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Clinical Pathology 2017 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is FIBRINOGEN increased with?

A
  • inflammation

- physiologic stress

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2
Q

What is FIBRINOGEN decreased with?

A
  • DIC
  • snake bites
    (less sensitive in detecting decreases)
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3
Q

Where are most plasma proteins synthesize?

A

liver

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4
Q

Where are immunoglobulins synthesized?

A

lymphoid organs

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5
Q

How are plasma proteins removed/lost?

A
  • catabolism
  • GI loss (protein losing enteropathy
  • renal loss (protein losing nephropathy)
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6
Q

How are plasma proteins replaced?

A
  • synthesis

- dietary intake

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7
Q

How does age affect plasma protein concentration?

A
  • albumins low at birth
  • globulins low until colostrum ingested/absorbed
  • geriatric generally lower
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8
Q

How does diet affect plasma protein concentration?

A
  • hypoalbuminemia can result when intake is less than need (NEB, malnutrition, malabsorption)
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9
Q

How does dehydration affect plasma protein concentration?

A
  • relative hyperproteinemia and erythrocytosis
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10
Q

How does external hemorrhage affect plasma protein concentration?

A
  • hypoproteinemia and anemia (all components lost equally, fluid replaced first)
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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
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12
Q

Albumin: low
Globulins: variable to normal
Cholesterol: low

A

liver failure

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13
Q

Albumin: low
Globulins: normal to high
Cholesterol: high

A

glomerular disease

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14
Q

`Albumin: low
Globulins: low
Cholesterol: low

A

GI disease

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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

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16
Q

What are positive acute phase proteins?

A

increased synthesis in response to inflammation

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17
Q

Examples positive acute phase proteins?

A

C-reaction protein (CRP) - complement activation
Serum amyloid A (SAA)
Fibrinogen

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18
Q

What are negative acute phase proteins?

A

decreased synthesis in response to inflammation

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19
Q

Examples negative acute phase proteins?

A

Albumin

Transferrin

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20
Q

Total protein: high

A:G ratio: normal

A

dehydration

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21
Q

Total protein: high

A:G ratio: low

A

hyperglobulinemia

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22
Q

Total protein: low

A:G ratio: normal

A

non-selective protein loss

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23
Q

Total protein: low

A:G ratio: low

A

selective - hypoalbuminemia

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24
Q

Four reasons for hypoproteinemia

A
  • decreased production
  • increased loss
  • sequestration
  • iatrogenic dilution
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25
Q

Hypoproteinemia d/t decreased production

A
  • chronic hepatic failure (usually only albumin)
  • inadequate protein intake/digestion (only albumin)
  • hypergammaglobulinemia (if high IG, body will downreg albumin)
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26
Q

Hypoproteinemia d/t increased loss

A
  • 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)
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27
Q

Hypoproteinemia d/t sequestration

A
  • body cavity effusion (only albumin)

- vasculopathy (only albumin)

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28
Q

Hypoproteinemia d/t iatrogenic dilution

A
  • IV fluid administration (albumin + globulins)
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29
Q

Two reasons for hypoglobulinemia

A
  • decreased production

- increased loss

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30
Q

Hypoglobulinemia d/t decreased production

A
  • severe, chronic hepatic failure
  • neonate before colostrum
  • humoral immunodeficiency (rare)
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31
Q

Hypoglobulinemia d/t increased loss

A
  • protein losing enteropathy

- whole blood loss

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32
Q

Four reasons for panhypoproteinemia

A
  • hemorrhage
  • protein losing enteropathy
  • severe exudative skin lesion
  • iatrogenic dilution
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33
Q

Hyperalbuminemia

A

Not clinically significant

ONLY occurs with hemoconentration (dehydration: albumin + globulins)

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34
Q

Hyperglobulinemia d/t increased immunoglobulins

A
  • inflammatory disease + antigenic stimulation = polyclonal

- neoplasia = monoclonal

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35
Q

PTH

A
  • increased Ca

- decreased P

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36
Q

Calcitriol/Vitamin

A
  • increased Ca

- increased P

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37
Q

Calcitonin

A
  • decreased Ca

- decreased P

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38
Q

Affect of hypoalbuminemia on calcium

A
  • decreases total calcium
  • no change in ionized calcium
  • decreases albumin bound calcium
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39
Q

Affect acidosis on calcium

A
  • no change in total calcium
  • increases ionized calcium
  • decreases albumin bound calcium
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40
Q

Affect of alkalosis on calcium

A
  • no change in total calcium
  • decreases ionized calcium
  • increases albumin bound calcium
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41
Q

Calcium changes with renal disease

A
  • 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)
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42
Q

Causes of hypocalcemia (acronym)

A 
"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
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43
Q

Signs of hypocalcemia

A
  • 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
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44
Q

CLASSIC signs of hypocalcemia in cats and cows

A

cats: intense facial rubbing
cows: flaccid paralysis with S shaped neck

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45
Q

Causes of hypercalcemia (acronym)

A

“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
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46
Q

Signs of hypercalcemia

A
  • PU/PD: high Ca blocks ADH
  • lethargy, weakness
  • constipation
  • mineralization of soft tissue
  • calcium containing uroliths
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47
Q

Hypercalcemia d/t primary hyperparathyroidism

A
  • 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
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48
Q

Hypercalcemia d/t hypervitaminosis D

A
  • vitamin D toxicity from dietary, medications, rodenticides, plants, granulomatous disease
  • increased vit D = Ca release from bone/intestinal absorption
  • increased Ca + P
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49
Q

Hypercalcemia d/t hypoadrenocorticism (addison’s disease)

A
  • SECOND MOST COMMON CAUSE IN DOGS
  • increased total Ca +/- ionized
  • tx with corticosteroids and/or volume replacement
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50
Q

Hypercalcemia of malignancy

A
  • MOST COMMON CAUSE
  • lymphoma = most common, usually T cell
  • apocrine gland adenocarcinoma of anal sac
  • multiple myeloma
  • associated with PTHrP
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51
Q

Causes of hyperphosphatemia (7)

A
  • 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)
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52
Q

Concerns with hyperphosphatemia

A
  • soft tissue mineralization when Ca x P > 70

- bone resorption, fibrous osteodystrophy

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53
Q

Causes of hypophosphatemia (9)

A
  • 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
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54
Q

Concerns with hypophosphatemia

A
  • intravascular hemolysis (decreased ATP)
  • intestinal ileus
  • weakness, ataxia, seizures
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55
Q

How does insulin affect phosphorus shifting?

A

shifts P into cells, decreasing serum P concentrations

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56
Q

How does alkalosis affect phosphorus shifting?

A

shifts P into cells, decreasing serum P concentrations

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57
Q

How does acidosis affect phosphorus shifting?

A

shifts P out of cells in order to shift excess H + into cells, increasing serum P concentrations

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58
Q

Two causes of hypomagnesemia

A
  • increased loss

- decreased intake

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59
Q

Hypomagnesemia d/t increased loss

A
  • MOST COMMON CAUSE SA
  • renal: diuresis, disease (#1)
  • GI: malabsorption, diarrhea
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60
Q

Hypomagnesemia d/t decreased intake

A
  • 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
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61
Q

Signs of hypomagnesemia

A
  • NM + cardiac abnormalities
  • hyperexcitability, tremors
  • fasciculations, ataxia
  • tetany
  • cardiac arrhythmias, possible arrest
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62
Q

Concerns with hypomagnesemia

A
  • secondary hypocalcemia d/t impaired PTH release + calcitriol resistance
  • secondary hypokalemia d/t renal wasting of K when Mg is low
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63
Q

Causes of hypermagnesemia

A

Less clinically significant
- iatrogenic
- decreased renal excretion (AKI/urethral obstruction)
Patients can develop CV, near, GI problems

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64
Q

Causes of hypernatremia

A
  • increased sodium (salt poisoning, sea water, fluids)

- decreased water (inadequate intake, loss of sodium poor fluid - effusion)

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65
Q

Signs of hypernatremia

A
  • depression, dementia, seizures, coma
  • MUST REHYDRATE SLOWLY to prevent cerebral edema (idiogenic osmoles)
  • dehydration (mild hypernatremia only)
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66
Q

Diseases associated with hypernatremia

A
  • lack of ADH or ADH resistance (diabetes insipidus)
  • hypotonic diarrhea/vomiting
  • inappropriate mixed milk-replacement in calves
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67
Q

Causes of hyponatremia

A
  • 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)
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68
Q

Signs of hyponatremia

A
  • usually d/t underlying disease: GI, renal

- rarely severe enough for signs for hypoosmolality

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69
Q

Diseases associated with hyponatremia

A
  • addison’s (hypoadrenocorticism)
  • lack of aldosterone and glucocorticoids
  • may present in hypovolemic shock
70
Q

What is pseudohyponatremia?

A

hyperosmolality not due to high sodium; draws water into ECF + dilutes measured sodium (though whole body Na normal)

71
Q

Causes of pseudohyponatremia

A
  • 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
Q

True hyponatremia vs pseudohyponatremia

A

True: Na LOW <290
Pseudo: Na normal or HIGH >290

73
Q

Causes of hyperkalemia

A
  • altered external balance
  • altered internal balance
  • spurious
74
Q

Hyperkalemia d/t altered EXTERNAL balance

A
  • 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
Q

Hyperkalemia d/t altered INTERNAL balance

A
  • leakage from cell with damaged membranes

- shifting from ICF to ECF: hyperchloremic metabolic acidosis, diabetes mellitus

76
Q

Signs of hyperkalemia

A
  • abnormal membrane electrical potential
  • decreased muscle electrical conduction
  • weakness, bradycardia, ECG changes, cardiac arrest
77
Q

Causes of hypokalemia

A
  • altered external balance
  • altered internal balance
  • spurious
78
Q

Hypokalemia d/t altered EXTERNAL balance

A
  • GI loss
  • increased renal excretion
  • decreased intake in LA
  • iatrogenic
79
Q

Hypokalemia d/t altered INTERNAL balance

A
  • shifts from ECF to ICF: metabolic alkalosis

- iatrogenic: bicarbonate admin, glucose + insulin

80
Q

Signs of hypokalemia

A
  • PU/PD (d/t medullar washout)
  • skeletal muscle weakness, respiratory arrest
  • ECG changes, arrhythmias
  • CAT: neck ventroflexion, nephropathy, polymyopathy
81
Q

When can hypokalemia be associated treatment of diseases?

A
  • treatment of male cat obstruction - post diuresis

- treatment of DKA (shifts into cells)

82
Q

Causes of hypochloremia

A
  • 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
Q

Causes of hyperchloremia

A
  • Na related increases (dehydration)
  • compensation for decreased bicarbonate (from GI or kidneys)
  • iatrogenic (hypertonic saline IV fluids)
  • spurious ( PBr admin)
84
Q

USG of canine

A

> 1.030

85
Q

USG of felines

A

> 1.040

86
Q

USG of large animals

A

> 1.025

87
Q

Hyposthenuria

A

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
Q

Isosthenuria

A

USG 1.008-1.012 (same as plasma)

Kidney doing nothing to urine, likely primary renal disease

89
Q

Normal results for urine sediment

A

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
Q

Dysuria

A

clinical sign of LOWER urinary tract disease; usually d/t inflammation, partial/complete urethral obstruction or neurological

91
Q

UMN dysuria vs LMN dysuria

A

UMN: tight distended bladder, difficult to express
LMN: large flaccid blades, easy to express

92
Q

Causes of PU/PD

A
  • loss of medullary gradient
  • decreased ADH secretion
  • ADH resistance
  • iatrogenic
  • psychogenic
93
Q

PU/PD d/t loss of medullary gradient

A
  • osmotic diuresis: CKD, diabetes mellitus, Fanconi syndrome, post-obstructive diuresis
  • medullary washout: any chronic PU/PD, liver failure
94
Q

PU/PD d/t decreased ADH secretion

A
  • central diabetes insipidus (rare - lack of increased BG, usually hyposthenuric)
  • congenital, sx, infection, inflammation, tumor, brain injury
95
Q

PU/PD d/t ADH resistance

A

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
Q

PU/PD d/t iatrogenic causes

A
  • diuretics
  • corticosteroids
  • anticonvulsants
  • excessive thyroid supplements
  • fluids
97
Q

Normal renal solute handling: net conservation

A

Na, Cl, H2O, HCO3, Ca, Mg
glucose
proteins
AA

98
Q

Normal renal solute handling: net excretion

A

urea
creatinine
K, H, NH4, PO4

99
Q

Function of the glomerulus

A

major route for solute/water excretion, plasma is filtered

100
Q

Function of renal tubules

A
  • regulate solute/water balance
  • ion exchange
  • mineral balance
  • acid-base balance
  • glucose/protein reabsorption
101
Q

Manifestations of glomerular disease

A

CAN STILL CONCENTRATE URINE

  • leak albumin: significant proteinuria
  • leak antithrombin 3: coagulopathies
102
Q

Manifestations of tubular disease

A

LOST ABILITY TO CONCENTRATE/DILUTE - PU/PD, dehydration

  • loss of electrolytes
  • acid/base abnormalities
  • inadequate USG
  • glucosuria without hyperglycemia
  • mild proteinuria
103
Q

Function of ADH

A
  • acts on kidney tubules + arterioles
  • decrease urine output
  • increases water reabsorption
  • constricts vessels to increase BP
  • decreases sweating
104
Q

Function of aldosterone

A
  • promotes Na reabsorption in exchange for K + H ions

- increases NaK ATPase activity

105
Q

Diseases associated with hormones of acting on the kidney

A
  • hyperCa interferes with ADH action at distal tubules

- Cushing’s, Addison’s, hyperthyroidism inhibit ADH effects

106
Q

Clinical findings with AKD

A
  • dehydrated, vomiting, depressed
  • initially anuric or oliguric, later polyuric
  • typically good BCS
107
Q

Lab findings with AKD

A
  • 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
Q

Clinical findings with CKD

A
  • dehydrated, vomiting, depressed
  • usually present with PU/PD
  • will become oliguric/anuric in end-stage
  • usually anemic d/t lack of EPO production
109
Q

Lab findings with CKD

A
  • 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
Q

Azotemia d/t uroabdomen

A
  • high BUN/creatinine (C 2x serum)
  • low Na
  • high K
111
Q

Azotemia d/t ethylene glycol intoxication

A
  • BUN/creatinine
  • low Ca
  • high anion gap
  • seizures
  • crystalluria: Ca oxalate monohydrate
  • anuria/oliguria 1-4 days post ingestion
112
Q

Azotemia vs uremia

A

azotemia: elevated BUN/creatinine
uremia: azotemia + clinical signs

113
Q

Azotemia characterized by decreased blood flow to kidney and high USG
Other findings: increased PCV, RBC, Na, CL, plasma proteins

A

pre-renal azotemia

114
Q

Pre-renal azotemia disease states

A
  • dehydration/hypovolemia
  • high protein diet (creatinine normal)
  • GI hemorrhage
115
Q

Azotemia characterized by decreased GFR and an inadequate USG (>1.008, NOT HYPOSTHENURIC)
Other findings: increased K + P, high anion gap, polyuric/oliguric/anuric

A

renal azotemia - can be masked by dehydration (clinically dehydrated should have max concentrated urine)

116
Q

Azotemia characterized by decreased GFR

Other findings: increased K + Mg, decreased Na, possible uroabdomen

A

post-renal azotemia d/t obstructed outflow/rupture in outflow tract

117
Q

Renal disease without azotemia

A

> 25% functional nephrons

  • need U/A with USG: reduced ability to concentrate in dehydrated animal
  • proteinuria
  • glucosuria without hyperglycemia
  • casts
118
Q

Causes of decreased BUN

A
  • hepatic failure
  • low protein diets
  • overhydration
    NOT indicator of renal disease
119
Q

Causes of creatinine increases

A
  • decreased GFR
  • pre-renal, renal, or post-renal causes that also increase BUN
  • severe muscle damage (myoglobin release)
120
Q

Causes of creatinine decreases

A
  • GFR increased
  • severe muscle atrophy/wasting
  • artifact of increased serum bilirubin (icterus)
  • pregnancy (via increased GFR)
121
Q

Is BUN or creatinine reabsorbed by the renal tubules?

A

BUN only

122
Q

decreased pH
increased PaCO2
increased HCO3

A

respiratory acidemia

123
Q

increased pH
decreased PaCO2
decreased HCO3

A

respiratory alkalemia

124
Q

decreased pH
decreased PaCO2
decreased HCO3

A

metabolic acidemia

125
Q

increased pH
increased PaCO2
increased HCO3

A

metabolic alkalemia

126
Q

Elevated anion gap physiology

A
  • build up of H+ (HCO3 not lost, Cl not conserved

- decreased HCO3, normal Cl (excess other acids)

127
Q

Causes of elevated anion gap (acronym)

A 
"P SKULE"
- phosphates
- sulfates
- ketones
- uremic acid
- lactic acid
- ethylene glycol metabolites
(titrational acidosis = where acids neutralize HCO3)
128
Q

Normal anion gap physiology

A
  • loss of HCO3 and compensation with increased Cl
129
Q

Causes of normal anion gap

A

“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
Q

Low anion gap physiology

A

Not clinically significant, normally d/t hypoalbuminemia

131
Q

Mixed acidosis/alkalosis physiology

A
  • decreased Cl and normal to increased HCO3
132
Q

Causes of mixed acidosis/alkalosis

A
  • combined alkalosis + high AG acidosis
  • high GI obstruction and lactic acidosis from shock
  • renal failure and vomiting that increases HCO3
133
Q

Two types of metabolic acidosis and associated anion gap

A
  • loss of HCO3 (conserve Cl) = normal anion gap

- build up of acids (HCO3 normal, Cl not conserved) = elevated anion gap

134
Q

Renal failure is an example of what type of acid/base disturbance?

A

metabolic acidemia

135
Q

Renal causes for increased potassium

A
  • anuric/oliguric RF
  • CKD in horses
  • uroabdomen
  • addison’s
  • hypoaldosteronism
136
Q

Renal causes for decreased potassium

A
  • increased aldosterone
  • increased distal tubular flow rate
  • renal tubular disease
  • polyuric RF
137
Q

Renal causes for increased sodium

A
  • osmotic/chemical diuresis

- RF

138
Q

Renal causes for decreased sodium

A
  • 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
Q

Urine dipstick: + bilirubin

A

NEVER NORMAL IN CATS

  • liver disease
  • hemolysis
  • pigmenturia, GI contamination
140
Q

Urine dipstick: + heme

A
  • RBCs (RBC in sediment, unless small # lysed d/t hyposthenuria)
  • damaged myocytes (clear plasma)
  • hemolysis (pink plasma)
  • catheterized sample or sperm present
141
Q

Urine dipstick: + glucose

A

INTERPRET WITH BG

  • without hyperglycemia = Fanconi syndrome
  • stress induced hyperglycemia in cats
  • vitamin C or cleaners
142
Q

Urine dipstick: + ketones

A
  • diabetes mellitus
  • bovine ketosis
  • pregnancy
  • NEB
143
Q

Urine dipstick: pH

A

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
Q

Urine dipstick: + protein

A

INTERPRET WITH USG + pH

  • blood in urine
  • hemorrhage (must have heme 3+)
  • glomerular or tubular disease
  • catheterized sample, alkaline, concentrated or sperm present
145
Q

Urine sediment: squamous epithelial cells

A
  • lower UT contamination from voided or catheterized samples
146
Q

Urine sediment: transitional epithelial cells

A
  • from bladder and proximal 2/3 urethra
147
Q

Urine sediment: caudate epithelial cells

A
  • pyelonephritis
  • calculi/stones in renal pelvis
    VERY SIGNIFICANT
148
Q

Urine sediment: renal tubular epithelial cells

A
  • renal damage or inflammation (tubular nephritis)

BIG DEAL, but hard to dx

149
Q

Urine sediment: casts in general

A
  • typically an early indicator of renal tubular disease

- counted per 10X

150
Q

Urine sediment: hyaline casts

A
  • renal dysfunction

- low # with exercise, hyperthermia

151
Q

Urine sediment: epithelial/cellular casts

A
  • nephritis/pyelonephritis (would expect USG to be low)

- there is also WBC casts

152
Q

Urine sediment: granular casts

A
  • normal degenerative process if 0-1/LPF

- renal tubular damage

153
Q

Urine sediment: waxy casts

A
  • chronic tubular lesion d/t local tubular obstruction, oliguria, CKD
154
Q

Urine sediment: fatty casts

A
  • often seen in cats

- hyperlipidemia: diabetes mellitus, nephrotic syndrome

155
Q

Urine sediment: hemoglobin casts

A
  • intravascular hemolysis (hemoglobinemia, hemoglobinuria) - usually something else going on at same time (DIC, renal ischemia)
  • post-transfusion
156
Q

Urine sediment: pseudocasts

A
  • mucous threads from horses

- microscopic fibers from dirty animals

157
Q

Progression of casts

A

cellular - coarsely granular - finely granular - waxy

158
Q

Urine sediment: calcium carbonate crystals

A

“radiant spheres/dumbells”

  • alkaline urine
  • normal in horses, rabbits, GP, elephant = excrete calcium in urine (RF if not seen!)
159
Q

Urine sediment: MAP/struvite crystals

A

“coffin lids”

  • alkaline urine
  • secondary to UTI in dogs
  • sterile cystitis in cats
  • refrigerated/storage
160
Q

Urine sediment: amorphous phosphate crystals

A

“sand”

- clinically insignificant

161
Q

Urine sediment: amorphous urate crystals/urates

A

“brown small spheroids or flat prisms of various shapes”

  • acidic urine
  • Dalmation, English Bulldogs = metabolic disorder, defective purine metabolism
162
Q

Urine sediment: dihydrate calcium oxalate crystals

A

“envelopes”

  • calciuresis = Cushing’s
  • can be normal usually NBD, oxalate containing plants
  • storage at RT/refrigerated
163
Q

Urine sediment: monohydrate calcium oxalate crystals

A

“picket fence posts”

  • acute ethylene glycol poisoning (3-18 hr post-ingestion)
  • calciuresis
  • storage
164
Q

Urine sediment: ammonium bitrate crystals

A

“golden-brown thorny apple”

  • severe hepatic disease: portovascular malformations, sago palm toxicity
  • Dalmatians, English bulldogs (uncommon)
165
Q

Urine sediment: bilirubin crystals

A

“reddish-brown granules or needle-like”

  • low # normal in canine urine (esp males, highly concentrated)
  • always significant in cat
  • liver disease
  • extravascular hemolysis
166
Q

Urine sediment: cystine crystals

A

“colorless hexagons”

  • LOOK FOR UROLITH
  • inherited defect in proximal tubule reabsorbing cystine
  • breed: Dachshunds, Enlish Bulldogs, Newfies, Siamese, Chihuahuas, Rottweilers
167
Q

Urine sediment: sulfa crystals

A

“haystack bundles or radiant spheres - pale yellow”

- sulfa-containing drugs

168
Q

Which stones can be diagnosed via radiographs - must check on ultrasound

A

cysteine

urates - amorphous, urates, ammonium biurate

169
Q

Lipid droplets on UA are common in which specie(s)?

A

cats - produced by tubular epithelium

170
Q

Two parasites seen on UA?

A
  • pearsonema place

- dioctyophyma renale

Clinical Pathology 2017 (4 decks)

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