Laboratory results, differentials and changes Flashcards
What is, what is the micropic appearance and what are the differentials for Asinocytosis?
Anisocytosis
What it is: Presence of RBCs of unequal size.
Microscopic appearance: Variably sized RBCs; can range from smaller to larger than normal RBCs.
Differentials:
Iron deficiency anemia (often with microcytosis and hypochromia)
Vitamin B12 deficiency or folate deficiency (macrocytosis)
Thalassemia (microcytic, hypochromic RBCs)
Chronic blood loss (microcytic, hypochromic)
What is, what is the micropic appearance and what are the differentials for Poikilocytosis?
What it is: Abnormal shapes of RBCs.
Microscopic appearance: RBCs with varied shapes (e.g., teardrop cells, sickle cells, target cells, spur cells).
Differentials:
Sickle cell anemia (sickle-shaped RBCs)
Hereditary spherocytosis (spherical RBCs)
Iron deficiency anemia (teardrop-shaped RBCs)
Thalassemia (target cells, basophilic stippling)
What is, what is the micropic appearance and what are the differentials for spherocytes?
What it is: Small, spherical RBCs with reduced central pallor.
Microscopic appearance: Spherical, lacking central pallor, and more dense.
Differentials:
Hereditary spherocytosis
Autoimmune hemolytic anemia (AIHA)
Hemolytic anemia (especially warm antibody type)
What is, what is the micropic appearance and what are the differentials for Target cells (codocytes) ?
What it is: RBCs with a bullseye appearance, increased central pallor.
Microscopic appearance: RBCs with a dark central area surrounded by a pale ring and then a dark outer rim.
Differentials:
Thalassemia Liver disease Iron deficiency anemia Hemoglobinopathies
What is, what is the micropic appearance and what are the differentials for sickle cells ?
What it is: RBCs shaped like a crescent or sickle.
Microscopic appearance: Crescent or sickle-shaped RBCs, often with irregular contours.
Differentials:
Sickle cell disease (Homozygous sickle hemoglobin, HbSS)
Sickle cell trait (heterozygous for HbS)
What is, what is the micropic appearance and what are the differentials for reticulocytes ?
What it is: Immature RBCs containing residual ribosomal RNA.
Microscopic appearance: Larger than mature RBCs, with a bluish tint or a reticular (network-like) pattern due to RNA.
Differentials:
Acute blood loss (e.g., trauma, surgery)
Hemolytic anemia (increased reticulocyte count)
Recovery from iron or vitamin B12 deficiency
What is, what is the micropic appearance and what are the differentials for basophilic strippling ?
What it is: RBCs with small, fine blue granules.
Microscopic appearance: RBCs with punctate blue granules throughout the cytoplasm.
Differentials:
Lead poisoning
Thalassemia
Alcoholism
Sideroblastic anemia
What is, what is the micropic appearance and what are the differentials for Howell-Jolly Bodies ?
What it is: Small, round remnants of nuclear DNA.
Microscopic appearance: Single, round, purple-staining bodies within RBCs.
Differentials:
Post-splenectomy
Severe anemia
Sickle cell disease
What is, what is the micropic appearance and what are the differentials for Howell-Jolly Schistozoites ?
What it is: RBC fragments caused by mechanical damage.
Microscopic appearance: Irregularly shaped, often jagged or triangular RBC fragments.
Differentials:
Microangiopathic hemolytic anemia (MAHA)
Thrombotic thrombocytopenic purpura (TTP)
Disseminated intravascular coagulation (DIC)
Hemolytic uremic syndrome (HUS)
What is, what is the micropic appearance and what are the differentials for Monocytosis ?
Monocytosis
What it is: Increased monocytes.
Microscopic appearance: Increased number of monocytes, larger and more abundant cytoplasm than lymphocytes.
Differentials:
Chronic infections (e.g., tuberculosis, endocarditis)
Autoimmune diseases
Myelodysplastic syndromes
Leukemia
what is a left shift?
A left shift refers to the presence of immature neutrophils (often bands or metamyelocytes) in the peripheral blood, which occurs when there is an increased demand for neutrophils due to infection or inflammation. It indicates that the bone marrow is releasing neutrophils into the bloodstream before they have fully matured.
what are key charachteristics of a left shift?
when do you see this?
Immature neutrophils (bands, metamyelocytes, myelocytes) are found in the peripheral blood, alongside mature neutrophils.
Associated conditions: Typically occurs in bacterial infections, severe inflammation, or bone marrow stimulation.
Neutrophil count: The total neutrophil count (including both mature and immature neutrophils) is often elevated
what is the microscopic appearance of a left shift?
Bands (neutrophils with a band-shaped nucleus) are the most common form.
In severe left shifts, you may also see metamyelocytes (nucleus less elongated than bands) and myelocytes (larger, with a rounder nucleus).
what are differentials for a left shift?
Bacterial infections (especially severe or overwhelming infections)
Abscesses
Severe inflammation
Leukemoid reaction (reactive, marked neutrophilia)
what is a stress leukogram?
A stress leukogram is a pattern of changes in the WBC count that reflects an acute stress response, typically due to corticosteroid release (either from the adrenal glands or exogenously administered corticosteroids). It is seen in conditions like physical stress, trauma, infection, or when corticosteroids are used as medication.
what are key charachteristics of a left shift?
Neutrophilia: An increase in neutrophil count, but without a significant increase in immature forms (no left shift).
Lymphopenia: A decrease in the number of lymphocytes.
Monocytosis: An increase in monocytes (less prominent than neutrophilia).
Eosinopenia: A decrease in eosinophils.
Microscopic appearance: There are no immature neutrophils (bands or metamyelocytes) in the blood smear.
what are differentials for a left shift?
Acute stress (e.g., physical trauma, surgery)
Corticosteroid therapy (either endogenous, like in Cushing’s disease, or exogenous)
Severe illness or systemic inflammation (e.g., sepsis)
Acute myocardial infarction
how to tell a left shift appart from a stress leukogram
. Immature Neutrophils:
Left shift: There will be a significant presence of immature neutrophils, such as bands, metamyelocytes, or myelocytes. Stress leukogram: There will be no immature neutrophils; neutrophils will be mature forms only.
- Neutrophil Count:Left shift: The neutrophil count will often be elevated, but with a high proportion of immature neutrophils.
Stress leukogram: The neutrophil count will also be elevated, but the neutrophils will be mostly mature, without a significant increase in immature forms. - Other WBC Components:Left shift: There is typically no marked change in lymphocytes or monocytes (though slight changes may be seen).
Stress leukogram: Lymphopenia (low lymphocytes) and monocytosis (increased monocytes) are typical features. Eosinopenia (low eosinophils) is also often seen in a stress leukogram. - Clinical Context:Left shift: More commonly seen in acute bacterial infections, inflammatory conditions, or severe infection.
Stress leukogram: Seen in response to physical or emotional stress, corticosteroid use, trauma, or acute systemic illness. It is more of a physiologic response to stress rather than an indicator of active infection or inflammation.
what is a transudate and what are the criteria that this must have?
Transudates are caused by imbalances in hydrostatic or oncotic pressure and are generally due to systemic conditions. They have low protein content and are typically clear and pale yellow.
Microscopic Features: Few cells, primarily macrophages, mesothelial cells, and lymphocytes. Occasionally, there may be neutrophils if mild inflammation is present.
what is an exudate
Exudates result from local inflammation, infection, or malignancy. They are typically high in protein and can be cloudy, yellow, or even bloody in appearance.
Often contains neutrophils (if bacterial infection), lymphocytes (if viral or neoplastic), and macrophages. Mesothelial cells may also be present.
compare transudate, modified transudate, exudate and septic exudate
Differentials for anaemia
HypoT
HypoA
Prolonged bleeding
Chronic renal failure (mild🡪life threatening) – ↓ EPO, toxic depression of BM, ↑RBC fragility
Secondary to inflammation ->Enhanced hemolysis
Utilisation of iron by bacteria
differentials for increased basophils
Concurrent w/ eosinophils in hypersensitivity disorders
Hyperlipoprotieinaemia
- DM
- Nephrotic syndrome
- Chronic liver dz
- Hypo-T
Some respiratory and skin disease
Mast cell tumors
Granulocytic leukemia
Heartworm disease or other systemic parasites
Differentials for increased eosinophils
Hyper-sensitivity disorders
Histamine release (allergic diease, mast cell Neoplasia, paraneoplastic diease)
Antigenic stimulation (sensitised by T-cells: hypersensitivity, migrating parasites)
Oestrus – esp bitch
Dz of the respiratory system, skin, GIT, female urogenital system
Hypo-A
Metastatic neoplasia
differentials for esinopaenia
Corticosteroids – less histamine release or prolonged release of corticosteroids = ↓ production in BM
Cushings/steroid treatment
Adrenaline release
Acute infections
BM disorder (hypoplasia, dysplasia, leukemia)
differentials for erythrocytosis
Relative
- Dehydration
- Splenic contraction
Absolute (10 or 20)
- 1’ = polycythemia vera
- 2’
- Pulmonary Disease
- DM
- Right 🡪 Left shunt
- High altitude
- HyperA
- HyperT
- Renal mass/cyst
when do you see decreased fibrinogen
In advanced hepatic insufficiency
Differentials for lymphocytosis
- Acute stress (especially cats)
- Lymphocytic leukemia
- Chronic infections →Response to antigen (chronic infection/inflammation)
- Hypoglycaemia
- Age – younger animals have higher leukocytes, especially lymphocytes (> 2000)
Differentials for lymphocytopaenia
- Endogenous corticosteroid release
- Stress, trauma, pain, shock, seizures, fever, etc → Glucocorticoid-induced redistribution of recirculating lymphocytes
- Exogenous corticosteroid or ACTH
- Acute systemic infection – usually viral infection
- Congenital immunodeficiency syndrome →T-cell immunodeficiency
- Less common: T-cell deficiency, loss of lymphocyte-rich lymph
- Impaired lymphocytopoeisis -> Cytotoxic drugs, irradiation
what is a differential for hyperchromasia
increase MCHC
Absolute increases aren’t usually seen, they may be artifact
- Presence of free Hb
- Intravascular haemolysis is the most common artefact
- Hyperlipidemia or Heinz bodies
- Spherocytosis
what is a differential for hypochromia (decreased MCHC) ?
Reticulocytosis
Iron deficiency
what are differentials for Macrocytosis (MCV)
Reticulocytosis
Cats infected w/ FeLV
what are differentials for microcytosis (MCV decrease)
Young animals
- They tend to have smaller erythrocytes and hence the lower MCV
- Esp foals 1-9 mnths (mean 34.5)
Animals w/ portosystemic shunts
Iron deficiency
what are the differentials for monocytosis ?
Endogenous corticosteroid release
- intense stress (corticosteroid release)
- Hyper-A
Response to GCS (dogs)
Inflammation: Acute or chronic infection or inflammation with tissue damage
Infarction or neoplasia
Suppurative disorders of body cavities
Necrosis
Internal haemorrhage
Haemolytic diseases
Immune mediated dz
Granulomatous disorders
Reduced production Neutropaenia
differentials for monocytopenia?
Endotoxaemia
BM disorder OR Viral or rickettsial infection (FeLV, Parvo, E. canis)
what are differentials for Neutrophilia?
1) Physiological = stress/epinephrine mediated stress:
a) Attributed to splenic contraction & increased BP which flushes the marginal pool
2) Chronic Stress & Corticosteroid mediated stress:
a) Shift MNP 🡪 CNP, ↓ migration from peripheral blood, ↑ from BM
b) Stress leukogram: ↑ N & M, ↓ L & E
c) HyperA= similar changes but magnitude ↓ with time
3) Regenerative anaemia
4) Inflammatory demand +/- left shift (septic or non-septic)
a) Immature:mature less than 1:16-18 (dog), 1:10-12 (cat), 1:12-16 (horse)
b) OR >1×109/L bands in dog (possibly cat), or >0.3×109/L for horse
c) Toxic changes – Dohle bodies (↑↑production), cytoplasmic basophilia/vacuolation (severe infection/inflamm e.g. pancreatic necrosis in dog), cytoplasm granulation (purple- toxaemia)
Differentials for neutropaenia?
Transient or persistent
1) ↓ survival, production, ineffective granulopoiesis, unknown mechanisms, sequestration
2) Severe infection: degenerative left shift (often see toxic changes)
3) Toxins/drugs: estrogen, chloramphenicol, chemotherapy
4) Primary BM disesase
5) Viral/rickettsial infections (FeLV, Parvo, E. canis)
what are the differentials for increased nucleated red blood cell count?
Occurs when there is an alteration of the blood-bone marrow barrier
If accompanied by reticulocytes:
- Regenerative anaemia
If unaccompanied by reticulocytes: consider a non-regenerative response due to
- Lead toxicoses
- Erythroid leukaemia
- Splenic disease/neoplasia
- Endotoxemia
differentials for increased ALT
Hepatocellular Damage
- Primary hepatocellular damage
-Infectious dz, hepatotoxic dz, neoplastic, obstructive, chronic active hepatitis
- Metabolic disorders w/ secondary liver dz
- DM, stress, hyper-A, feline hyper-thyroid, hepatic lipidosis
- Circulatory disorder w/ secondary liver dz
- Portosystemic shunt, severe anemia, shock
- Drug therapy
-Corticosteroids
- Muscle disease (compare with CK)
- Dog: induced by corticosteroids & some anti-convulsants (↑ membrane permeability)
- Can be mildly elevated with congenital liver shunts
- Not used to determine hepatocelluar damage in horses due to limited elevations in liver Dz
- Muscle disease (compare with CK) 🡪 common in the horse, hard to interpret
Differentials for decreased albumin
- Decreased protein intake/production
- Intestinal malabsorption
- Starvation
- Exocrine pancreatic insufficiency →Maldigestion
- Liver disorders
a) Mild↓ in acute hepatic dz
b) Marked ↓in chronic liver dz
- Intestinal malabsorption
- Increased protein loss
- In urine (primary glomerular dz) → proteinuria
- In the gut (PLGE)
- Hemorrhage → albumin and globulins lost
- Ascites
Will lead to low serum Ca levels (reduction in the protein-bound fraction
Differentials for increased ALP
- Cholistasis
- Levels high in neonatal pups/kittens (colostrum levels) -> only measure if >2weeks old
- Usually elevated before hyperbilirubinaemia or significant bilirubinuria
- Bone and gut isoenzymes – bone growth in puppies for example or diseases can = 2-3×↑ in ALP
- Dog: elevations in
- Hyperadrenocorticism (Cushing’s); (may have levels > 2000 U/L)
- DM (fatty change)
- Exogenous corticosteroids
- Anticonvulsants, volatile anaesthetics, barbiturates - Cat: ANY ELEVATION IS SIGNIFICANT 🡪 Cats have lower levels in hepatocytes & shorter plasma t ½
- Hyperthyroidism
- Acromegaly
- DM (fatty change) - Drugs
- Anticonvulsants
differentials for ALT increase
- Hepatocellular Damage
- Primary hepatocellular damage
- Infectious dz, hepatotoxic dz, neoplastic, obstructive, chronic active hepatitis
- Primary hepatocellular damage
- Metabolic disorders w/ secondary liver dz
- DM, stress, hyper-A, feline hyper-thyroid, hepatic lipidosis - Circulatory disorder w/ secondary liver dz
- Portosystemic shunt, severe anemia, shock - Drug therapy
- Corticosteroids - Muscle disease (compare with CK)
- Dog: induced by corticosteroids & some anti-convulsants (↑ membrane permeability)
- Can be mildly elevated with congenital liver shunts
- Muscle disease (compare with CK) 🡪 common in the horse, hard to interpret
Differentials to increases anion gap
- Titration acidosis: Most common cause of an increased anion gap.
- Alkalemia: loss of protons from plasma proteins (unmeasured anions) increases their negative charge. -Alkalemia also stimulates lactic acid production. The increase in AG is very mild.
- Dehydration: Will increase plasma protein concentration (especially albumin).
- Sodium containing drugs: Sodium salts, penicillin.
- Age: Anion gap is higher in foals than adult horses.
- Decreased cations: magnesium and calcium. Have minimal affect on the anion
what are the differentials for decreased anion gap?
- Acidemia: Causes dissociation of protons from plasma proteins, decreasing their negative charge.
- Hypoalbuminemia
- Hypercalcemia
- Assay artefacts: Artefactually elevated chloride, e.g. bromide therapy.
- Dilution: Dilutes plasma proteins
- Increased unmeasured cations: Calcium, magnesium, gamma globulins, lithium. (These rarely cause an increased anion gap as most increases are incompatible with life. It is unusual to see a low anion gap in multiple myeloma)
whatare differentials for increased AST found?
If it is elevated, what steps should you take?
present in hepatocytes, muscle, RBC
- Liver dz (Hepatocellular)
- GI dz (reflux into the liver leading to mild hepatocellular disease)
- Muscle inflammation or necrosis (IM injection or exercise)
-RBC hemolysis
NOTE: if this is elevated, check for hemolysis then look at ALT
what are the main liver enzyme changes seen in hepatic lipidosis that are prognostic
ALT increased
ALP increased
GGT NORMAL
