Final Flashcards
T/F: you should always interpret abnormalities on blood panels in light of your clinical picture
True
How can you compartmentalize the CBC? Chem?
CBC:
-erythron
-leukom
-thrombon
Chemistry+urine+blood gas:
-protein metabolism
-energy metabolism
-renal
-minerals
-electrolytes and acid base
-liver
-muscle
-pancreas and GI
How should you interpret proteins?
In context of the chemistry- look at protein metabolism
What is the difference between hematocrit and PCV?
Hematocrit is calculated by machine
-disagree in cases of IMHA due to agglutination. MCV will also be affected if HCT is affected (MCV used to calculate the hematocrit)
-In the case of IMHA, trust the PCV not the hematocrit
What values should you look at to determine if an anemia is regenerative?
Reticulocyte count, percent, morphological changes
What is a test you can send out blood for to farther classify an anemia?
Iron panel
What should be the proportion between hemoglobin and hematocrit?
Hemoglobin X 3 = hematocrit (+/- 1-3)
-when this is not the case, this is likely due to hemolysis
How can you differentiate in vitro vs in vivo hemolysis?
In vivo- patient may have icterus which would indicate actual hemolysis in the patient
What is one reason that a patient with a systemic infection may have a low lymphocyte count?
Stress
-can have simultaneous corticosteroid and inflammatory leukogram
What should you do if you are worried about an erroneous platelet result?
Do a blood smear
In what species is enlarged platelets (increased MPV) normal?
Cat
What is the cause of giant platelets? What will they look like on a CBC?
Due to megakaryocyte replenishing of platelets (due to consumption in most cases)
-will appear as an increased RBC count
What can decreased fibrinogen indicate?
Impaired liver function, impaired coagulation, inflammation
T/F: globulins are measured for a Chemistry
False- just total protein minus albumin
How do you determine if fibrinogen is increased due to inflammation or due to dehydration?
PP:F Ratio (PP- fibrinogen)/Fibrinogen
-In horses <15 is inflammation, >20 is dehydration
-In cattle <10 is inflammation, >15 is dehydration
If between the two values, both are probably present
How can serum protein electrophoresis help you better determine a patients protein status?
To better determine what is happening with globulin proteins, specifically beta 2 and gamma
-cancer may cause monoclonal increase, vs if polyclonal more likely from infectious process
How can you evaluate energy metabolism?
Look at carbohydrates and lipids
Why may animals with diabetes have low glucose in the urine?
Due to osmotic diuresis
-always have to keep in mind the hydration status of the patient
What is included in the primary vs secondary renal panel?
Primary: creatinine, BUN, UPC on urinalysis, SDMA (dont rely on only this, often reflects other values)
Secondary: Albumin, Minerals, Electrolytes, acid-base
What mineral is very affected by increased or decreased GFR?
Phosphorus
What does 3/4 loss of renal loss lead to? 2/3?
3/4: azotemia
2/3: Isosthenuria
What makes up the primary and secondary renal panel?
Primary: calcium, phosphorus, magnesium
Secondary: Albumin, ALP, Renal Profile
What calcium is reflected on a blood panel?
Total calcium
-composed of ionized calcium (50-55%), protein bound calcium (35-45%), and complexed calcium (5-10%)
T/F: if albumin is lost, calcium should drop proportionally
True
What is the synonym for total CO2?
Bicarb
-used to calculate ion gap (sum of positive things minus negative things)
Can you tell anything about respiratory alkalosis or acidosis on a chemistry?
NO
-can only look at metabolic components
What does a lot of chloride mean? too little?
Excess chloride: metabolic acidosis
Too little chloride: metabolic alkalosis
** chloride behaves as an acid. If chloride decreases bicarb will increase to compensate
T/F: Uremic acids are the same thing as BUN
False- they are the other acids that are not measured on blood panel
-ex: citrates and sulfates
How do you calculate corrected chloride? Why do you do this?
To determine if the chloride is following the sodium. Can help you determine if there is a true alkalosis or acidosis.
(average Na/measured Na) X measured Cl
What are the main things you look for on the liver panel?
Liver injury (ALT,AST, GDH, SDH, LDH)
Liver function (Albumin, BUN, Glucose, cholesterol, coag factors, conjugated bilirubin, fibronogen, ammonia, bile acids, RBCs)
Cholestasis (indicated by increased GGT, ALP)
T/F: in horses you can use ALT and AST as a marker of liver function
F- because very influenced by red blood cells
T/F: you can have a patient with liver dysfunction without liver injury
TRUE
-also can have lots of liver injury with a functional liver
How can liver dysfunction lead to anemia?
The liver plays a large role in iron metabolism
Should you worry about liver enzymes being low?
NO- should only care when they are above the reference interval
With bad muscle injury, what may you see on urinalysis?
Myoglobin
What are the markers of the exocrine pancreas?
Lipase, amylase, Trypsin-like immunoreactivity (TLI), pancreatic lipase immunoreactivity (PLI), cobalamin, folate
What are the two things that can cause increased lipase or amylase?
Decreased GFR (usually more mild changes) or increased acinar pancreatic damage
What causes increased TLI and PLI? Decreased?
Increased: acinar pancreatic damage, decreased GFR
Decreased: chronic pancreatitis, acinar atrophy
What does decreased cobalamin and increased folate indicate?
Exocrine pancreatic insufficiency
How should you approach toxicology cases?
Look into what body systems are affected, onset time, morbidity and mortality
-history is critical- analysis is expensive so must have very defined differentials
What are the main categories of toxicants in small animal? Large animal?
Small animal: human or veterinary medicines and foods, insecticides and rodenticides, house and garden products
Large animal: metals and minerals, toxic plants, mycotoxins, feed additives and contaminants
What does 16 ounces equal?
1 pound/pint
How many pints are in a quart?
2
How much does 1 milliliter weight?
1 gram
What does percent equal?
gram or mL per 100 grams or mL
What is 1 fluid ounce equivalent to?
30 mL
What is 1 ppm equivalent to?
1 mg/kg
How do you determine a mg/kg dose in feed?
ppm in feed X percent BW eaten per day
What organ system do insecticides target?
Nervous system
What insecticides target the sodium or chloride channels?
Pyrethroids, avermectins, fipronel
What insecticides target acetylcholine receptors?
Organophosphates, Carbamates, Neonicotinoids
-mainly cause parasympathomimetic signs (pupil constriction, hypersalivation, decreased HR)
How can you diagnose Organophosphate or Carbamate Toxicity?
Give preanesthetic dose of atropine (0.01-0.04 mg/kg IV). If signs resolve this is not the cause
-If no change, give antidotal dose (0.2 mg/kg)
-can also measure acetylcholinesterase activity of heparinized whole blood and/or brain tissue to confirm (70% reduction of activity is reasonably diagnostic)
What is the treatment for cholinesterase inhibitor toxicity?
Atropine is the first treatment to counteract signs
-be careful not to overdose and cause atropine toxicity (treat with diazepam)
-give initial dose of 0.1-0.5 mg/kg. can give 1/4 IV and rest IM or SQ to prevent overdose
2-PAM (pralidoxime) secondarily
-regenerates of AChE
-20-50 mg/kg early
-works against nicotinic signs
Are there any anecdotes for pyrethrins? What species is the most affected?
NO- must do empiric treatment (decontamination)
Cats are the most affected
What are the 5 main Rodenticides that you worry about in small animals? What do they target?
- Bromethalin: targets nervous system, no anecdote. Important to calculate amount ingested and decontaminate
- Vitamin K Antagonists: target hematopoietic system, treat with vit K.
- Cholecalciferol: targets kidney
- Strychnine: targets nervous system (causes tetanic seizures)
- Zinc Phosphide: changes to a volatile gas and causes respiratory problems
How should a DVM act if there is a suspected metal or mineral toxicosis?
-obtain history, review signs, assess site
-perform physical
-review unique characteristics of metals and minerals that may be involved
-prioritize suspected toxicants
-collect appropriate samples for testing. Collect from animal and the environment
-confirm with toxicology testing
What are the possible metal toxicities, what are their sources, and what do they target?
Lead: acute and chronic exposure from many sources. Has multi system effects (CNS, GI, kidneys)
Sodium: CNS toxicity from water deficiency (can be affected by ionophores)
Copper: in copper wire, chronic exposure via feed additive with acute released from liver especially in stressed sheep
Zinc: in galvanized meal, metallic nuts and bolts. Has hematopoetic effects
Arsenic: in soils, ores, and ash of treated wood, targets GI tract
Iron: in drugs, fertilizers, and metal objects that rust. Target GI tract and liver
Selenium deficiency: chronic from deficient soil, targets muscle
How do you treat lead toxicity?
Calcium EDTA 75 mg/kg
-3 days of and 3 days off dosing
-not allowed to use in Food animals as it remains in meat for years
T/F: in tox cases, you should only treat animals with clinical signs
True in most cases
What are seven important mycotoxins that can contaminate animal feed/food?
Aflatoxin: hot, dry season, mainly in corn, GI and liver target
Vomitoxin: cool, set season production mostly in small grains, GI target
Zealenone: co exists with vomitoxin, repro system target
Slaframine: produced in clover, limited cholinergic effect
Penitrem A: in rotting dairy products, garbage, neurotoxic
Roquefortine: in rotting compost, garbage, neurotoxic
Fumonisin: moldy corn products, neurotoxic
**food/feed contaminations can also include bacteria and their toxins
T/F: There is no diagnostic test for mycotoxins in biological samples from animals exposed
True- must save the food
Describe the toxicity of bulbs
-includes daffodils, tulips, iris, hyacinths, crocus, amaryllis, gladiolas
-toxicity: not well characterized, usually not lethal. Includes irritant resins, alkaloids and/or insoluble calcium oxalate
-clinical signs: mostly in dogs, onset time <1 hr. Causes salivation, vomiting, diarrhea
-treatment: decontamination, multiple doses activated charcoal, cerenia
What is the mechanism of action of bulb toxicosis?
Contact irritant, allergen, centrally acting emetic, decreased protein synthesis
Describe onion and garlic toxicity
Also a bulb
-toxic in all forms (toxic dose 0.5% body weight or 5 g/kg)
-cats and cattle affected more than dogs
-MOA: metabolism to disulfides cause oxidative damage to RBCs–> lysis
Signs: odor on breath, vomiting, anemia, hemoglobinuria
Treatment: decontamination and symptomatic
Prognosis is dose dependent
What system is affected by Christmas plants?
GI tract
-but Christmas trees can cause hepatic nephrosis, and nephrosis (due to phenols and pine oils)
Which toxins are the most toxic to cats of the following list:
1. tulips
2. Onions
3. Mistletoe
4. Pine
Onions and pine
What are the main cardiotoxic plants?
-Christmas kalanchoe, oleander, foxglove, lily of the valley
-cardioactive steroids (digoxin and oleandrin)
What is the lethal dose of oleander?
0.005% of body weight
What is the mechanism of action of cardiotoxic plants?
All parts of the plant are toxic, and all animals are susceptible
-GI irritants
-inhibition of NA/K ATPase pumps
-increases intracellular sodium and calcium –> positive ionotrope
-increased extracellular potassium leads to a decreased resting membrane potential and impaired conduction
-causes bradycardia and dysrhythmias
What are the clinical signs associated with cardiotoxic plants?
-anorexia, hypersalivation, vomiting/diarrhea, colic, depression/lethargy, marked weakness
-various arrythmias: Bradycardia/AV block/tachycardia
-weak irregular pulses
-death usually from asystole and Vfib
How can you diagnose cardiotoxic plant toxicosis?
-history, clinical signs, presence of plant in GIT
-clin path shows hyperkalemia
-serum analysis/urine analysis for specific toxin (immunoassays for digoxin and digitoxin)
-ECG abnormalities
What is the treatment for cardiotoxic plants?
Activated charcoal, atropine and glycopyrrolate (to increase HR), lidocaine
In small animals can use Digibind (antibody to bind digitalis and others)-very expensive
What are some other cardiotoxic plants can affect cattle and horses?
-Dogbane, common milkweed can end up in haybales
-diagnose same way as small animals (unlike to do ECG though)
Describe tobacco poisoning in small animals
Frequently occurs from puppies licking ashtrays
-alkaloid toxicity
-effects on CNS, GI, indirectly cardiovascular
-can be toxic at 1 mg/kg
-signs include nausea, salivation, irritation of mouth and stomach, weakness, staggering, resp problems, erratic heart rate and BP
-treatment: remove residual tobacco, assist resp, stabilize heart and BP
What occurs with Yew toxicosis?
-all parts of plant are toxic (taxine alkaloid)
-direct affect on myocardium with depression of AV node conduction–> bradycardia, hypotension and diastolic cardiac arrest
-fast onset (15 min-24 hr)
-signs: dyspnea, bradycardia, convulsions, trembling, diarrhea, incoordination, depression, lethargy, SUDDEN DEATH
-can often diagnose with necropsy by analyzing GI contents. Other options are taxine analysis of stomach contents
-treatment: atropine, activated charcoal, saline cathartic
-guarded prognosis even if they don’t die right away
What are the toxic shrubs we discussed? How do they cause toxicosis?
Rhododendron, Azaleas, Mountain Laurel
-contains grayanotoxins (all parts of plants toxic), sheep and goats most likely to be affected
-causes heart arrythmias and vomiting through stimulation of the vagus nerve (decreases HR)
-diagnose mainly through clinical signs. Die due to heart effects
What is the treatment for rhododendron, azalea and mountain laurel?
-stop vomiting with acepromazine
-then give activated charcoal and a saline cathartic
-appropriate drugs for arrythmias (lidocaine for tachycardia, atropine for bradycardia)
Describe buckeye toxicosis
-all parts are toxic
-aesculin is toxin
-unknown MOA
-clinical signs: goose stepping (hypermetra), ataxia, muscle tremors, paralysis, hyperesthesia
-diagnose on necropsy of stomach contents
-treat with sedative until signs resolve
-morbidity not mortality problem
What species does black walnuts affect?
Horses- can be used as bedding and horses can ingest
-causes enhanced constriction of blood vessels of the woof wall which can lead to laminitis
-diagnose through analysis of wood shavings in bedding (dark, chocolate brown color)
-treatment: activated charcoal, cathartics, mineral oil, acepromazine, DMSO, pain meds, prazosin (vasodilator)
What part of oak trees causes toxicity problems?
Acorns
-tannic acid causes inactivation of phenols and denatured proteins
-causes gastroenteritis and ulceration as well as severe kidney damage (proximal tubule damage)
-only tends to cause problems in cattle
-clinical signs: ventral edema, dyspnea, black diarrhea, colic
-diagnosis: evidence of renal failure (elevated BUN/creatinine, decreased sodium, chloride, calcium, increased magnesium)
-treatment: fluid therapy, electrolyte replacement, vitamin B, transfaunation, calcium hydroxide
-major differential is pigweed
How can you avoid acorn toxicosis?
Pasture management
Which maple tree is the most toxic?
Red maple in horses
-causes oxidative damage and heinz body formation, methemoglobin formation and hemolysis
-clinical signs: cyanosis, heinz body anemia, methemoglobinemia
-long onset (1-2 days after ingestion)
-lesions: icterus with hepatic, centrilobular necrosis, splenomegaly, reddish-black kidneys (similar to copper)
How do you diagnose and treat maple toxicosis?
-diagnosis through history and clin path (decreased PCV, increased bilirubin, AST, SDH, BUN, creatinine)
-treatment: activated charcoal, saline cathartic, blood transfusions, ascorbic acid (antioxidants), fluid therapy, pain meds (NO STEROIDS)
-causes more morbidity than mortality
What are the cyanogenic plant sources?
Prunus (cherries) and sorghum species
What happens with cyanide toxicity?
-glucuronidation in the rumen causes separation of the sugar from cyanide
-most toxic in the wilting stage when the cyanide becomes volatile
-can cause sudden death in ruminants, especially goats
-prevents oxygen from leaving the blood leading to cherry red blood, and inability of oxygen to be used by tissues (brain is very sensitive to low oxygen)
-ddx: nitrate poisoning (but blood will be brown in that case)
-clinical signs: bright red mucous membranes, CNS signs, coma, sudden death
-treat with thiosulfate, nitrite, B12
What happens behind the scenes in a clin path lab?
-test validation
-test comparison
-quality management
-reference intervals
-development of new methodologies and applications
Describe how reference intervals are obtained?
Ideally by sampling at least 120 individuals within a population (several breeds, equal male/female, all ages)
-take average of population and take 2 standard deviations above and below to determine interval
-can have reference intervals for different life sages
-reference intervals vary with equipment, methodology, location and patient
T/F: reference interval is very specific to the region you are in and equipment you are using
True
What should you do if there is not a reference interval available for the species you are working with?
Can compare to reputable sources on the internet
What is the minimum animals accepted to determine a reference interval?
40- often done in minor species as its hard to find 120 normal animals for a study
-with exotic animals, may have to reduce numbers farther and do fancy statistics to increase clinical relevance
What are the 3 types of lab errors?
- Preanalytical (46-68%)
- Analytical (7-13%)
- Post-analytical (19-47%)
What are some examples of pre-analytical errors?
-inappropriate test request
-order entry error or error on request form
-misidentification or labelling error
-inappropriate container or sample
-insufficient volume
-inadequate transport or storage
-sample processing before analysis
If you have a small or fractious patient, how can you prioritize tests?
Based on differentials
-only have a limited amount of blood, cant run all the tests with not enough blood
What can excess EDTA in a purple top tube cause?
Errors in morphology (lots of echinocytes)
-decreased MCV and HCT
-hypocalcemia,hyperkalemia
What is the concern for lack of blood in a citrate tube?
Will dilute the sample and lead to false clotting results
How can you avoid preanalytical errors?
-SOPs
-training of personnel
-communication with clients