Veterinary Clinical Pathology

Course instructors

• Melinda Wilkerson, DVM, MS, PhD, ACVP (Anatomic/Clinical pathology)
  • Professor and co-course director
  • Office location: St. George’s Hall, Rm 219
  • Email: mwilkers@sgu.edu
  • Office telephone number: +1473 439 2000 xtn 3673
  • Office hours: email to schedule an appointment or online weekly office hours  
• Richard M. Kabuusu, DVM, MPH, CPH, PhD
  • Professor and co-course director
  • Office location: St. George’s Hall, Rm 215
  • Email: rkabuusu@sgu.edu
  • Office telephone number: +1473 439 2000 xtn 3672
  • Office hours: schedule an appointment via email
• Dawn Seddon, BVSc, MSc (VetPath), ACVP (Clin Path), MRCVS, NHD Micro Professor
  • Office location: St. George’s Hall, Rm 211
  • Email: dseddon@sgu.edu
  • Office telephone number: +1473 439 2000 xtn 3676
  • Office hours: email to schedule an appointment possible weekly office hours if online

Laboratory Technicians:

• Ms. Ruth Alexander, BSc.
  • ​​​​​​​Office location: Clinical Pathology Laboratory
  • Email: ralexander@sgu.edu
  • Office telephone number: +1473 439 2000 xtn 3489
•  Ms. Lucinda Ogilvie
  • Office location: Clinical Pathology Laboratory
  • Email: logilvie@sgu.edu
  • Office telephone number: +1473 439 2000 xtn 3540     

Secretary:

• Ms. Cindy Edwards 
  • Office location: St. George’s Hall, Rm 22
  • Email: cedwards@sgu.edu, Office telephone number: +1473 439 2000 xtn 3339

Sis Hall (East)

• Online location—Sakai resources (i.e. Resources will contain ppt pdfs and supplemental materials, Panopto for recordings, Zoom links for online Labs and office hours, Lessons for lectures and labs – particularly the Chemistry section after Midterms, Tests & Quizzes for formative and Lab quizzes).  
• Top Hat will be used for the first half of the course (Hematology, Hemostasis, and Cytology) - Lessons in Sakai will be used for all chemistry / endocrinology & urinalysis

• Resources:  pdfs of the power-point lectures, panoptos will also be recorded.
• Laboratory activities and explanations will be provided in Lesson Pages in Sakai
• Supplemental resources will be available in Sakai resources and in some cases in Lesson Pages

• Laptop specs need functional microphone and camera
• Thrall MA, Weiser G, Allison RW and Campbell TW. (2012). Veterinary hematology and clinical Chemistry, 2^nd Edition. Wiley-Blackwell.
• **Stockham SL and Scott MA (2008). Fundamentals of veterinary clinical pathology. 2^nd Edition.  Blackwell Publishing (Dr. Wilkerson follows this textbook very closely)  
• *eclinpath website; online textbook. Website: http://www.eclinpath.com/  
• Villers E, Ristic J and Blackwood L (2016).  BSAVA manual of canine and feline clinical pathology.3^rd Edition. https://mycampus.sgu.edu/group/mycoach-vet/integrating-example

1. Students with disabilities who need accommodations should contact Student Accessibility and Accommodations Services (SAAS), located in the Welcome Center, inside the International Students Office.  
2. Information can be found at mycampus.sgu.edu/group/saas

Daily, veterinarians mostly in small and large animal practice, but in other practices (diagnostics, research, teaching, exotics) are required to select appropriate tests and reliable referral laboratories for common and rare diseases of their patients. They are expected to collect specimens that include (but not limited to), blood, urine and fine needle aspirates and to ensure that the samples are examined before they deteriorate, and thereby yielding inaccurate or misleading results. Most importantly veterinarians are expected to interpret results correctly with due regard to biological and non-biological factors which can influence results. Generally, clinical pathology, sometimes known as laboratory medicine, allows the veterinarian to evaluate the status and function of internal organs by assessing and interpreting laboratory analyte results from whole blood, serum or plasma, urine, and fluids, and cytologic samples. Clinical pathology, the subspecialty that deals with the use of laboratory methods (clinical chemistry, hematology, urinalysis, cytology) for the diagnosis and treatment of disease, is integral to nearly all diagnostic investigations.

Upon successful completion of this course, the student will be able to:

CLOA. Identify and explain the most common pre-analytical and analytical errors and principles of select laboratory analytes 

CLOB. Interpretation of Lab Data by identifying/recognizing abnormalities/patterns, applying concepts, and classifications.

CLOC. Describe/recognize the pathogenesis (the series of events that lead to the disease or pathologic state) of the laboratory data abnormalities and propose pathologic states, physiologic conditions, or specific diseases that might cause the abnormalities

CLOD. Identify/recognize cells, artifacts  and urinary sediment findings (crystals, casts, etc) microscopically, digitally or abnormalities in cells that are of diagnostic/pathologic importance including microscopic features of cells in blood films, cavitary effusions, urine and aspirates from lesions in tissues (marrow, lymph nodes, & common inflammatory or neoplastic lesions.

Detail description of CLOs

CLOA. Explain pre-analytical and analytical errors and principles of laboratory analytes. A student should be able to explain when the reported laboratory data represent poor sample handling, poor sample quality, unique sample properties, or the limitations of an analytical procedure when there are interferents or errors. A student show also be able to describe the basis of the analytical principle of the assay for each laboratory analyte that is described in the lecture content. 

CLOB. Be able to interpret Laboratory Data, there are two recurring tasks for the cases.

• State appropriate terms to describe abnormalities and use classifications if appropriate (e.g., acute inflammatory leukogram, renal azotemia, hypernatremia or hypoglycemia)
• Propose appropriate pathologic states, physiologic conditions, pathologic syndromes, or specific diseases that might cause the defined abnormalities. The specificity of the proposed disorders should be appropriate for the available information (or the conclusion that can be justified); e.g., the leukogram justifies a conclusion that the animal has an inflammatory disease (but do not know where, why, or the cause), or the data can justify a conclusion of acute bacterial cystitis.

CLOC. Describe pathogeneses of laboratory data found in common clinical disorders and conditions (most objectives of this course fall into this area).

• Be able to identify or distinguish how a variety of clinical disorders and conditions can produce the same laboratory test result.
• Describe the hows and whys of pathogenic states so that laboratory data can provide clues to the variety of clinical disorders and conditions that occur in animals. Pathogenesis (patho- disease; -genesis origin, creation, production) is the sequence of events that occur during the development of or the response to a disease. In the context of clinical pathology, pathogenesis of laboratory data starts with the initial pathologic event that causes changes in tissues, cells, or body fluids which eventually produce abnormal laboratory data.

The different pathogenesis levels can be divided as follows.

• Organ: changes in an organ that creates the abnormal laboratory data – rarely an adequate explanation in this course
• Cellular: what happens to cells; or how do cells create the abnormality – common level for abnormal cell concentrations or the microscopic features of cells
• Physiologic: what are the cellular or physiologic responses to hormones, to tissue damage, or to cellular or tissue dysfunction – common level for clinical chemistry abnormalities 
• Biochemical: what happens in biochemical pathways – occasional level for either clinical chemistry abnormalities or microscopic features of cells
• Molecular: what happens with a molecule’s interaction with other molecules – this level of understanding is usually not needed for clinical disorders or conditions
• Other major pathogenesis concepts should be remembered when describing the processes that result in abnormal laboratory data.
• An abnormal analyte concentration in a body fluid typically represents a disruption of equilibrium. Blood concentrations in health reflect a balance between an analyte entering the blood and the analyte leaving the blood. An abnormal concentration indicates an imbalance in those processes.
• An abnormal analyte concentration in a body fluid was caused by either an initial event (e.g., pathologic, physiologic, or pharmacologic) or a physiologic response to the initial change (e.g., destruction of pancreatic β-cells leads to decreased insulin release which lead to decreased glucose utilization by cells which leads to hyperglycemia). Therefore, to understand pathogeneses, we need to know what the initial event is.
• When considering potential reasons for abnormal blood analyte concentrations, one should think of basic processes that might cause such concentrations.
  • If there is an increased analyte concentration, is it due to increased rate of entering blood (if so, how?) or a decreased rate of leaving blood (if so, how?).
  • If there is a decreased analyte concentration, is it due to decreased rate of entering blood (if so, how?), an increased rate of leaving blood (if so, how?), or destruction within the blood (if so, how?).

CLOD. Be able to identify normal and abnormal cells. A student should be able to identify cells or abnormalities in cells that are of diagnostic importance using a microscope. This would include microscopic features of cells in blood films, cavitary effusions, and aspirates from lesions in tissues (marrow, lymph nodes, & common inflammatory or neoplastic lesions.

1. Introductory concepts  

1. Identify and/or differentiate between blood samples and blood tubes necessary for          hematology, coagulation, or chemistry assays
2. Identify examples of qualitative, semi-quantitative, and quantitative types of assays
3. Define reference intervals and describe how they are obtained.  
4. Identify which analytes have Gaussian and/or non-Gaussian reference interval distributions and what these look like graphically
5. Distinguish between preanalytical, analytical, and post analytical errors
6. Define analytical precision, accuracy, analytical sensitivity, analytical specificity and detection limit properties of assays
7. Introduction to CBC (Erythrogram, leukogram, thrombogram)

2. Erythrocytes (Review erythron pools, iron, and Classify Anemias) 

1. Define the function of the bone marrow and the tissue pools and contrast species differences in the spleen 
2. Describe the transport of iron to erythroblasts and identify tissue stores
3. Define and identify reticulocytes and polychromatophils on blood films with or without special stains and explain their significance
4. Interpret erythrocyte data and provide a classification of the anemia using marrow responsiveness ([Retic]), morphologic criteria (Wintrobe Indices) or pathophysiologic criteria

3. Erythrogram (Wintrobe Indices)

1. Recognize which analytes impedance analyzers measure (MCV, RBC, Hgb) and define the significance of the analytes
2. Recognize which analytes are calculated by analyzers (HCT, MCHC, MCH) and describe how they can be affected by lipemia, hemolysis, or agglutination
3. Be able to calculate absolute reticulocyte concentration from [RBC] and Retic.percentage

4. Erythrocytes morphology of RBCs and hemoparasites

1. Identify on blood films and define significance of discocytes, rubricytosis, hypochromia, anisocytosis (macrocytes, microcytes, spherocytes) and inclusions such as basophilic stippling & Howell jolly bodies 
2. Identify on blood films and define significance of abnormal erythrocyte shapes (poikilocytes): schizocytes, spherocytes, ecchinocytes, elliptocytes, codocytes, acanthocytes, eccentrocytes, pyknocytes, keratocytes
3. Identify hemoparasites on blood films (Anaplasma marginale, A. centralie, Cytauxzooan, Babesia, Mycoplasmas sp.) and recognize which animal species they infect

5. Nonregenerative & regenerative anemias

1. Identify disorders that cause nonregenerative anemias (inflammation, renal failure, bone marrow disease such as erythroid hypoplasia or ineffective erythropoiesis)  
2. Describe pathogenesis of nonregenerative anemias due to inflammation, renal failure, bone marrow disease
3. Identify the disorders that cause regenerative anemias (blood loss and hemolytic anemia) 
4. Describe the pathogenesis of acute and chronic blood loss disorders (iron deficiency)
5. Describe the pathogenesis of extravascular and intravascular hemolytic anemias and the identify the clinical and blood film findings associated with each

6. Analytical Methods In-Office Hematology (Dr. George Daniel, Abaxis – if time permits, information will be online and prerecorded)

a. Describe the basic principles of hematology analysis of red blood cell mass [RBC], [Hct], [Hgb], WBC, and Platelets using:

• Impedance analyzes* (SGU uses these analyzers, Most important)
• Dual impedance/optical or flow cytometry-based analyzers
• Be able to interpret the platelet histogram for clumps

7. Hemolytic anemia disorders

1. Identify the disorders that cause hemolytic anemia (immune mediated, infectious agents, erythrocyte metabolic defects due to oxidative injury, vasculitis or causes of fragmentation anemia)
2. Explain the difference between Rouleaux and agglutination, clinical significance and which laboratory tests can differentiate (saline replacement test)
3. Identify the tests to determine if immune mediated hemolytic anemia is present (Coombs tests or flow cytometry for dog erythrocyte IgG)
4. Describe pathogenesis and expected erythrocyte morphology with:
   1. Immune mediated  o Infectious agents
   2. erythrocyte metabolic defects due to oxidative injury results in Heinz body anemia, hypophosphatemia, eccentrocytic anemia 
   3.  erythrocyte fragmentation

8. Erythrocytes (Fe tests/Erythrocytosis)

1. Interpret [Fe], TIBC, ferritin, and stainable Fe in the context of Fe deficiency, inflammation, and hemolysis. 
2. Identify erythrocytosis in a CBC
3. Describe the pathogenesis of erythrocytosis

9. Intro to Leukocytes (pools, migration, analytic principles, and neutrophil shifts)

1. Describe the myeloid bone marrow pools and time spent in each neutrophil pool in health and during inflammation (monocyte pools are similar)
2. Describe and contrast 3 lymphocyte migration paths 
3. Describe how [nRBC] > 10 interferes with [WBC]
4. Describe how you determine differential white cell counts and concentrations
5. Define left shifts of neutrophil concentrations (regenerative vs degenerative) and the clinical significance
6. Describe reasons for hypersegmented neutrophils

10. Leukocytosis (Neutrophilia, lymphocytosis, monocytosis, eosinophilia, and basophilia)

1. Describe features of toxic neutrophils and the clinical significance (i.e. accelerated neutropoiesis) 
2. Recognize leukogram patterns (acute inflammatory, chronic inflammatory, steroid (stress) and physiologic) in a CBC
3. Describe the pathogenesis of acute inflammatory, chronic inflammatory, steroid (stress) or physiologic leukograms
4. List diseases and conditions that cause lymphocytosis.
5. Describe pathogenesis of chronic lymphocytosis, physiologic (shift) lymphocytosis, and lymphoproliferative lymphocytosis
6. Describe reactive lymphocytes and significance
7. List common causes of monocytosis, eosinophilia, and basophilia

11.  Leukopenia (neutropenia and lymphopenia)

1. List diseases and conditions that cause neutropenia.
2. Describe pathogenesis of inflammatory (overwhelming) neutropenia
3. Describe pathogenesis of granulocytic hypoplasia
4. List diseases and conditions that cause lymphopenia.
5. Describe pathogenesis of inflammatory lymphopenia, stress lymphopenia, and depletion lymphopenia

12. Leukocytes, abnormal morphology, organisms, and leukemia

1. Describe and identify leukocyte organisms
2. Describe and contrast myeloid, lymphoid, erythroid, and megakaryocytic leukemia
3. Recognize CD molecules that distinguish acute from chronic leukemia
4. Identify CD molecules that distinguish myeloid from monocytic from lymphocytic (T and B cell) leukemias
5. Recognize the purpose of the PARR test

13. Thrombogram (analytical principles, thrombocytopenia and thrombocytosis)

1. Identify/describe the basic physiology and functions of platelets
2. Describe the analytical principles of determination of platelet concentration via impedance, optical, and manual methods (slide estimate)
3. Describe the preanalytical causes of platelet clumping and how it effects the accuracy of the platelet concentration
4. Identify/recognize canine breeds (e.g. CKC) that have macroplatelets and pseudothrombocytopenia
5. List the causes of thrombocytopenia
6. Describe the pathogenesis of immune medicated and consumptive thrombocytopenia.
7. Describe the pathogenesis of inflammatory, Fe deficiency, and exercise induced thrombocytosis

14.  Proteins Introductory concepts

1. Describe production sites for proteins
2. Describe physiologic functions and clinical importance of albumin, globulins, fibrinogen
3. Define Inflammatory protein groups (Acute phase proteins and Delayed response)
4. Describe analytical principles of measuring TP (plasma and serum), albumin, globulin, and fibrinogen o Observe video and describe how to perform a plasma total protein by refractometer
   • Recognize interferences in refractometry (other total solids-glucose, urea, and electrolytes) and BCG (globulins)
   • Be able to interpret serum protein electrophoresis (SPE) patterns
   • Differences between total solids concentration and total protein concentration 

15. Proteins Hyper and hypoproteinemia

1. Define and explain processes that cause dysproteinemias (hyperproteinemia and pathologic states)
2. Interpret serum and plasma protein concentrations that indicate:
   1. Protein loss e.g. PLD, PLN, PLE, decreased synthesis or protein catabolism 
3. Describe the pathogenesis of the serum/plasma protein concentrations in  PLD, PLN, PLE, decreased synthesis or protein catabolism (hepatic insufficiency, malabsorption, cachexia) 

16: Overview of hemostasis 

1. Describe the process that leads to the formation of a platelet plug
2. Outline the main function of platelets in primary hemostasis
3. Outline the antithrombotic and prothrombotic properties of endothelial cells 
4. Outline the main goal of secondary hemostasis
5. Outline the main regulatory proteins of the secondary hemostasis   
6. Describe the main steps of the cell-based model of thrombin generation
7. Compare and contrast cell-based model and coagulation cascade 
8. List the role (and factors) of the contact pathway 
9. Outline the main goal of tertiary hemostasis (fibrinolysis)
10. Outline the main regulatory proteins of the tertiary hemostasis
11. List the anticoagulant properties of thrombin
12. List major differences between bleeding and thrombosis

17: Laboratory evaluation of hemostasis disorders

1. Interpret tests used to assess thrombi formation and/ or antithrombotic processes   
2. Interpret CBC and coagulation test results in clinically healthy animals 
3. List and interpret qualitative tests used to assess primary hemostatic disorders 
4. List and interpret quantitative tests used to assess primary hemostatic disorders
5. List and interpret tests used to assess intrinsic and common pathway disorders 
6. List and interpret tests used to assess extrinsic and common pathway disorders
7. List and interpret tests used to assess common pathway
8. List and interpret tests used to assess fibrinolysis  

18: Disorders of hemostasis 

1. List hemorrhagic patterns associated with primary hemostatic disorders
2. List hemorrhagic patterns associated with secondary hemostatic disorders 
3. Describe the main clinical pathology abnormalities of primary hemostatic disorders
4. List key differential diagnoses for extrinsic pathway disorders 
5. List major differentials diagnoses for intrinsic pathway disorders
6. List some differential diagnoses for primary hemostatic disorders
7. Outline the major causes of thrombosis
8. Describe the relationship between hemostasis and inflammation

19: Principles of cytological examination

1. Describe good aspiration, imprint and smearing techniques
2. List the indications, advantages for cytology, and limitations
3. Outline the “systematic approach” to the interpretation of cytologic specimens
4. Describe characteristics of good cytologic preparations
5. Describe characteristics of non-diagnostic preparations
6. Recognize artifacts in cytologic preparations
7. Describe common cytological stains and staining procedures

20: Characteristics of inflammatory processes

1. Apply “cytologic algorithm” criteria to cutaneous masses
2. Describe the components of inflammatory processes
3. Recognize common microorganisms in septic inflammatory lesions
4. Memorize specific stains used to identify organisms
5. Recognize degenerate neutrophils
6. Recognize non-degenerate neutrophils
7. Describe the biologic behavior of neoplastic lesions

21: Characteristics of neoplasms and lymph node-aspiration

1. Outline features (criteria) for malignancy
2. Identify features of epithelial, neuroendocrine and mesenchymal cell neoplasms
3. Recognize round cell neoplasms in images and cytology preparations
4. List examples of benign neoplasms
5. List the various round cell neoplasms
6. List the biologic behavior of round cell neoplasms 
7. Describe distinct features of round cell neoplasms
8. List some special stains for round cell neoplasms
9. List specific antigen markers for common neoplasms
10. List the common indications for lymph node aspiration
11. Categorize lymphadenopathy based on cytology 
12. List advanced diagnostic techniques for lymphomas

22: Cytology of selected internal organs and respiratory tract 

1. List the common indications for aspiration of internal organs and the risks
2. Recognize the major features of neoplastic or inflammatory lesions
3. Stage estrus in a dog based on cytologic findings 
4. Recognize the major cytologic findings in the prostatic diseases
5. List common cytologic findings in major hepatopathies 
6. List the sampling techniques for the respiratory tract
7. Recognize oro-pharyngeal contamination of samples
8. Classify respiratory samples as neoplastic or inflammatory based on images 
9. List or identify common gastrointestinal cytologic findings

23: Pathogenesis of body cavitary effusions

1. Outline the major mechanisms for analyzing fluids
2. Discuss the pathogenesis of fluid accumulation within these spaces
3. Differentiate between protein-poor and protein-rich transudates
4. Describe the relationship between renal failure and fluid accumulation
5. Differentiate between neoplastic and inflammatory effusions 
6. Recognize mesothelial cells 
7. List several causes and features of protein-poor transudates 
8. List several causes and features of protein-rich transudates

24: Specific body cavitary effusions

1. List several causes and features of exudates
2. List major causes and features of septic exudates
3. Differentiate between neoplastic and inflammatory effusions
4. Differentiate iatrogenic from pathologic hemorrhage
5. Differentiate chyle from pseudochyle
6. Classify equine peritonitis based on cytological findings
7. Describe cytologic features of FIP 
8. Describe cytologic features in uropreritoneum
9. Describe cytologic features in bile peritonitis

25: Synovial fluid cytology and cerebrospinal fluid

1. Describe the collection and handling of synovial fluid
2. Describe the major cells in normal joint fluid
3. Describe the major cells in acute and chronic arthritis
4. Differentiate thixotropism from mucin clot)
5. Describe techniques unique to joint fluid analysis
6. Describe the collection and handling of CSF samples
7. Explain the basis for urgent analysis of CSF
8. List the key elements and unique tests of CSF analysis
9. Describe the common findings in “normal” CSF
10. Explain the underlying causes for abnormal findings in CSF

26: Review of hemostasis and cytology

27. Lab evaluation of the Kidney: Concentrating ability of the Nephron (Specific Gravity & Osmolality)

1. Describe or explain the physiologic processes of nephron regarding: GFR, resorption/excretion of water and solutes, osmolality of nephron segments
2. Describe analytical principles of Urine Specific Gravity & Osmolality and their relationship
3. Describe mechanisms of polyuria in various disorders (i. e Chronic renal failure, diabetes mellitus, diabetes insipidus, hypercalcemia, hyperadrenocorticism)
4. Lab Eval Kidney 2   Urinary 
   1. Define azotemia and uremia
   2. Define and recognize acute and chronic renal insufficiency/ failure based on lab data
   3. Interpret UN & CREAT concentrations in serum with/without USG_ref and urinalysis;  o Describe mechanisms of pre-renal, renal, and post renal azotemia  o List tests that evaluate renal disease 
5. Interpret Urinalysis data regarding: 
   1. physical characteristics of urine, qualitative or semi-quantitative chemical characteristics of urine (pH, protein, glucose, ketone, bilirubin, urobilinogen, heme)
   2. USG_ref - < 1.007, 1.008 – 1.013, > 1.013 in dehydrated states, 
   3. USG_ref > 1.013 when glucosuria or proteinuria is present  
   4. Interpret significance in urine sediment findings (i.e. cells, casts, crystals, organisms)
   5. Interpret Protein/Creatinine Ratio in PLN and hematuria (voided sample)
   6. Differentiate between pre – renal and post renal proteinuria
   7. Urinalysis – Videos for urine chemistry  / sediment  https://www.youtube.com/watch?v=jhmzkUcAbIM  (8mins, 44 secs)
   8. Idexx – the urine sediment examination https://www.youtube.com/watch?v=dswfnZXb3nM  (10mins, 43 secs)

30.Interpret Urinalysis data regarding:

Sediments including cells, crystals, bacteria, casts

31. Electrolytes, total body sodium, Chloride and bicarbonate (HCO₃^- or TCO₂) body water, osmolality

1. Recognize, list, and explain causes of hyper / hypo / normo - natremia, and chloremia
2. Interpret Na and CL- data from a clinical scenario, recognize abnormalities and provide possible pathogenesis (mechanisms). 
3. Calculate and interpret osmolality
4. Interpret serum chemistry data (especially electrolyte and total solute concentrations) that indicate or suggest:
   • Different forms of dehydration (i.e., hypertonic, isotonic, & hypotonic)
   • Hypoadrenocorticism
   • Metabolic acidoses and alkaloses
   • Uroperitoneum
   • Oliguric or anuric renal failure
   • Anorexia
   • Ketoacidotic diabetes mellitus
   • Equine sweating
   • Upper gastro-intestinal obstruction in dogs, cats, or ruminants
   • Lactic acidosis
   • Ethylene glycol toxicosis
5. Recognize, list, and explain causes of increased or decreased bicarbonate.  Be able to interpret HCO₃^- or TCO₂^- data from a clinical scenario, recognize abnormalities and provide possible pathogenesis (mechanisms).

32. Electrolytes K & Anion gap

1. Recognize, list, and explain causes of hyperkalemia and hypokalemia.  
2. Be able to interpret K data from a clinical scenario, recognize abnormalities and provide possible pathogenesis (mechanisms). 
3. Recognize, list, and explain causes of increased or decreased anion gap.  Be able to interpret anion gap (AG) data from a clinical scenario and determine which anions are most likely (i.e. inorganic vs organic) and the conditions responsible.
4. Calculate the AG

33, 34. Blood gases / Acid Base

1. Define Acidemia, Alkalemia, Acidosis, Alkalosis, Hypercapnia, Hypocapnia, Hypoxemia, Hypoxia
2. Interpret blood gas data including:
   • Increases and decreases in plasma pH values
   • Increases and decreases in plasma Paco₂
   • Increases and decreases in plasma Pao₂ • Increases and decreases in serum / plasma HCO₃₋ / Total CO₂ concentrations
3. Interpret blood gas data that indicate or suggest:
   • Metabolic acidosis, with or without compensatory respiratory alkalosis
   • Metabolic alkalosis with or without compensatory respiratory acidosis
   • Respiratory acidosis with or without compensatory metabolic alkalosis
   • Respiratory alkalosis with or without compensatory metabolic acidosis
   • Hypoxemia due to pulmonary disease
   • Hypoxemia due to impaired respiratory exchange of gases
4. Explain, list, or recognize the reasons for:
   • Decreased serum HCO₃₋ concentration due to poor sample handling 
   • Decreased PaCo₂ due to sample being exposed to air or when collected with excess heparin 
   • Increased PaO₂ due to sample being exposed to air or when collected with excess heparin 
   • Decreased PaO₂ and decreased pH when there is delayed analysis of a heparinized blood sample 
   • Increased PaCo₂ due to respiratory disease or disorders that restrict respiration or as a compensation to alkalemia 
   • Decreased PaCo₂ as a response to hypoxemia or acidemia 
   • Acidemia due to disorders that cause lactic acidosis, ketoacidosis, renal failure, or extensive pulmonary disease 
   • Alkalemia due to disorders that cause gastric or abomasal loss of HCl, bovine renal failure, or hypoxemia 
   • Decreased PaO₂ due to pulmonary disease 
   • Increased PaO₂ during gas anesthesia 
   • PaO₂ within reference interval when anemia is causing hypoxia 
   • Tissue hypoxia when there is no hypoxemia 

35, 36. Calcium, magnesium, Vit D, PTH, PTHrp, 

a. Recognize typical total calcium and phosphorus concentrations, and their regulatory hormone [iPTH, PTHrp, vit. D] data that suggest or indicate:

• Primary hyper & hypo -parathyroidism
• Humoral hypercalcemia of malignancy
• Secondary hyperparathyroidism 
• Hypervitaminosis D
• Renal insufficiency/failure in dogs, cats, cattle, and horses
• Milk fever

1. Interpret Ca, fCa Vit D3, and their regulatory hormone data including: o Hypercalcemia and hypocalcemia⁺⁺] in horses compared to other
2. Explain the difference in the regulation of [fCa species.
3. Explain, list, or recognize the physiologic and pathologic processes or mechanisms that cause:
   • Hypercalcemia in hyperparathyroidism, malignancies, cholecalciferol & other toxicosis, equine renal failure, canine hypoadrenocorticism, and canine renal failure, hyperproteinemia 
   • Hypocalcemia in hypoparathyroidism, chronic renal disease (dogs, cats, and cattle), post parturient state or during early lactation, toxic causes
   • Alterations in free Ca²⁺ concentrations due to acidemia or alkalemia  
   • Increased iPTH concentrations due to parathyroid neoplasm, chronic renal disease, or a diet with a low Ca^2+:PO4 ratio, and Increased PTHrp concentrations due to malignancies
   • Explain, list, or recognize the reasons for hypocalcemia due to hypoproteinemia and/or hypoalbuminemia 
   • Pseudo hypocalcemia due to collection of blood into an EDTA anticoagulant 
   • Decreased fCa²⁺ concentration when blood sample collected with excess heparin 
   • Altered fCa²⁺ concentrations when blood or serum sample is not handled anaerobically 

37.  Phosphorus & Magnesium

1. Interpret phosphorus, magnesium, and their regulatory hormone data including:
   • Hyperphosphatemia and hypophosphatemia
   • Hypermagnesemia and hypomagnesemia
2. Hyperphosphatemia due to dehydration, renal failure, uroperitoneum, urinary tract obstruction, hypoparathyroidism, and myopathies 
3. Hyperphosphatemia due to in vitro hemolysis or delayed blood sample handling
4. Hypophosphatemia due to anorexia, hyperparathyroidism, hyperinsulinism, and milk fever 
5. Explain, list, or recognize the reasons for  hypomagnesemia due to hypoproteinemia and/or hypoalbuminemia 
6. Hypomagnesemia due to renal failure 
7. Interpret serum magnesium for

• Decreased GFR
• Hemolysis
• Hypoproteinemia
• Osmotic diuresis
• Ketonuria
• Bovine grass tetany

38. Enzymology including Muscle, Liver, pancreas

1. Define and identify leakage enzymes vs. inducible enzymes
2. Identify different liver enzymes used for evaluating liver disease in small and large animals. 
3. Different enzyme data when assays are performed at different temperatures or with different substrates
4. Interpret serum enzyme data including increased activities of ALP, ALT, AMS, AST, CK, GGT, GMD, ID, LD, and LPS

39.  Muscle

1. Explain, list, or recognize the reasons for:
   • Alterations in AST, LD, or CK activities due to in vitro hemolysis or delayed blood sample handling
   • Increased activities of AST, LD, CK, or ALT due to muscular disorders 
2. Interpret serum enzyme data that indicate or suggest:  Muscle damage

40.  Liver Enzymology 

a. Explain, list, or recognize the physiologic and pathologic processes or mechanisms that cause the following:

• Increased activities of ALP, ALT, AST, GGT, GMD, ID, and LD due to hepatic, biliary, or hepatobiliary disorders or conditions 
• Increased activities of ALP due to glucocorticoids in dogs and hyperthyroidism in cats 

b. Interpret serum enzyme data that indicate or suggest

• Hepatocellular damage
• Cholestasis
• Hepatic lipidosis
• Muscle damage
• Changes associated with glucocorticoids
• Decreased glomerular filtration rate

41. Liver function

1. Explain, list, or recognize the physiologic and pathologic processes or mechanisms that cause the following:
   • Hypoproteinemia due to hepatic disorders
   • Ammonium biurate crystalluria due to hepatic disorders 
   • Hyposthenuria due to hepatic disorders 
   • Hyperbilirubinemia due to in vivo hemolysis, anorexia (horses, cattle), and cholestasis (obstructive or functional) 
   • Bilirubinuria due to in vivo hemolysis or cholestasis 
   • Increased bilirubin, unconjugated bilirubin, conjugated bilirubin, or δ-bilirubin concentration in pathologic or physiologic states 
   • Hypercholemia (increased bile acid concentration) due to portosystemic shunts, diffuse liver disease, and cholestasis (obstructive or functional) 
   • Hyperammonemia or increased bile acids due to portosystemic shunts, diffuse liver disease, and, in horses, intestinal disease 
2. Interpret CBC, serum chemistry, or urinalysis data that suggest or indicate 
   • Hepatic dysfunction including evidence of:
     • Raised bile acids  o Hepatic lipidosis in cats
   • Decreased number of functional hepatocytes o Portosystemic shunt
   • Decreased hepatocyte uptake of bilirubin
   • Decreased biliary excretion of bilirubin or bile acids o Extravascular hemolysis o Intestinal disease in horses
   • Explain, list, or recognize the reasons for:
     • Falsely decreased serum bilirubin concentration after sample is exposed to daylight 
     • False elevations or decreases in bile acid concentrations due to lipemia or hemolyzed blood samples respectively

42. Lipids  

a. Explain, list, or recognize the physiologic or pathologic mechanisms and interpret increases and decreases of cholesterol and / or triglycerides that are associated with the following:

• hypercholesterolemia
• protein-losing nephropathy, hypothyroidism, cholestasis, diabetes mellitus, lipid metabolism disorders in specific breeds, liver disease (cholestasis) and eating a meal 
• Hypertriglyceridemia – post prandial, equine & camelid hyperlipemias, acute pancreatitis, lipid metabolism disorders in specific breeds, and diabetic disorders
• Hypocholesterolemia due to hepatic insufficiency.
• Explain the mechanism of production of ketones and NEFAs in ruminants during negative energy balance with hepatic lipidosis.

43. Pancreas (exocrine, inflammatory) pancreatitis

a. Explain, list, or recognize the physiologic or pathologic processes or mechanisms that cause the following:

• Hyperamylasemia, hyperlipasemia, increased PLI concentration in acute pancreatitis 
• Increased TLI concentration, amylase and lipase in azotemic dogs  b. Interpret 
• increased serum AMS & LPS activities
• increased PLI concentration
• Increased activities of AMS or LPS due to pancreatic disease, dehydration, or renal disease 
• Increases in PLI concentration due to pancreatic disease 

44.  Pancreas (exocrine, non-inflammatory) - Intestinal disorders 

1. Interpret laboratory test results related to exocrine pancreas and intestine that suggest or indicate:
   1. Exocrine pancreatic insufficiency / Pancreatic acinar cell damage
   2. Azotemic disorders (decr GFR)
      Diffuse or segmental disease of intestinal mucosa
   3. Protein-losing enteropathy
2. Explain, list, or recognize the reasons for:
   • Increased TLI concentrations in a nonfasted dog 
   • False feline TLI (or PLI) data if a canine assay is used 
   • False folate concentration if there is in vitro hemolysis 
   • False cobalamin concentration if the sample is exposed to daylight 
   • Decreased TLI concentration in chronic pancreatitis or pancreatic acinar cell atrophy (exocrine pancreatic insufficiency)
   • Decreased cobalamin or folate concentrations due to pancreatic or intestinal disorders 
   • Increased fecal α1-PI concentration in dogs and cats with intestinal diseases (PLE)
   • decreased serum TLI concentration
   • decreased cobalamin concentration
   • decreased and increased folate concentration
   • Flat glucose absorption curves in horses with intestinal diseases 
   • Microbial dysbiosis

45. Endocrine pancreas - hyperglycemia

a. Explain, list, or recognize the physiologic, pathologic, or pharmacologic processes or mechanisms that cause the following:

• Hyperglycemia due to excitement, eating a meal, stress, β-cell destruction, feline pancreatic insular amyloidosis, acute pancreatitis, hyperadrenocorticism, equine hyperpituitarism, pheochromocytoma, steroid therapy, intravenous glucose therapy, xylazine & detomidine therapy, and insulin overdose 
• Increased fructosamine concentration in persistent hyperglycemic states  
• Decreased fructosamine concentration in persistent hypoglycemic states, hypoproteinemic states, or hyperthyroidism (cats)
• Hypoinsulinemia due to β-cell damage or hypoglycemic disorders 

46. Endocrine pancreas – hypoglycemia

1. Explain, list, or recognize the physiologic, pathologic, or pharmacologic processes or mechanisms that cause the following:
   • Hypoglycemia due to functional β-cell neoplasm, hypoadrenocorticism, hepatic insufficiency, xylitol toxicosis, spontaneous bovine ketosis, and insulin overdose, hypoglycemia in sepsis, young animals, small breeds 
   • Hyperinsulinemia (inappropriate) relative to glucose in functional β-cell neoplasm and insulin in hypoglycemic disorders  
2. Interpret serum (blood, plasma) glucose, ketoamine, and insulin concentrations including:
   • Hypoglycemia
   • decreased fructosamine concentration
   • Hyperinsulinemia
3. Interpret serum (blood, plasma) glucose, ketoamine, and insulin concentrations that indicate or suggest:
   • Recent ingestion of a meal
   • Diabetes mellitus due to a variety of disorders
   • Functional β-cell neoplasm
   • Hepatic insufficiency/failure
4. Explain, list, or recognize the reasons for:
   • Pseudo hypoglycemia due to delayed removal of serum from clotted blood, marked leukocytosis, or marked erythrocytosis 
   • Artifactual hypoglycemia due to collection of blood into NaF-oxalate tubes.

47. Adrenal hormones - Hyperadrenocorticism 

1. Explain, list, or recognize the physiologic, pathologic, or pharmacologic processes or mechanisms that cause the following:
   • • Typical hematology and Chemistry changes seen in hyperadrenocorticism
     • The common presentation in terms of organ involved – ie primary, secondary and tertiary organ
     • Normocortisolemia in a dog with hyperadrenocorticism 
     • Increased urinary cortisol to creatinine ratio (UCCR) due to hyperadrenocorticism or nonadrenal disease 
     • Increased ACTH concentration in hyperadrenocorticism 
     • Decreased ACTH concentration in hyperadrenocorticism 
2. Interpret serum or plasma cortisol and ACTH concentrations and urine cortisol:creatinine ratios (UCCR) that indicate or suggest:
   • Hyperadrenocorticism due to pituitary neoplasm
   • Hyperadrenocorticism due to adrenal neoplasm
   • Iatrogenic hyperadrenocorticism
   • Primary hypoadrenocorticism
   • Iatrogenic hypoadrenocorticism
   • Nonadrenal disease that is causing hypercortisolemia or secondary hyperadrenocorticism

2. Interpret serum or plasma cortisol in the following
   • Inadequate cortisol suppression in LDDST in PDH, FAN, or nonadrenal disease 
   • Escape from suppression in LDDST or HDDST 
   • Adequate cortisol suppression in PDH or nonadrenal disease  o  Exaggerated cortisol response to ACTH in PDH, FAN, or nonadrenal disease 
     • Poor cortisol response to ACTH in FAN 
     • Normal cortisol response to ACTH in PDH, FAN, or nonadrenal disease  • Explain, list, or recognize the reasons for:
     • Falsely low ACTH concentrations if sample is not handled properly 
   • Interpret serum or plasma cortisol and ACTH concentrations and urine cortisol:creatinine ratios including:
     • Hypercortisolemia
3. Differentiate between tests and be able to apply to disease syndromes associated with hyperadrenocorticism
4. Describe the sensitivity and specificity of tests used for diagnosis of hyperadrenocorticism

48. Adrenal hormones - Hypoadrenocorticism (Addison’s disease) 

1. Explain, list, or recognize the physiologic, pathologic, or pharmacologic processes or mechanisms that cause the following:
2. • Typical hematology and Chemistry changes seen in hypoadrenocorticism
   • The common presentation in terms of organ involved – ie primary, secondary and tertiary organ
   • Poor cortisol response to ACTH in hypoadrenocorticism
   • Increased ACTH concentration in hypoadrenocorticism 
3. Differentiate between tests and be able to apply to disease syndromes associated with hypoadrenocorticism
4. Describe the sensitivity and specificity of tests used for diagnosis of hypoadrenocorticism

49.  Endocrine Hypothyroidism (dogs)

1. Describe the feedback mechanism in control of thyroid hormones and list which hormones are the most active and which ones are involved in the feedback mechanism
2. Describe why freeT4 by equilibrium dialysis is the gold standard test for assessing the thyroid.
3. Explain, list, or recognize the physiologic, pathologic, or pharmacologic processes or mechanisms that cause the following:
4. The most common organ involved – i. e. primary, secondary or tertiary organ
5. Important changes in hematology and chemistry associated with hypothyroidism 
6. Understand euthyroid sick syndrome and list the factors that cause this
7. Hypothyroxemia or decreased free [T4] due to lymphocytic thyroiditis (or other causes of thyroid gland damage), nonthyroidal disease, and some drug treatments 
8. Increased TSH concentrations due to lymphocytic thyroiditis (or other causes of thyroid gland damage) 
9. Increased anti T4AA concentration due to lymphocytic thyroiditis 
10. List the main breeds of dogs which have lower RIs for T4
11. Explain, list, or recognize the reasons for:
    • Positive interference by anti T4 thyroxine autoantibodies on measurement of thyroxine (T4) concentration 
12. Interpret serum thyroxine, free thyroxine (by equilibrium dialysis), TSH, and TgAA concentrations including: o Hypothyroxemia 
    • Hypothyroxemia with concurrent free thyroxine concentrations o Increased TSH concentration
    • Increased TgAA concentration

50. Endocrine Hyperthyroidism (cats)

1. Describe the feedback mechanism in control of thyroid hormones and list which hormones are the most active and which ones are involved in the feedback mechanism
2. Describe why freeT4 by equilibrium dialysis is the gold standard test for assessing the thyroid.
3. Explain, list, or recognize the physiologic, pathologic, or pharmacologic processes or mechanisms that cause the following:
4. The most common organ involved – i. e. primary, secondary or tertiary organ
5. Important changes in hematology and chemistry associated with hyperthyroidism 
6. Hyperthyroxemia due to thyroid neoplasm or administration of TSH 
7. Absence of hyperthyroxemia in feline hyperthyroidism due to thyroid adenoma 
8. Failure to suppress [T4] with T3 treatments in a cat
9. Interpret serum thyroxine, free thyroxine (by equilibrium dialysis), (TSH)concentrations including:
   • Hyperthyroxemia 
   • Hyperthyroxemia with concurrent free thyroxine concentrations o Decreased TSH concentration

ALL LABORATORIES ARE MANDITORY UNLESS YOU HAVE AN APPROVED ABSENCE

Learning outcomes for the laboratory sessions

Lab 1. See Online Videos (Sakai). In lab activities will be recorded live (Micro lab)

• Observe, perform, describe how to handle EDTA blood samples appropriately 
• Observe, perform, describe, how to make an adequate blood film 
• Observe, perform, describe how to perform a spun HCT (PCV) 
• Be able to determine the HCT of microhematocrit tube using microhematocrit reader (exercise in Lab 1)
• Observe and be able to describe the basic principles of the Abaxis HM5 hematology analyzer for RBC, HCT, Hgb, and WBC concentration determinations via PowerPoint and online video

Lab 2. Blood film evaluation of healthy animals (dog, cat, and horse) (in lab recorded live – Micro lab).  Glass slides in Microbiology lab and prior PowerPoint lectures  Digital slides will be showcased during the lab for all students (online and in person)

• Identify and describe the morphologies of RBCs (crenation/echinocytes from healthy animals
• Identify and describe the morphologies of platelets from healthy animals
• Identify and describe the morphologies of WBCs from healthy animals  
• Be able to perform or describe how to do a differential WBC count and an absolute WBC count
• Perform platelet estimates via blood film review
• Compare obtained results with data from HM5 (dog and cat samples)

Lab 3. Interpretation of Anemic cases (3 dog films) Digital slides will be showcased during the lab for all students (online and in person)

• Identify morphologic abnormalities of RBC (anisocytosis, macrocytes, microcytes, hypochromasia, polychromasia, spherocytes, and platelets (clumping) and describe clinical significance 
• Recognize a left shift and be able to identify leukocyte patterns
• Practice interpretation of the hematology data
• Be able to classify anemia, leukocyte patterns, and thrombogram

Lab 4.

Instructor will moderate student discussions of select cases in this lab, activate participation by TEAMS will be encouraged. Live discussion will be recorded. Charter Hall lab. Cases will be posted to Sakai in Lab Resources

Lab 5 Leica online slide hosting site (Cytology Glass Slides and online images Lab 5 – Micro lab) 

• Recognize bacteria in a digital image  
• Recognize degenerate and non-degenerate neutrophils in digital images
• Identify “criteria for malignancy” using digital images
• Recognize epithelial and mesenchymal neoplasms using digital images
• Describe characteristics of discrete round cells neoplasms using digital images

Lab 6 (Charter Hall lab)

• Cytology case discussions including on cytology using digital images that emphasize cytological findings suggestive of malignant and benign neoplasms, acute, septic, or chronic inflammation 

Lab 7. UA (Micro lab and Zoom)

Online activities (19 mins)

• Distinguish artifacts from significant findings  
• Interpret urinalysis, CBC and serum chemistry results • Urinalysis – chemistry & Sediment “how to” videos https://www.youtube.com/watch?v=jhmzkUcAbIM (8mins, 44 secs)
• Idexx – the urine sediment examination https://www.youtube.com/watch?v=dswfnZXb3nM    (10mins, 43 secs)

Lab 8, 9 (Zoom online) 3- 4 pm

• Case discussions including interpretation abnormal laboratory findings and describe  • pathogenesis of the laboratory abnormalities (Chemistry and Endocrine analytes)

Lab 10 (Zoom online) Case Discussions 3-4 pm

Assessment Points:

Total            117

Final grading will be based on cumulative performance in all examinations.  Grades posted in Gradebook in sakai are not final until confirmed by CAPPS.

A grade reduction of 5% will be applied to that exam if a student does not observe the parameters listed in the Assessment Policy for Students:  *This syllabus is subject to change

Relative to other term three courses, clinical pathology is a difficult course. It depends mostly on a student’s ability to understand and apply learned material. Only a small part of it depends on strict memorization of material. 

Students are encouraged to determine their individual learning styles (visual, tactile or auditory) and apply these appropriately. Briefly; a visual learner likes to see the information they are trying to understand, to take notes or makes chats when reading; a tactile learner likes a hands-on approach (lab sessions – this terms labs will be converted to video and digital technology to view glass slides) while an auditory learner prefers to listen or talk to others (study groups). 

Students are also encouraged to study the material sooner rather than later and to set studying schedules and stick to them.  

We also recommend practicing applying the learned concepts to the cases that are posted to Sakai for the laboratories and presentations.

The student is expected to review the online lectures prior to the zoom sessions.  

Students are expected to conduct them themselves professionally during forums, labs, zoom sessions, and during exams. If in doubt, please refer to the student and lab manuals, as well as to the syllabus.

All students are responsible for knowing and complying with the University’s Code of Conduct and the guidelines.

Students are expected to be available during the standard 8:30- 5:20 pm AST school day, to virtually attend, engage with online content, and participate in all classes and clinical rotations for which they have registered. Employment is not an excusable absence. Although attendance, engagement, and participation may not be recorded at every academic activity, attendance, engagement, and participation is graded for mandatory sessions. Students’ lack of attendance, engagement, and participation may adversely affect their academic status as specified in the grading policy. 

If failure to attend, engage, or participate in individual classes, examinations, and online activities, or from the University itself is anticipated, or occurs spontaneously due to illness or other extenuating circumstances, proper notification procedures must be followed. 

Laboratory session attendance is mandatory: any student failing to attend without an approved absence from the Dean's Office and agreed upon makeup assignment will receive 0.5 points deduction.  

Students who fail to attend an examination or submit an assignment by the deadline without a valid reason (see student manual: SGUSVM POLICY ON AN EXCUSED ABSENCE (EA) FOR STUDENTS) will receive a score of “0” points for the examination.

Students who have technical issues during the examination MUST inform the Course Director (rkabuusu@sgu.edu, mwilkers@sgu.edu) and IT (tellexaminationservices@sgu.edu OR support@sgu.edu OR call 1-631-665-8500 ext. 4444 (US, NU, International) OR 1-473-439-2000 ext. 4444 (Grenada), AND Dean of Students (DOS@sgu.edu) during the open period for the examination. Failure to do so immediately will result in the student receiving the highest score recorded at the time, but NOT being eligible to take a completion examination.

Scheduling of examinations (regular, re-sit, completion, comprehensive, or exemption) is at the discretion of the School. Completion exams will be scheduled within 7 days of the original exam date. Re-sit examination will be scheduled in the first week of the following term

All students are responsible for knowing and complying with the University’s Code of Conduct and the guidelines. Students must read and then sign the Honor Code statement at the start of examinations to indicate that they will comply with the University Code of Conduct. 

Prior to Exam Day

1. Each student is required to have a laptop for the purpose of taking computer-based examinations (e-Exams) at SGU. Students must ensure that their laptops meet the current minimum system requirements prior to exam day:
2. Examinees must use their MY SGU Member Center username and password to access the Custom Home Page (www.examsoft.com/sgu) created by ExamSoft for the University.
3. Examinees are responsible for downloading and registering the latest version of Examplify on their laptop prior to exam day. Once Examplify has been successfully downloaded, examinees are strongly encouraged to familiarize themselves with the software by downloading and taking practice exams.
4. Examinees are responsible for setting their laptop up for ExamMonitor prior to the exam (see links below).
5. Examinees will be notified via MyCourses, of all exam related information. Email notifications will also be sent from ExamSoft Support to examinees, notifying them of examinations available for downloading.
6. Examinees experiencing difficulties with their laptop are encouraged to visit the IT department for assistance prior to exam day. Examinees needing a laptop must visit the Office of Institutional Advancement (OIA) to request an exam loaner.
7. Examinees should visit the following information to familiarize themselves with the online proctored exam format and set up their baseline photo.
   1. A Examsoft/ExamID quick guide for students (Please note that the current Examplify version is 2.3.8)
   2. The Examsoft student perspective video 30mins
   3. The Examsoft/ExamID FAQ  
   4. Examsoft information page
   5. The general Reminders/Guidelines  
   6. The general Reminders/Guidelines