Module 4 Clin Path and Focussed U/S Flashcards
Identify and interpret a complete blood count
THE ERYTHROGRAM;
PCV;Packed Cell Volume. This is the direct measure of red blood cell volume as a percentage of the whole, from the haematocrit tube. Will be slightly higher than haematocrit as despite spin, will have slight amount plasma. Assess in conjunction with TP (total protein) using refractometer.
HCT;Haematocrit. Approximates PCV, but haematocrit is a calculation. Thus PCV is considered more accurate.
HCT=(MCV x RBC)/10 . MCV may be falsely elevated if rbc’s swell due to storage. Haemolysis due to processing, may falsely decrease RBC, this is why PCV considered more reliable.
HB;The haemoglobin concentration in all the RBC’s. Direct measure by machine. Most ACCURATE assessment of the red blood cell mass. If MCHC is normal, it should be approx 1/3rd of the haematocrit, as haemoglobin makes up 1/3rd of the rbc’s. Is however falsely elevated by lipaemia. Becomes less accurate than pcv or haematocrit in cases of true intravascular haemolysis.(because machine reads hb by lysing cells thus hb = hb in cells lysed by machine + hb which was lysed by animal or collection and this is obviously higher in IMHA but this hb is not functional and so not an indicator of rbc mas).
MCV;mean corpuscular volume (average single rbc volume)
MCH;mean corpuscular haemoglobin.Amount of hb in an average rbc. If large number of reticulocytes, have many larger volume rbc’s but less MCHC so value of MCH becomes more important than MCHC.
MCHC;Mean corpuscular haemoglobin concentration. Unlike MCH, MCHC expresses how much hb is in an rbc, by correlating it to the size of the rbc.
RDW;Red Blood Cell Distribution Width. This represents the standard deviation of erythrocyte volumes. ie most sensitive marker of an increased variability in rbc size (anisocytosis).Increased in regenerative anaemia and in iron deficiency anaemia.
THE LEUKOGRAM;
MAST CELLS if seen in circulation, ddx inflammation (low numbers) or mast cell neoplasia if in high numbers.
BASOPHILS appear in ddx inflammation or allergy, hypothyroidism, diabetes,
NEUTROPHILS
LYMPHOCYTES
THE THROMBOGRAM
MPV=mean platelet volume;average volume of a single platelet. Tends to be an inverse relationship with average platelet size and platelet numbers.
Outline differential diagnoses for complete blood count changes
ERYTHROCYTOSIS;increased haematocrit, hb and rbc count.a)relative. caused by splenic contraction or isotonic dehydration.
b)Absolute. 1. Primary
2. Secondary due to increased erythropoietin either appropriate due to chronic hypoxia or inappropriate eg due to renal neoplasia
ANAEMIA: decreased haematocrit, hb and rbc count.
a) regenerative. ddx haemorrhage or haemolysis. Takes 3-5 days for regeneration to occur. Is regenerative if CRP=>1% in dogs, and >0.4% in cats.
CRP= corrected reticulocyte percentage=
(patient hct/pcv)/(normal hct/pcv).
Normal hct/pvc is 45% for dogs and 35% for cats.
b) non regenerative. ddx bone marrow dz, anaemia of chronic dz, decreased epo.
POIKILOCYTOSIS;variation of rbc shapes. ddx turbulent blood flow, intravascular fibrin deposition, liver dz (esp in cats), drugs eg doxorubicin.
a) Acanthocytes have 2 or more blunt -tipped projections on the rbc membrane.v important marker for dog with haemangiosarc esp in liver/spleen, but can be other neoplasia, lipid, gdv, anaemia, liver dz,heart dz etc.
b)eccentrocytes-transparent crescent shape on one side of the rbc.oxidative injury eg onion. Can occur in sick dogs prior to anaemia.
c) echinocytes;uniform multiple blunt/sharp spicules from rbc membrane. ddx artifact (common), envenomation,renal dz, neoplasia, drugs (furosemide, phenylbutasone)
d) Elliptocytes-elongated rbc’s. ddx lipidosis, liver dz, progenitor anaemias,myelofibrosis, genetic defect, neoplasia, artifact.
e) Keratocytes (helmet cells)-rbc has a bite shaped defect with 2 “horn” spurs on bite’s edge.ddx fragmentation ionjury, oxidative injury, liver (hepatic lipidosis cats)
f)Schistocytes;irregular rbc fragments. ddx intravascular fibrin, turbulent flow, iron deficiency anaemia, doxorubicin. Rare in cat (if present, usually liver dz).
g) Spherocytes; smaller, globoid rbc’s which lack central pallor. ddx immune mediated anaemia (p-rimary or secondary-must always look for the cause), oxidative injury, abnormal macrophage fn, snakebite, beesting. normal in small numbers.
h)Stomatocytes; central pallor is like a smile.ddx regenerative anaemia, liver dz, toxin, inherited defect, artifact.
i)Codocytes (target cells). looks like a target. ddx regenerative anaemia, iron deficiency anaemia, lipid disorder, hypothyroid (high cholesterol), hepatic dz, renal dz
LEUKOCYTOSIS-increased white cells, most commonly neutrophilia.
STRESS LEUKOGRAM; (corticosteroid response). Combinations of all or some; neutrophilia, lymphopaenia, monocytosis, eosinophilia.
Most common is lymphopaenia, then neutrophilia. Neutrophilia usually raised 1 x ref limit but may be up to 3 x. Increased alkp (dogs) often present, occasionally hyperglycaemia.
ADRENALINE RESPONSE;(excitement/fear/stress);usually juveniles. Neutrophilia, lymphocytosis, eosinophilia & basophilia (cats), hyperglycaemia. resolves after 30 min.
LEUKEMOID RESPONSE;(aka extreme neutrophilia).Absolute neutrophil count >70 x 10tothepower9/L for dogs and >50 x 10tothe9power/L for cats.ddx marked inflammation/infection. Poor px esp if neoplastic cause.
LEFT SHIFT;increased number of immature circulating neuts. When they exceed mature neuts, is called a Degenerative Left Shift, which = severe inflammation.
ACUTE INFLAMMATORY RESPONSE;Neutrophilia in response to a dz process. +/- degenerative left shift, +/- toxic changes, +/- lymphopaenia. ddx bacterial, fungal, virus, protozoa, neoplasia, immune mediated, hypoxaemia/necrosis, migrating fb eg grasseed.
TOXIC CHANGE;of neuts,only assessible via microscope, increased dohle bodies, increased cytoplasmic basophilia (=bluer), cytoplasmic vacuolation, nuclear immaturity. Something causes accelerated granulopoiesis, resulting in dysplasia.Usually due to inflammation. Is helpful in ruling out a corticosteroid or adrenaline response.
HYPERSEGMENTATION OF NEUTROPHILS; > 5 lobes to a nucleus. Normal aging. Not usually seen in circulation. May be increased with steroids, fiv, myelodysplasia, vit b def, congenital some poodles.
NEUTROPENIA WITH LEUKOPAENIA;overwhelming demand with increased migration from circulation to tissues/third space eg pyometron/pyothorax etc, or insufficient production (bone marrow issue), or decreased cell survival eg fiv, parvo, protozoa, endotoxic shock, anaphylaxis, collie cyclic haemopoeisis disorder (grey coat, usually die very young), chloramphenical, oestrogens, phenylbutazone.
LYMPHOCYTOSIS ddx chronic antigen stimulation, transient post vacc, hypoA, adrenaline in youngs, protozoa, lymphoid leukaemia (if lymphoid count > 20 x 10tothepowerof9/L =pathognomonic for).
LYMPHOPAENIA ddx stress/steroids, fiv/feleuk, chylothorax/lymphangiectasia, acute inflammation, sepsis, chronic renal failure, immune mediated disorder, immunosuppressive meds, congestive heart disease, etc
EOSINOPHILIA; ddx IgG hypersensitivity, migrating parasites, paraneoplastic (eg cats lymphoma/ intestinal or disseminated mast cell tumour), hypoA, idiopathic hypereosinophilia dz, eosinophilic leukaemia, cat chronic renal failure/cardiac dz,
EOSINOPAENIA ddx stress/steroids
THROMBOCYTOSIS most commonly due to anaemia (eg iron deficiency or chronic gi bleed, due to increased erythropoeitin release and there being cross reactivity b/n erythropoitin and thrombopoeitin. May also be rebound effect after haemorrhage or thrombocytopaenia. May also occur secondary to stress/inflammation. Fairly common in hyperA.
THROMBOCYTOPAENIA ddx haemorrhage, impeded production (drugs, bone marrow disorder), destruction eg immune-mediated, sequestration in spleen (rare). May be normal for some breeds eg cavalier.
Discuss how to perform and evaluate a blood smear
Have a method.
1. Inspect thick end (where blood drop was) at 10x objective. Check for microfilaria and large abnormal cells.
2.Inspect feathered edge for microfilaria, platelet clumps, white cell clumping and any large abnormal cells. 10x objective
3. estimate total wbc count in mid smear on 10 x objective by counting 3 windows, divide by 3=n (average). Then n/4=Estimated wbc count x10tothepowerof9/L.
4.Differential white cell count on 40Xobjective lens.Count 100wbc’s and record numbers of segmented neuts, band neuts, lymphocytes, monocytes, eosinophils and basophils.Write as percentage. Also note nRBC’s and if >5, a corrected white cell count should be done.
CorrectedWBCcount=nRBCx[100/(nRBC+100)].
5. On 100xobjective (with oil) check platelets.Check 10 fields . Then average.
Average number of platelets per hpf x20000=number of platelets x10tothepowerof9/L. Check for clumps as this will lower the count artifactually.
8-20platelets per hpf should be sufficient.
6. on oil. assess white cell morphology and check for toxic change and or parasites etc. Check absolute counts if wish (checks machine readings).
Multiply differential count by estimated WBC count
* E.g. if 88% segmented neutrophils and estimated WBC count is 15x109
cells/L → 0.88x15 = 13.2x109
segmented neutrophils/L
Interpret a serum biochemistry profile and outline differential diagnoses for abnormalities
ALBUMIN AND GLOBULIN;
1. Albumin and globulins both increased;
ddx dehydration or neonate.
2.Increased albumin, normal globulins (increased A:G);
ddx dehydration or lab error (lipaemia/haemolysis)
3.Increased globulins only;
ddx acute phase reaction, polyclonal gammopathy, monoclonal gammopathy.
4.Both albumin and globulin decreased (Panhypoproteinaemia)
ddx haemodilution, haemorrhage, excessive protein loss (burn, gi loss, renal loss, 3rd space effusion)
5.Decreased globulins and normal albumin;
ddx pre colostral neonate, primary immunodeficiency, IgA deficiency, some breed variation eg Greyhounds normally maybe, infection (felv,fiv,toxo,distemper)
6.Decreased albumin +/- decreased globulin
ddx inadequate diet, failure to synthesise albumin eg severe liver dz
7.Decreased albumin with increased globulins
=acute phase response.
LIPIDS comprise triglicerides (t) and cholesterol (c). Liver source of cholesterol synthesis.
1.Post Prandial hyperlipidaemia-normal.
2. Primary hyperlipidaemia-rare but see in some breeds eg Schnauzer(t), Rottie/sheltie/rough collie/dobi (c).
3.Secondary hyperlipidaemia; ddx hypoT (c,t), diabetes m (c,t), pancreatitis (mainly t), hyperA (c, t), hepatic dz/cholestasis (c), protein losing nephropathy (c), pregnant, obese, sepsis, steroids and some other drugs.
4. Hypolipidaemia; frequently of no significance but can also be significant and ddx impaired liver fn (cirrhosis/shunt), malabsorbtion, protein losing enteropathy, hypoA.
BLOOD UREA NITROGEN (BUN);urea produced by liver as end result of protein catabolism. Increased when increased protein catabolism eg burns, sepsis, corticosteroids, starvation. Increased with increased protein digestion eg gi haemorrhage/ high protein meal.Increased when there is decreased filtration (pre/renal/post). Decreased when there is reduced synthesis (ddx severe liver dz/shunt, reduced protein intake), increased loss (eg polyuria leading to medullary washout) or haemodilution.
CREATININE comes primarily as an end product of muscle metabolism, a tiny amount is ingested. If have larger muscle mass (eg greyhound), will normally be a bit higher. Because under normal circumstances it is released at set rate, so it can be assumed that any change in level reflects a change in glomerular filtration rate (ie increased approximates reduced gfr).
AZOTAEMIA=increased Bun, +/- increased creatinine.
1. Pre-renal ie decreased renal perfusion eg shock, reduced cardiac output, dehydration. ie If dog usg >1.030 or cat >1.035, renal ability likely ok. May have increased pcv and tp. Or increased protein catabolism (usually only causes mild azotaemia)
2. Renal-75% nephron functionality lost before gfr is affected to level that can see changes in labwork. Dog usg 1.008-1.029, cat usg 1.008-1.034. Will also have clinical signs of either polyuria, oliguria or anuria.
3. Post renal; urinary obstruction or leakage distal to kidneys. Commonly hyperkalaemic. If ruptured, may have increased peritoneal potassium and creatinine cf serum (but if had significant obstruction prior to rupture, serum will obviously be eleavted also.
AMYLASE-non specific enzyme. Increases over 3-5 x normal may indicate pancreatitis (canine only), but ddx intestinal/uterine/renal disorder. Will be increased in renal failure.
LIPASE-increases may indicate pancreatitis but ddx gastric/hepatic/renal or post abdominal surgery. Increased in renal failure. Normal level does not exclude pancreatitis.
CANINE PANCREATIC LIPASE-negative test rules out pancreatitis, but positive may be pancreatitis or other primary abdominal issue secondarily causing pancreatitis.
ALANINE AMINO TRANSFERASE (ALT);mainly from liver, also heart and muscles. Considered most liver specific indicator of liver damage.Less than 4x increases can be normal with drug induction eg phenobarb. Moderate muscle damage may result in mild increases. Half life3 hour to 4 days. After trauma, if elevated, 4 days after if reduced by 50%, is considered good prognostic indicator. Should be normal after 3 weeks or if still elevated= ongoing liver issue. May be decreased in hepatic insufficiency.
ASPARTATE AMINO TRANSFERASE (AST) from muscle liver or rbc’s. Increased with increased alt=liver, elevated without increased alt= extrahepatic. check alongside ck.
ALKALINE PHOSPHATASE (ALKP or ALP)-primarily liver or bone. Membrane bound, does not increase with injury.
a) Hepatic isoenzyme of alp:
1.Dog; sensitive for cholestasis. ddx severe hepatic necrosis, hepatocellular swelling, phenobarb, hyperA, steroids, diabetes meliitus, hypoT.
2. Cat; only 6 hour half life. Elevations are very significant in cat. ddx neutrophilic cholangitis, cholestasis, hepatic lipidosis, hyperT (treat hyperT and alkp should normalise)
b) Bone isoenzyme of alp; normal increase in kittens <15 weeks and pups up to 8 months. if increased in olders, ddx arthritis, osteomyelitis, osteosarcoma, primary/secondary hyperparathyroidism.
c) steroid induced isoenzyme of alp; does not occur in cats. ddx endogenous or exogenous.
BILIRUBIN levels are proportional to rate of haem production/turnover, and inversely proportional to the rate of bilirubin clearance. Bilirubin is unconjugated in the blood, the liver conjugates it (makes it water soluble), then excretes it into the bile.
Unconjugated bilirubin is bound to albumin and is the main form of bilirubin in the blood. Conjugated bilirubin is usually only a very small fraction of total bilirubin in the blood as once conjugated by the liver, it is usually excreted into bile. Conjugated bilirubin will spill into the urine. Often see bilirubinaemia prior to bilirubinaemia. 1+ bilirubin in concentrated dog urine may be normal, higher than this abnormal. Any bilirubinuria in cat is abnormal.
Hyperbilirubinaemia;
a)Retention hyperbilirubinaemia; primarily unconjugated. ddx haemolysis or hepatic issue prior to conjugation.
b)Regurgitation hyperbilirubinaemia; primarily conjugated. Issue post conjugation. eg intra/exta hepatic cholestasis, liver failure, biliary tract blockage etc
c) Mixed pattern;most animals present with mixed ie increase in both conjugated and unconjugated bilirubin due to system saturation by time of presentation.
CREATININE KINASE (CK)-half life approx 6 hours. Any muscle damage. if ongoing, = ongoing myonecrosis.
Outline the interpretation of the coagulation profile
PT;measures extrinsic and factor vii and common pathways. Factors need to be at <30% normal to show abnormal test result. If have low fibrinogen, can prolong PT irrespective of levels of factors of interest.
APTT; measures intrinsic (xii,xi, ix and x) and common pathways. Low fibrinogen cal prolong APTT irrespective of factors of interest levels. Factors need to be <30% normal to cause prolonged time, OR mild deficiencies along both common and intrinsic pathways can cause prolonged APTT. Difficult venupuncture can increase APTT.
ACT;done in diatomaceous earth tube. Tests same path as APTT but does require platelets (but low platelets may only cause mild increase in time)and time is prolonged when factors <10% normal.
BUCCAL MUCOSAL BLEEDING TIME-crude test of all factors in path including platelets.
PROLONGED PT AND NORMAL APTT; ddx inherited factor vii deficiency (does not cause clinical bleeding), early vitamin K deficiency (early rodentacide toxicity), DIC (esp cats), liver failure.
PROLONGED APTT AND NORMAL PT; ddx Artifact –
difficult venipuncture.
* Iatrogenic – unfractionated heparin therapy
* Inherited deficiency – haemophilia A (FVIII deficiency) and haemophilia B (FIX deficiency)
in dogs. FXII deficiency in cats (common – not required for physiologic haemostasis, so will
not cause haemorrhage)
* Disseminated intravascular coagulopathy – especially in dogs
* Anti-phospholipid antibodies – dogs with systemic lupus erythematosis
* Liver failure
PROLONGED PT AND PROLONGED APTT; ddx Multiple factor deficiencies, affecting both extrinsic and intrinsic pathways or common
pathway factor deficiencies.
o Vitamin K deficiency – e.g. rodenticide toxicity
o Disseminated intravascular coagulopathy
o Liver failure
o Hypofibrinogenaemia
-Snake envenomation (black snake).(browns and tigers are pro-coagulatory which can lead to consumption of factors, then dic and prolonged pt and aptt).
Identify artefact that may affect clinical pathology results in terms of animal breed, sample artefact and laboratory artefact
6
Describe aFAST and tFAST techniques
aFAST;used for quick initial evaluation esp for trauma patient. To detect free fluid in abdomen. Can also be used for non trauma patients with suspected abdominal fluid eg cardiac ascites, bleeding abdo mass, peritonitis etc.For trauma, free fluid is usually blood or urine. Usually done via Lisciandro technique which is right lateral recumbency and sequentially view the 4 windows:
Step 1)
Cranial part of the abdomen at the gall bladder diaphragmatic-hepatic (DH) view. Under xiphoid. Fan through. Can also see if any pericadrial effusion.
Step 2)
Probe is then moved caudally and laterally to assess the left ‘gutter’ spleno-renal (SR) view. Find left kidney, let it almost fill screen, fan around.
Step 3)
After this, the probe is moved caudally to assess around the urinary bladder cysto-colic (CC) view. Cranial part of bladder.
Step 4)
And finally, the probe is moved ventrally and cranially to assess around the dependent kidney (right)
in the hepato-renal (HR) view.Need to get under patient.
Since the right kidney can be very difficult to locate in a patient in right lateral recumbency,
identifying it is not necessary since the purpose is to identify free fluid pockets.
Can also do 5th view which is at umbilicus-fan down to view any dependent pooling (if push too hard, fluid will move away from probe).
Look for triangles of fluid (anechoic).
No shaving necessary (BUT does help). apply alcohol to skin.
tFAST; normally cannot transmit u/s through normal lung. Therefore do rapid assessment to identify abnormalites such as pneumothorax, pleural effusion, pericardial effusion, chest wall defects, and other intrathoracic abnormalities.
Usually follow the vetBLUE TECHNIQUE;
Outline the abdominal fluid scoring system
From aFAST exam;
Score the fluid seen;
0 = absence of fluid
1 = fluid at one site
2 = 2 sites
3 = 3 sites
4 = all four sites have fluid
There is a correlation with patients with a score of 3 or 4 requiring more intensive management such
as requiring more blood products, damage control surgery, and potentially antifibrinolytic agents
such as tranexamic acid.
Describe and outline VetBLUE including the acoustic windows
The 4 major lung regions that are assessed on the left and right sides are:
▪ Dorso-caudal lung region
▪ Perihilar region
▪ Middle lung region
▪ Cranial lung region
Patient to be in sternal recumbency (or standing)
o Can be done without clipping the hair and the use of alcohol/lube applied directly to
the contact points
o Holding the probe horizontally to the body wall, begin with the probe placed on the
dorso-caudal abdominal region, just caudal to the last rib.
o At this point you should move it cranially until the normal curtain sign is visualised.
This where the lung starts to slide in and out of view in time with respiration. This
highlights the most caudal aspects of the thoracic cavity.
o From here the probe is moved cranially two ribs, this is the dorso-caudal lung region
o Then the probe is moved cranially and ventrally to the perihilar region, followed by the
middle lung lobe region, and finally the cranial lung lobe region
o With the cranial lung lobe region, you may have to move the probe up under the axilla
to properly assess this region
o At each of the four regions, the probe is moved 1-2 intercostal spaces back/forth and
1-2cm ventrally and dorsally, to assess the lung.
o This is repeated on the other side of the chest, giving the 8 sites
Identify lung ultrasound signs - A lines, B lines, glide sign
A-LINES;cannot normally penetrate more than 1-3mm. therefore get horizontal reverberation artifact lines parellel to pleural interface. Normal in dry lungs
B-LINES;(lung rockets) hyperechoic streaks penetrating deeper into lungs. More than 2 is abnormal. Greater number= greater severity. (very severe merges into one =white lung or infinity rockets))Caused by fluid/cells in the outermost 3mm of lungs. If B lines are present, pneumothorax is not.
Bilateral rockets ddx cardiogenic or non cardiogenic pulmonary oedema. Unilateral rockets is usually lung contusion or pneumonia (aspiration pneumonia is usually middle right lobe).
GLIDE SIGN;normal movement of lung with insp/exp. Absence suggests pneumothorax.Proceed to emergency thoracocentesis.
LUNG POINT-explores transition from abnormal to normal lung in pneomothorax to determine extent.Glide signs recur in normal zone.
Describe likely disease processes using the regionally based respiratory pattern
a) All lung fields DRY:
o Rules out clinically relevant left-sided congestive heart failure
o Suggests upper airway obstruction
▪ E.g. upper airway foreign body, feline asthma, chronic obstructive
pulmonary disease, pulmonary thromboembolism, non-respiratory
disease.
b) Dorsal, perihilar and middle lung lobe regions WET:
o Cardiogenic pulmonary oedema
▪ DDx: LSCHF, iatrogenic fluid overload
c) Dorsal lung lobe region WET:
o Non-cardiogenic pulmonary oedema
▪ E.g. Neurogenic, smoke inhalation, electrical
d) Ventral fields WET +/- shred sign/ tissue sign (consolidation):
o Pneumonia
e) Solitary nodule:
o Primary pulmonary neoplasia
f) Multiple nodules:
o DDx: metastatic pulmonary neoplasia or granulomatous disease
STEP SIGN is where the glide sign deviates from the normal linear continuity of pulmonary-pleural
interface and suggests a partial pneumothorax, or concurrent thoracic injury such as haemothorax,
rib fractures, intercostal muscle tear, pulmonary contusions, or diaphragmatic hernia.
Describe focused echocardiography and the use of this technique
Focused echocardiography is a bedside or crash bench assessment of the heart to help determine 4
things:
1. Degree of contractility to assess for dilated cardiomyopathy
2. Assessment of chamber sizes to indicate left or right sided heart failure
3. Assessment of chamber wall thickness for hypertrophic cardiomyopathy
4. Presence or absence of pericardial effusion
The focused echocardiogram has 3 basic views - all obtained from the right parasternal acoustic
window.
The right parasternal acoustic window is located between the right 3rd and 6th intercostal spaces
(usually 4th or 5th) and between the sternum and costochondral junctions. where the patient’s elbow touches the sternum can sometimes be helpful in locating the acoustic window.
Once the heart is located, generally the probe does not need to be moved on the skin, only the angle
and orientation of the probe is altered.
In cats, pericardial effusion is usually due to congestive heart failure, does not require drainage, and usually precedes pleural effusion.
