Clinical Pathology Flashcards

1
Q

Where is albumin produced and what is its major function?

A

Albumin is made in the liver and is slightly bigger than pores separating blood and urine. It serves to regulate oncotic pressure and is cleared by metabolically active tissue

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2
Q

What types of proteins make up globulins?

A

-Immunglobulins
-Complement proteins
-coagulation proteins
-haptoglobulin
-transferrin

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3
Q

Where are globulins made and what do they primarily do?

A

Globulins are made by B lymphocytes, plasma cells, and by the liver
They most function during inflammatory responses

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4
Q

What are positive acute phase proteins?

A

Most globulins

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5
Q

What are negative acute phase proteins?

A

Albumin

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6
Q

What are positive delayed response proteins?

A

immunoglobulins

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7
Q

T/F Negative delayed response proteins don’t really exist

A

True

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8
Q

What are the three methods we can measure total proteins?

A

Refractometer
Chemistry
Electrophoresis

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9
Q

What are common causes of panhypoproteinemia?

A

-hemorrhage
-protein losing enteropathy

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10
Q

What are common causes of selective hypoalbuminemia?

A

-Inflammation
-protein losing NEPHROPATHY
-liver failure

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11
Q

What are common causes of selective hypoglobulinemia?

A

Failure of passive transfer

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12
Q

What are common causes of panhyperproteinemia?

A

DEHYDRATION

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13
Q

What are common causes of selective hyperalbuminemia?

A

Dehydration

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14
Q

What are common causes of selective hyperglobulinemia?

A

-inflammation
-b cell lymphoma
-plasma cell neoplasia

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15
Q

What is indicated by polyclonal gammopathy?

A

antigenic stimulation

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16
Q

What is indicated by monoclonal gammopathy?

A

lymphoid neoplasia

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17
Q

When are EDTA tubes selected for fluid collection?

A

Fluid analysis and cytology

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18
Q

When are tubes with no additive selected for collection?

A

Culture
Biochemical testing

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19
Q

What are the two important to note based on gross appearance of fluid?

A

Color
Clarity

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20
Q

What are important measured concentrations of fluid analysis?

A

Total protein
Total nucleated cell count
RBC count

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21
Q

What are important things to ID upon microscopic examination of fluid?

A

Cell ID
Infectious agents
Acellular material

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22
Q

What percentage of a normal, healthy, adult animal’s weight is composed of water, how does this change in neonates?

A

In adults, 60% of weight is comprised of water
In neonates, this number reaches 80% (D+ more severe and can lead to death

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23
Q

What composes extracellular fluid?

A

1/3 of total body water
Blood
Intracellular fluid
Transcellular fluid
GI tract

24
Q

What composes intracellular fluid?

A

2/3 of total body water
Fluid within cells

25
Q

What are 3rd spaces?

A

Abdominal cavity, pleural space, pericardial space

26
Q

What are distinguishing factors of pure (protein poor) transudate?

A

Appearance: clear, colorless, light yellow
TP: <2.0 g/dL
TNCC: < 1,500/microL
Typically mononuclear
Pathogenesis: Dec. oncotic pressure, inc. capillary hydrostatic pressure, dec lymphatic drainage
Etiologies: protein losing nephropathy, protein losing enteropathy, liver failure

27
Q

What are distinguishing factors of modified (protein rich) transudate?

A

Appearance: clear, hazy, or cloudy, usually yellow
TP: > 2.0 g/dL
TNCC < 5,000 /microL
typically neutrophils present
Pathogenesis: inc capillary hydrostatic pressure, dec lymphatic drainage
Etiology: hypertensive disorders, lymphadenopathy, FIP etc

28
Q

What are distinguishing factors of septic exudate?

A

Appearance: hazy, cloudy, flocculent, yellow, tan, cream, orange
TP: >2.0 g/dL
TNCC: >5,000 /microL
Neutrophils and infectious agents
Pathogenesis: inc interendothelial spaces and diapedesis of neutrophils
Etiologies: Visceral tissue (IN -> OUT)
-pleuropneumonia, esophageal perf, GI perf/necrosis, ruptured bladder
Parietal tissue (OUT -> IN)
-penetrating wounds/FB, hematogenous

29
Q

What are distinguishing features of sterile exudate?

A

Appearance: hazy, cloudy, yellow, tan, cream, orange
TP: > 2.0 g/dL
TNCC: >5,000/microL
Neutrophils, but NO infectious agents
Pathogenesis: Inc. interendothelial spaces, diapedesis of neutrophils
Etiologies: pancreatitis, enteritis/colitis, displaced organs/tissues, ruptured bladders, FIP, neoplasia

30
Q

What are distinguishing features of hemorrhagic effusions?

A

Appearance: opaque, red
TP: > 2.0 g/dL
RBC: >1,000,000 / microL
Looks like blood smear upon microscopic examination with erythrophagia and hemosiderin
Pathogenesis: leakage of blood
Etiology: Trauma, displaced organs/tissues, hemorrhaging neoplasms, coag disorders, idiopathic

31
Q

What are distinguishing features of a chylous effusion?

A

Appearance: hazy, cloudy, opaque, pinkish white, white
TP: > 2.0 g/dL
TNCC: variable
small lymphocytes
Chemistry: triglycerides >100mg/dL
Pathogenesis: leakage of lymphatics that drain the GI tract
Etiology: idiopathic, trauma, heart disease, displaced organs/tissues, lymphadenopathy, neoplasms

32
Q

What are distinguishing features of a uroperitoneum/uroabdomen?

A

Appearance: clear, hazy, cloudy, pale yellow, yellow
TP: variable
TNCC: variable
Micro. exam: variable
Fluid Chemistry: creatinine
Pathogenesis: ruptured bladder
Etiologies: uroliths, mucus plugs, trauma, neoplasms

33
Q

What are distinguishing features of a bilious effusion?

A

Appearance: hazy, cloudy, flocculent, yellow, tan, orange, green, brown
TP: > 2.0 g/dL
TNCC: >5,000 /microL
Bile on micro examination
Fluid chemistry: Bile
Pathogenesis: ruptured biliary tract
Etiology: choleliths, mucocele, trauma, neoplasms

34
Q

What are distinguishing features of a neoplastic effusion?

A

Appearance: clarity and color is variable
TP: variable, but often > 2.0 g/dL
TNCC: variable, but often > 5,000 /microL
Neoplastic cells on microscopic examination

35
Q

What are the 4 types of noninflammatory cells?

A
  1. Round: individualized and rounf
  2. Epithelial: cell to cell, individualized, round, polygonal
  3. Mesenchymal: Matrix, individualized, spindle, stellate
  4. Naked nuclei: fragile cells with invisible borders, round nuclei, uniform nuclei
36
Q

What are the criteria of malignancy?

A
  1. Anisokaryosis (variation in size of nuclei)
  2. Pleomorphism (variability in size and shape)
  3. High nucleus to cytoplasm ratio (N:C)
  4. Mitotic figures present
  5. Atypical nuclei
  6. Coarse chromatin
  7. Nuclear molding (adjacent cell nuclei conform to eachother)
  8. Multinucleation
37
Q

What are key features of enzymes?

A

-measure in serum or plasma
-catalyze cellular reactions
-originate from cells
-measure ACTIVITY, not quantity
-induced or “leakage”
-tissue and species specificity
-varied half life
-only worry about increases not decreases

38
Q

What can cause increased enzymatic activity?

A

-Injury (leakage): bleb, leak, necrosis
-Induction
-Decreased clearance
-Hyperplasia
-Ingestion
-Xenobiotic or endogenous chemical induction

39
Q

Creatine Kinase

A

Results from cell injury
Muscle and hemolysis
Short half life (2-3 hrs)

40
Q

AST

A

Cell injury
Liver and muscle and hemolysis
Small and large animals

41
Q

SDH

A

Cell injury
Liver
Replaces ALT for animal
Sample handling is critical

42
Q

ALT

A

Cell injury
Mostly liver specific
Small animal specific

43
Q

GGT

A

Induced
Hepatobiliary
Cholestasis -> decreased bile flow

44
Q

ALP

A

Induced
Hepatobiliary
Cholestasis -> Decreased bile flow
SMALL ANIMALS ONLY
1. Tissue unspecific isoenzyme
liver, bone, placenta, renal
2. Intestinal isoenzyme
GI, K9 c-steroid induced

45
Q

cALP

A

DOGS ONLY
Intestinal ALP gene, but in liver
Drug induced production
-corticosteroids, phenobarbital, or cholestasis

46
Q

Canine ALP Interpretation

A

< 4x increase -> nonspecific
>4x increase -> cholestasis and/or glucocorticoids, anticonvulsants

47
Q

LPS

A

Cell injury
Exocrine pancreases (pancreatitis)
2 hr half life in canines
Use in conjunction with amylase
Pancreatitis -> increase 3-8X
Corticosteroids -> increase up to 5X

48
Q

PLI

A

Cell injury
More specific for exocrine pancreases than LPS
cPLI -> canine pancreatitis

49
Q

AMS

A

Cell injury
Exocrine pancreases (pancreatitis) and other tissue types

50
Q

T/F Acids donate H+ while bases accept H+

A

True

51
Q

What are normal blood pH parameters and what qualifies as alkalemia and acidemia?

A

Normal Blood pH: 7.35-7.45
Alkalemia: pH > 7.45
Acidemia: pH < 7.35

52
Q

How is blood pH metabolically regulated?

A

Kidneys: Excrete H+, retain HCO3-, take hours to days
Blood Buffers: Titrate H+ in seconds

53
Q

What are the metabolic acid base testing options?

A

Blood gas: pH, Bicarbonate (HCO3-)
Biochemistry: TCO2, anion gap, sodium vs. chloride
Urinalysis: Urine pH

54
Q

What are respiratory acid base testing options?

A

Blood gas: pH, pCO2

55
Q

What are requirements for testing blood gas?

A

-Heparinized whole blood
-Patient body temp
-Anaerobic conditions and ready for rapid processing