ECC/ Tox Flashcards
Exam 1
What is normal [Na] in the plasma? (dogs and cats)
Dogs: 142-151mEq/L
Cats: 153-158mEq/L
T/F: Na is the most abundant electrolyte in the extracellular space.
True
Dysnatremia is most often due to an imbalance in what? (don’t just say sodium)
Water
3 causes of Hypernatremia
- excessive water loss (urine + gi) [diabetes insipidus most common]
- excess sodium intake [playdough, beef jerky]
- inadequate water intake [usually a sole problem like getting locked in the garage]
2 causes of Hyponatremia
- Increased water retention - requires elevated ADH [inadequate circulatory volum, diuretic therapy, addison’s disease]
- Excess water intake [iatrogenic]
Clinical signs of dysnatremia
- obtundation
- disorientation
- head pressing
- seizures
- coma
- death
How to calculate plasma osmolality?
Osmo = (2 Na) + (BUN/ 2.8) + (glc/ 18)
What molecule contributes most to plasma osmolality?
Sodium
How do cells defend against changes in cell size and shape?
they have internal mechanisms (physical structures) that prevent shape/ size change (microtubules and such)
Treating Hypernatremia
- administer electrolyte-free water source @ 7-10mL/kg*hr w/ 5% dextrose (until neuro signs resolve)
- treat as ‘stable hypernatremia’ w/ 3-7ml/kg*hr to return [Na] to normal within 48 hrs
- monitor [Na] on a single machine to prevent errors
Treating Hyponatremia
- hypertonic slaine treatment until clinical signs begin to diminish
- diuretic therapy w/ furosemide/ mannitol
Psuedohyponatremia
- does not require treatment
- results from hyperglycemia (every 100 increase in glc causes a ~2mEq/L drop in Na
T/F: a majority of the K in the body is intracellular
T
T/F: K is super tightly regulated within the body
T
T/F: Hyperkalemia usually presents with musculoskeletal signs while Hypokalemia presents cardiac
F: Hyper presents with cardiac signs and Hypo presents with musculoskeletal
Causes of Hyperkalemia
- inadequate excretion (renal or post-renal, Addison’s, chronic body cavity effusions)
- Excessive intake (iatrogenic)
- Rarely w/ metabolic acidosis
ECG changes with Hyperkalemia
- tall, tented T waves
- loss of P waves
- bradycardia
- widening of QRS
- A. systole or v. fib (death)
Treatment of Hyperkalemia
- cardioprotection (IV calcium gluconate)
- Elimination via IV fluid therapy –> Increase GFR
- Drugs to shift K into cell (insulin + dextrose) (terbutaline)
Pseudohyperkalemia
- thrombocytosis (platelet degranulation leads to K release)
- Japanese Breeds w/ hemolysis of RBCs
Causes of Hypokalemia
- kidney failure (CKD)
- diuretics or other causes of PU/PD
- Diarrhea, vomiting or , dec intake
Toxin (Rare) - beta agonist
Clinical signs of Hypokalemia
- muscle weakness (cervical ventroflexion)
- ECG changes (short T waves, tall P waves)
Treatment of Hypokalemia
- supply IV potassium in fluids + treat underlying disease
- Kmax = 0.5mEq/kg*hr (do not exceed unless actively monitoring the ECG)
T/F: Chloride is the major extracellular anion and often comes close to matching [ ] with Na
T
Causes of change in [Cl]
- change in free water balance
- met. alkalosis w/ hypochloremia w/ loss of HCl (pyloric outflow obstruction)
- GI or kidney loss of bicarb
- Iatrogenic
Pseudohyperchloremia
- KBr administration, the Br will falsely read as Chloride on the machine
Treatment of hypochloremic met alkalosis
- 0.9% NaCl to help kidney eliminate bicard
Treatment of hyperchloremic met. acidosis
- LRS, fluids w/ low [Cl]
Calcium functions in the body
- coagulation
- cardiac contractility
- muscle contraction
Causes of Hypocalcemia
- Eclampsia (puerperal tetany)
- CKD
- pancreatitis
- iatrogenic (blood transfusions)
Clinical signs of hypocalcemia
mild: none
moderate: facial pruritis, muscle tremors, ‘tetany’
severe: seizures, obtundation, cardiac dysrrhythmias, death
Treatment of hypocalcemia
IV calcium fluids
Hypercalcemia causes acronym
HARD IONS
3 main types of shock
- Vasoconstrictive
- Metabolic
- Vasodilatory/ Distributive
What are the 6 perfusion parameters
- Mentation
- CRT
- mucous membrane color
- extremities temp
- peripheral pulse quality
- heart rate
Hypovolemic Shock (pathogenesis)
- decreased venous return -> dec preload -> dec SV -> dec CO -> dec tissue perfusion
Causes of Hypovolemic shock
- hemorrhage
- ongoing water losses
- third space losses
Common Causes of obstructive shock
- GDV
- cardiac tamponade
- tension pneumothorax
- thrombus
- space occupying lesions
Causes of Cardiogenic Shock
- poor contractility
- HR too low or too high
- valvular insufficiency
T/F: All types of vasoconstrictive shock can be treated isotonic fluids
F: cardiogenic shock cannot be treated with isotonic fluids
Most common cause of vasodilatory shock
- Septic shock
Shock resuscitation goals
- O2 therapy
- vascular access or intraosseus catheters
Isotonic fluids Shock dose
Dogs: 80-90mL/kg
Cats: 40-60mL/kg
When to use hypertonic saline
- large animals w/ hypovolemic shock
- treat cerebral edema
Contraindications of hypertonic saline
- cardiogenic shock
- hypernatremic
- dehydrated patients
Max rate = 4mL/kg over 5 min.
Colloids fucntion
- increase plasma oncotic pressure
indications for colloids
- hypovolemic shock
- obstructive shock
- septic shock
- shock w/ hypoalbuminemia
Contraindications for colloids
- cardiogenic shock
- acute kidney injury
- coagulopathy (interferes w/ vWF)
2 sources of heat production
- basal metabolic rate (dec w/ shock and inc w/ disease)
- increased muscle activity (excercise, resp distress)
Forms of heat loss
- convection (through air)
- conduction (direct contact)
- radiation
- evaporation (humidity dependent)
Factors affecting heat loss
- body SA/ mass
- insulation (BCS)
- external temperature
- relative humidity
Heat stress vs Heat stroke
Heat stress: lethargy, weakness, vomiting, diarrhea, tremors
Heat stroke: evidence of CNS dysfunction +/- liver dysfunction
Critical temps vs heat-time product
- max temp is probably around 112F
- heat-time product refers to the amount of time spent at a certain temperature
Heat stroke pathogenesis
- direct thermal injury to endothelial cell and proteins -> cytokines activate WBC + coagulation -> microvascular thrombosis -> inflammation, ischemia, direct thermal injury -> MODS (multi-organ dysfx syndrome) -> death
Hyperthermia treatment
- room temp fluids
- cool the patient with whole water bath
- measure BG
- check plasma for coagulopathies
- IV fluids for dehydration, dec BG, electrolytes
Prognosis for hyperthermia (neg indicators)
- seizures
- nRBC
- hypoglycemia
- DIC
- AKI
Primary vs Secondary Hypothermia
Primary - exp. to low environmental temps
Secondary - d/t disease, drugs, surgery, etc
Physiological effets of hypothermia
- bradycardia (SA node is temp dependent)
- initial vasoconstriction, then loss
- dysrhythmias
- hypovolemia from cold diuresis
- coagulopathy in sever hypothermia
Rewarming (passive vs active)
Passive: reduce heat loss, blankets
Active: applies exogenous heat, forced air blanket, IV warm fluids
Complications w/ rewarming
- can causes vasodilation -> hypotension
- counter by administering fluids during rewarming
Therapeutic hypothermia
- used post CPR
- during great vessel occlusion
Drowning (aspiration rate)
- 90% of patients aspirate fluids into lungs while 10% do not, but rather die of hypoxia from laryngospasm
Dysnatremia from drowning
Hypernatremia in salt water
Hyponatremia from fresh water
Canine blood typing
- roughly 13 subtypes
- DEA 1 and DAL have very high incidence w/ no naturally occurring antibodies
Feline blood typing
either A, B, or AB
What would happen if you give A blood to a B type cat?
- it will kill the cat
What would happen if you give B blood to an A type cat?
- cat would just get sick, but most likely would not die
Indications for cross-matching blood types
- unknown transfusion hx
- > 7 days since first transfusion
- unknown donor type
- if donor DEA7 type unknown
What is the Major Cross-match
- donor RBCs mixed w/ recipient serum
What is the Minor Cross-match
- donor serum mixed w/ recipient RBCs
Fresh Whole Blood (contents, indications, pros, cons)
Contents - everything within normal blood
Indications - hemorrhage 2ary to coag, vWD, thrombopathy
Pros - contains everything
Cons - not readily avialable, need a lot
Packed RBCs (contents, indications, pros, cons)
Contents - RBCs and WBCs
Indications - Anemia (hemolysis, hemorrhage, dec EPO)
Pros - High PCV and available
Cons - contains nothing else
Fresh Frozen Plasma (contents, indications, pros, cons)
Contents - clotting factors, albumin, vWF
Indications - coagulopathy, vWD, hypoalbuminemia
Cons - expensive, adverse rxns
Platelet Rich Plasma (contents, indications, pros, cons)`
Contents - platelets, clotting facotrs, and albumin
Indications - hemorrhage from thrombocytopenia, DIC
Pros - High [platelets]
Cons - short shelf life, short T1/2
Cryoprecipitate (contents, indications, pros, cons)
Contents - contains factors 7, 13, fibrinogen, vWF
Indications - vWD, hemophelia A/B
Pros - High [vWF]
Cons - expensive, not readily available
Cryopoor Plasma (contents, indications, pros, cons)
Contents - does not contain 5, 8, vWF
Indications - VIt-K dependent coagulopathy, hypoproteinemia
Acute hemolytic transfusion reaction
- intra/extra vascular hemolysis
- IgM/G mediated reaction
- clinical signs (restlessness, vomiting, hypotension, collapse, hemoglobinemia/uria, vasodilatory shock, AKI)
T/F: cats are more resistant to anticoagulant rodenticides than dogs.
T
MOA of Anticoagulant rodenticides
- prevents activation of Factors 2, 7, 9, 10 (vit. k dependent clotting factors)
What elevates first w/ anticoag rodenticides (pt or ptt)
PT elevates first because Factor 7 has the shortest half life
Clinical signs of anticoag rodenticides?
- lag period of 3-5 days, but signs can occur as early as 24hrs
- determined by site, volume, and rate of hemorrhage
- elevated PT/PTT
Treatment of anti-coag rodenticides (asymptomatic patient)
- induce vomiting + activated charcoal
- vit k1 therapy
Treatment of anti-coag rodenticides (symptomatic patient)
- provide clotting factors via transfusion
- O2 therapy
- Vit. K1 therapy
T/F: cats are more susceptible to bromethalin rodenticides than dogs
T
Clinical Sings of bromethalin rodenticides (high dose, low dose)
- dose dependents
- high dose - tremors hyperexcitability, seizures, hyper-reflexia, depression
- low dose - hind limb ataxia and paresis, loss of deep pain, CNS depression
Diagnosis of bromethalin rodenticides
detection of metabolite in fat, brain, liver, or baits
vacuolar myelinopathy from the edema
Treatment of bromethalin rodenticides
- control CNS signs
- no antidote
- prognosis is v poor
Cholecalciferol toxicity (clinical signs)
- anorexia, vomiting, diarrhea, PU/PD, ECG changes
Cholecalciferol toxicity (Diagnosis)
- clinical signs
- hx of exposure
- metastatic calcification
Cholecalciferol toxicity (Treatment)
- decontam. if possible
- monitor serum [Ca] and treat hypercalcemia if necessary
What is the first course of action on an animal coming in for potential toxicity?
- make sure they are stable/ stabilize the patient
Ethylene Glycol (MOTA)
- metabolites bind to Ca to form Calcium oxylate crystals –> AKI
- parent compound is slightly CNS depressing
Ethylene Glycol (clinical signs, phase 1-3)
Phase 1 - CNS depression
Phase 2 - severse acidosis, inc RR
Phase 3 - AKI + renal failure
Ethylene Glycol (diagnosis)
- detection of parent compound
- very elevated kidney [Ca]
Ethylene Glycol (treatment)
- prevent metabolism of EG into metabolites w/ ethanol or fomepizole (inactivate alcohol dehydrogenase)
Xylitol (Clinical Signs)
- emesis, lethargy
- hypoglycemia
- elevated liver enzymes and bilirubin
- coagulopathy, thrombocytopenia
Xylitol (diagnosis)
- hx of exposure
- relevant clinical signs
Xylitol (Lesions)
- gross hemorrhage
- microscopic hemorrhage, acute hepatic necrosis
Xylitol (treatment)
- decontamination - emesis, AC not useful
- treat hypoglycemia
- treat coagulopathy
- hepatoprotectants
Methylxanthines (clinical signs)
- vomiting and diarrhea
- hyper-reflexia,
- tachycardia, possible PVCs
Mainly cardio and CNS excitability (over-caffeinated)
Methylxanthines ( Diagnosis)
- alkaloids in tissues, urine, or stomach contents
Methylxanthines (Treatment)
- decontamination
- control seizures
- treat tachycardia and PVCs
- B-blockers such as metaprolol
Amanitin (target organ)
- liver
Amanitin (MOA)
- bind eukaryotic DNA-dependent RNA polymerase II which inhibits RNA elongation essential for transcription
Amanitin (Clinical Disease)
- asymptomatic incubation of 6-12 hrs
- GI phase (12-24 hrs) - diarrhea, vomiting, abd pain, dehydration
- Hepatotoxic phase ( 24-48 hrs) - liver damage and coagulopathy
- Hepato-renal phase - hemorrhage, convulsions, fulminant hepatic failure, coma and death
Amanitin (clin-path findings)
- HIGH [AST]
- hypoglycemia
- coagulopathy
Amanitin (treatment)
- AC
- IV fluids, correct hypoglycemia
- antiemetics
Cycad Palms (target organ)
- gi and hepatic necrosis
Kalanchoe (target organ)
- cardiac glycoside (like oleander)
Easter Lily (target organ)
- kidney/ nephrotoxic
Philodendron (target organ)
- insoluble Ca-oxylates (mechanical irritation)
Acetaminophen (target organ)
Cats - RBCs d/t formation of methemoglobin
Other - hepatotoxic
Acetaminophen (Clinical Signs)
- methemoglobin ( cyanosis, resp distress)
- heinz body anemia
- hematuria and hemoglobinuria
- Edema of face and paws
Acetaminophen (Diagnosis)
- History, clinical presentation, detection of drug in plasma
Acetaminophen (treatment)
- N-acetylcysteine is antidotal by binding directly to toxic metabolite
SSRIs (MOA)
- inhibits re-uptake of serotonin
SSRIs (Seratonin Syndrome Signs)
- agitiation, vocalizaiton
- vomiting, tremors
- hyperthermia, transient blindness
SSRIs (treatment)
- decontamination
- counter clinical signs such as tachycardia, hypertension, tremors
- counter w/ cyprohepatine
Amphetamines (Clinical Signs)
- sympathomimmetic toxidrome
- CNS overstimulation (hyperexcitability, agitation, tachycardia, hyperthermia)
- rarely depression, weakness, bradycardia
Amphetamines (treatment)
- control clinical signs –> mainly tremors/ seizures induing hyperthermia
Amphetamines (Diagnosis)
- urine samples
Albuterol (clinical signs)
- tachycardia v common
- VPCs less common
- hypokalemia (can be concerning)
Albuterol (treatment)
- w/ propanolol for tachycardia and hypokalemia
Cannabis (clinical signs)
- CNS signs ( CNS depression, ataxia, disorientation, mydriasis)
- urinary incontinence
- emesis
Cannabis ( Diagnosis)
- hx of exposure
- delta9-THC in urine
Cannabis (treatment)
- decontamination
- no antidote
Opioid Toxicity (clinical signs)
- emesis, defecation, salivation, CNS depression, miosis, ataxia
- Severe: resp. depression, constipation, hypothermia, coma, death
Opioid Toxicity (treatment)
- Naloxone
Opioid Toxicity (species sensitivity)
- cats are super sensitive
pRBC administration volume
pRBC (Volume) = 90 * BW * ( change in PCV/ donor PCV)
Treating Acute Hemolytic Transfusion Reaction
- 0.1 mg/kg dexamethasone
- fluid therapy for vasodilatory shock
