmenturia, GI contamination
140
Urine dipstick: + heme
- RBCs (RBC in sediment, unless small # lysed d/t hyposthenuria)
- damaged myocytes (clear plasma)
- hemolysis (pink plasma)
- catheterized sample or sperm present
141
Urine dipstick: + glucose
INTERPRET WITH BG
- without hyperglycemia = Fanconi syndrome
- stress induced hyperglycemia in cats
- vitamin C or cleaners
142
Urine dipstick: + ketones
- diabetes mellitus
- bovine ketosis
- pregnancy
- NEB
143
Urine dipstick: pH
normals
carnivores/suckling herbs: 5.5-7.5
herbivores: 7.0-8.5
- aging or presence of contaminant/pathogenic bacteria will alkalinize over time*
144
Urine dipstick: + protein
INTERPRET WITH USG + pH
- blood in urine
- hemorrhage (must have heme 3+)
- glomerular or tubular disease
- catheterized sample, alkaline, concentrated or sperm present
145
Urine sediment: squamous epithelial cells
- lower UT contamination from voided or catheterized samples
146
Urine sediment: transitional epithelial cells
- from bladder and proximal 2/3 urethra
147
Urine sediment: caudate epithelial cells
- pyelonephritis
- calculi/stones in renal pelvis
VERY SIGNIFICANT
148
Urine sediment: renal tubular epithelial cells
- renal damage or inflammation (tubular nephritis)
| BIG DEAL, but hard to dx
149
Urine sediment: casts in general
- typically an early indicator of renal tubular disease
| - counted per 10X
150
Urine sediment: hyaline casts
- renal dysfunction
| - low # with exercise, hyperthermia
151
Urine sediment: epithelial/cellular casts
- nephritis/pyelonephritis (would expect USG to be low)
| - there is also WBC casts
152
Urine sediment: granular casts
- normal degenerative process if 0-1/LPF
| - renal tubular damage
153
Urine sediment: waxy casts
- chronic tubular lesion d/t local tubular obstruction, oliguria, CKD
154
Urine sediment: fatty casts
- often seen in cats
| - hyperlipidemia: diabetes mellitus, nephrotic syndrome
155
Urine sediment: hemoglobin casts
- intravascular hemolysis (hemoglobinemia, hemoglobinuria) - usually something else going on at same time (DIC, renal ischemia)
- post-transfusion
156
Urine sediment: pseudocasts
- mucous threads from horses
| - microscopic fibers from dirty animals
157
Progression of casts
cellular - coarsely granular - finely granular - waxy
158
Urine sediment: calcium carbonate crystals
"radiant spheres/dumbells"
- alkaline urine
- normal in horses, rabbits, GP, elephant = excrete calcium in urine (RF if not seen!)
159
Urine sediment: MAP/struvite crystals
"coffin lids"
- alkaline urine
- secondary to UTI in dogs
- sterile cystitis in cats
- refrigerated/storage
160
Urine sediment: amorphous phosphate crystals
"sand"
| - clinically insignificant
161
Urine sediment: amorphous urate crystals/urates
"brown small spheroids or flat prisms of various shapes"
- acidic urine
- Dalmation, English Bulldogs = metabolic disorder, defective purine metabolism
162
Urine sediment: dihydrate calcium oxalate crystals
"envelopes"
- calciuresis = Cushing's
- can be normal usually NBD, oxalate containing plants
- storage at RT/refrigerated
163
Urine sediment: monohydrate calcium oxalate crystals
"picket fence posts"
- acute ethylene glycol poisoning (3-18 hr post-ingestion)
- calciuresis
- storage
164
Urine sediment: ammonium bitrate crystals
"golden-brown thorny apple"
- severe hepatic disease: portovascular malformations, sago palm toxicity
- Dalmatians, English bulldogs (uncommon)
165
Urine sediment: bilirubin crystals
"reddish-brown granules or needle-like"
- low # normal in canine urine (esp males, highly concentrated)
- always significant in cat
- liver disease
- extravascular hemolysis
166
Urine sediment: cystine crystals
"colorless hexagons"
- LOOK FOR UROLITH
- inherited defect in proximal tubule reabsorbing cystine
- breed: Dachshunds, Enlish Bulldogs, Newfies, Siamese, Chihuahuas, Rottweilers
167
Urine sediment: sulfa crystals
"haystack bundles or radiant spheres - pale yellow"
| - sulfa-containing drugs
168
Which stones can be diagnosed via radiographs - must check on ultrasound
cysteine
| urates - amorphous, urates, ammonium biurate
169
Lipid droplets on UA are common in which specie(s)?
cats - produced by tubular epithelium
170
Two parasites seen on UA?
- pearsonema place
| - dioctyophyma renale
