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VET 433a - Small Animal Stream 1 > ECC/ Tox > Flashcards

ECC/ Tox Flashcards

Exam 1

1
Q

What is normal [Na] in the plasma? (dogs and cats)

A

Dogs: 142-151mEq/L
Cats: 153-158mEq/L

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2
Q

T/F: Na is the most abundant electrolyte in the extracellular space.

A

True

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3
Q

Dysnatremia is most often due to an imbalance in what? (don’t just say sodium)

A

Water

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4
Q

3 causes of Hypernatremia

A
  1. excessive water loss (urine + gi) [diabetes insipidus most common]
  2. excess sodium intake [playdough, beef jerky]
  3. inadequate water intake [usually a sole problem like getting locked in the garage]
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5
Q

2 causes of Hyponatremia

A
  1. Increased water retention - requires elevated ADH [inadequate circulatory volum, diuretic therapy, addison’s disease]
  2. Excess water intake [iatrogenic]
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6
Q

Clinical signs of dysnatremia

A
  1. obtundation
  2. disorientation
  3. head pressing
  4. seizures
  5. coma
  6. death
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7
Q

How to calculate plasma osmolality?

A

Osmo = (2 Na) + (BUN/ 2.8) + (glc/ 18)

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8
Q

What molecule contributes most to plasma osmolality?

A

Sodium

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9
Q

How do cells defend against changes in cell size and shape?

A

they have internal mechanisms (physical structures) that prevent shape/ size change (microtubules and such)

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10
Q

Treating Hypernatremia

A
  1. administer electrolyte-free water source @ 7-10mL/kg*hr w/ 5% dextrose (until neuro signs resolve)
  2. 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
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11
Q

Treating Hyponatremia

A
  • hypertonic slaine treatment until clinical signs begin to diminish
  • diuretic therapy w/ furosemide/ mannitol
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12
Q

Psuedohyponatremia

A
  • does not require treatment

- results from hyperglycemia (every 100 increase in glc causes a ~2mEq/L drop in Na

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13
Q

T/F: a majority of the K in the body is intracellular

A

T

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14
Q

T/F: K is super tightly regulated within the body

A

T

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15
Q

T/F: Hyperkalemia usually presents with musculoskeletal signs while Hypokalemia presents cardiac

A

F: Hyper presents with cardiac signs and Hypo presents with musculoskeletal

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16
Q

Causes of Hyperkalemia

A
  • inadequate excretion (renal or post-renal, Addison’s, chronic body cavity effusions)
  • Excessive intake (iatrogenic)
  • Rarely w/ metabolic acidosis
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17
Q

ECG changes with Hyperkalemia

A
  • tall, tented T waves
  • loss of P waves
  • bradycardia
  • widening of QRS
  • A. systole or v. fib (death)
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18
Q

Treatment of Hyperkalemia

A
  • cardioprotection (IV calcium gluconate)
  • Elimination via IV fluid therapy –> Increase GFR
  • Drugs to shift K into cell (insulin + dextrose) (terbutaline)
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19
Q

Pseudohyperkalemia

A
  • thrombocytosis (platelet degranulation leads to K release)
  • Japanese Breeds w/ hemolysis of RBCs
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20
Q

Causes of Hypokalemia

A
  • kidney failure (CKD)
  • diuretics or other causes of PU/PD
  • Diarrhea, vomiting or , dec intake
    Toxin (Rare) - beta agonist
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21
Q

Clinical signs of Hypokalemia

A
  • muscle weakness (cervical ventroflexion)

- ECG changes (short T waves, tall P waves)

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22
Q

Treatment of Hypokalemia

A
  • supply IV potassium in fluids + treat underlying disease

- Kmax = 0.5mEq/kg*hr (do not exceed unless actively monitoring the ECG)

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23
Q

T/F: Chloride is the major extracellular anion and often comes close to matching [ ] with Na

A

T

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24
Q

Causes of change in [Cl]

A
  • change in free water balance
  • met. alkalosis w/ hypochloremia w/ loss of HCl (pyloric outflow obstruction)
  • GI or kidney loss of bicarb
  • Iatrogenic
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25
Q

Pseudohyperchloremia

A
  • KBr administration, the Br will falsely read as Chloride on the machine
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26
Q

Treatment of hypochloremic met alkalosis

A
  • 0.9% NaCl to help kidney eliminate bicard
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27
Q

Treatment of hyperchloremic met. acidosis

A
  • LRS, fluids w/ low [Cl]
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28
Q

Calcium functions in the body

A
  • coagulation
  • cardiac contractility
  • muscle contraction
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29
Q

Causes of Hypocalcemia

A
  • Eclampsia (puerperal tetany)
  • CKD
  • pancreatitis
  • iatrogenic (blood transfusions)
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30
Q

Clinical signs of hypocalcemia

A

mild: none
moderate: facial pruritis, muscle tremors, ‘tetany’
severe: seizures, obtundation, cardiac dysrrhythmias, death

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31
Q

Treatment of hypocalcemia

A

IV calcium fluids

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32
Q

Hypercalcemia causes acronym

A

HARD IONS

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33
Q

3 main types of shock

A
  1. Vasoconstrictive
  2. Metabolic
  3. Vasodilatory/ Distributive
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34
Q

What are the 6 perfusion parameters

A
  1. Mentation
  2. CRT
  3. mucous membrane color
  4. extremities temp
  5. peripheral pulse quality
  6. heart rate
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35
Q

Hypovolemic Shock (pathogenesis)

A
  • decreased venous return -> dec preload -> dec SV -> dec CO -> dec tissue perfusion
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36
Q

Causes of Hypovolemic shock

A
  • hemorrhage
  • ongoing water losses
  • third space losses
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37
Q

Common Causes of obstructive shock

A
  • GDV
  • cardiac tamponade
  • tension pneumothorax
  • thrombus
  • space occupying lesions
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38
Q

Causes of Cardiogenic Shock

A
  • poor contractility
  • HR too low or too high
  • valvular insufficiency
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39
Q

T/F: All types of vasoconstrictive shock can be treated isotonic fluids

A

F: cardiogenic shock cannot be treated with isotonic fluids

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40
Q

Most common cause of vasodilatory shock

A
  • Septic shock
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41
Q

Shock resuscitation goals

A
  • O2 therapy

- vascular access or intraosseus catheters

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42
Q

Isotonic fluids Shock dose

A

Dogs: 80-90mL/kg
Cats: 40-60mL/kg

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43
Q

When to use hypertonic saline

A
  • large animals w/ hypovolemic shock

- treat cerebral edema

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44
Q

Contraindications of hypertonic saline

A
  • cardiogenic shock
  • hypernatremic
  • dehydrated patients
    Max rate = 4mL/kg over 5 min.
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45
Q

Colloids fucntion

A
  • increase plasma oncotic pressure
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46
Q

indications for colloids

A
  • hypovolemic shock
  • obstructive shock
  • septic shock
  • shock w/ hypoalbuminemia
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47
Q

Contraindications for colloids

A
  • cardiogenic shock
  • acute kidney injury
  • coagulopathy (interferes w/ vWF)
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48
Q

2 sources of heat production

A
  • basal metabolic rate (dec w/ shock and inc w/ disease)

- increased muscle activity (excercise, resp distress)

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49
Q

Forms of heat loss

A
  • convection (through air)
  • conduction (direct contact)
  • radiation
  • evaporation (humidity dependent)
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50
Q

Factors affecting heat loss

A
  • body SA/ mass
  • insulation (BCS)
  • external temperature
  • relative humidity
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51
Q

Heat stress vs Heat stroke

A

Heat stress: lethargy, weakness, vomiting, diarrhea, tremors

Heat stroke: evidence of CNS dysfunction +/- liver dysfunction

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52
Q

Critical temps vs heat-time product

A
  • max temp is probably around 112F

- heat-time product refers to the amount of time spent at a certain temperature

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53
Q

Heat stroke pathogenesis

A
  • 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
54
Q

Hyperthermia treatment

A
  • room temp fluids
  • cool the patient with whole water bath
  • measure BG
  • check plasma for coagulopathies
  • IV fluids for dehydration, dec BG, electrolytes
55
Q

Prognosis for hyperthermia (neg indicators)

A
  • seizures
  • nRBC
  • hypoglycemia
  • DIC
  • AKI
56
Q

Primary vs Secondary Hypothermia

A

Primary - exp. to low environmental temps

Secondary - d/t disease, drugs, surgery, etc

57
Q

Physiological effets of hypothermia

A
  • bradycardia (SA node is temp dependent)
  • initial vasoconstriction, then loss
  • dysrhythmias
  • hypovolemia from cold diuresis
  • coagulopathy in sever hypothermia
58
Q

Rewarming (passive vs active)

A

Passive: reduce heat loss, blankets
Active: applies exogenous heat, forced air blanket, IV warm fluids

59
Q

Complications w/ rewarming

A
  • can causes vasodilation -> hypotension

- counter by administering fluids during rewarming

60
Q

Therapeutic hypothermia

A
  • used post CPR

- during great vessel occlusion

61
Q

Drowning (aspiration rate)

A
  • 90% of patients aspirate fluids into lungs while 10% do not, but rather die of hypoxia from laryngospasm
62
Q

Dysnatremia from drowning

A

Hypernatremia in salt water

Hyponatremia from fresh water

63
Q

Canine blood typing

A
  • roughly 13 subtypes

- DEA 1 and DAL have very high incidence w/ no naturally occurring antibodies

64
Q

Feline blood typing

A

either A, B, or AB

65
Q

What would happen if you give A blood to a B type cat?

A
  • it will kill the cat
66
Q

What would happen if you give B blood to an A type cat?

A
  • cat would just get sick, but most likely would not die
67
Q

Indications for cross-matching blood types

A
  • unknown transfusion hx
  • > 7 days since first transfusion
  • unknown donor type
  • if donor DEA7 type unknown
68
Q

What is the Major Cross-match

A
  • donor RBCs mixed w/ recipient serum
69
Q

What is the Minor Cross-match

A
  • donor serum mixed w/ recipient RBCs
70
Q

Fresh Whole Blood (contents, indications, pros, cons)

A

Contents - everything within normal blood
Indications - hemorrhage 2ary to coag, vWD, thrombopathy
Pros - contains everything
Cons - not readily avialable, need a lot

71
Q

Packed RBCs (contents, indications, pros, cons)

A

Contents - RBCs and WBCs
Indications - Anemia (hemolysis, hemorrhage, dec EPO)
Pros - High PCV and available
Cons - contains nothing else

72
Q

Fresh Frozen Plasma (contents, indications, pros, cons)

A

Contents - clotting factors, albumin, vWF
Indications - coagulopathy, vWD, hypoalbuminemia
Cons - expensive, adverse rxns

73
Q

Platelet Rich Plasma (contents, indications, pros, cons)`

A

Contents - platelets, clotting facotrs, and albumin
Indications - hemorrhage from thrombocytopenia, DIC
Pros - High [platelets]
Cons - short shelf life, short T1/2

74
Q

Cryoprecipitate (contents, indications, pros, cons)

A

Contents - contains factors 7, 13, fibrinogen, vWF
Indications - vWD, hemophelia A/B
Pros - High [vWF]
Cons - expensive, not readily available

75
Q

Cryopoor Plasma (contents, indications, pros, cons)

A

Contents - does not contain 5, 8, vWF

Indications - VIt-K dependent coagulopathy, hypoproteinemia

76
Q

Acute hemolytic transfusion reaction

A
  • intra/extra vascular hemolysis
  • IgM/G mediated reaction
  • clinical signs (restlessness, vomiting, hypotension, collapse, hemoglobinemia/uria, vasodilatory shock, AKI)
77
Q

T/F: cats are more resistant to anticoagulant rodenticides than dogs.

A

T

78
Q

MOA of Anticoagulant rodenticides

A
  • prevents activation of Factors 2, 7, 9, 10 (vit. k dependent clotting factors)
79
Q

What elevates first w/ anticoag rodenticides (pt or ptt)

A

PT elevates first because Factor 7 has the shortest half life

80
Q

Clinical signs of anticoag rodenticides?

A
  • 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
81
Q

Treatment of anti-coag rodenticides (asymptomatic patient)

A
  • induce vomiting + activated charcoal

- vit k1 therapy

82
Q

Treatment of anti-coag rodenticides (symptomatic patient)

A
  • provide clotting factors via transfusion
  • O2 therapy
  • Vit. K1 therapy
83
Q

T/F: cats are more susceptible to bromethalin rodenticides than dogs

A

T

84
Q

Clinical Sings of bromethalin rodenticides (high dose, low dose)

A
  • dose dependents
  • high dose - tremors hyperexcitability, seizures, hyper-reflexia, depression
  • low dose - hind limb ataxia and paresis, loss of deep pain, CNS depression
85
Q

Diagnosis of bromethalin rodenticides

A

detection of metabolite in fat, brain, liver, or baits

vacuolar myelinopathy from the edema

86
Q

Treatment of bromethalin rodenticides

A
  • control CNS signs
  • no antidote
  • prognosis is v poor
87
Q

Cholecalciferol toxicity (clinical signs)

A
  • anorexia, vomiting, diarrhea, PU/PD, ECG changes
88
Q

Cholecalciferol toxicity (Diagnosis)

A
  • clinical signs
  • hx of exposure
  • metastatic calcification
89
Q

Cholecalciferol toxicity (Treatment)

A
  • decontam. if possible

- monitor serum [Ca] and treat hypercalcemia if necessary

90
Q

What is the first course of action on an animal coming in for potential toxicity?

A
  • make sure they are stable/ stabilize the patient
91
Q

Ethylene Glycol (MOTA)

A
  • metabolites bind to Ca to form Calcium oxylate crystals –> AKI
  • parent compound is slightly CNS depressing
92
Q

Ethylene Glycol (clinical signs, phase 1-3)

A

Phase 1 - CNS depression
Phase 2 - severse acidosis, inc RR
Phase 3 - AKI + renal failure

93
Q

Ethylene Glycol (diagnosis)

A
  • detection of parent compound

- very elevated kidney [Ca]

94
Q

Ethylene Glycol (treatment)

A
  • prevent metabolism of EG into metabolites w/ ethanol or fomepizole (inactivate alcohol dehydrogenase)
95
Q

Xylitol (Clinical Signs)

A
  • emesis, lethargy
  • hypoglycemia
  • elevated liver enzymes and bilirubin
  • coagulopathy, thrombocytopenia
96
Q

Xylitol (diagnosis)

A
  • hx of exposure

- relevant clinical signs

97
Q

Xylitol (Lesions)

A
  • gross hemorrhage

- microscopic hemorrhage, acute hepatic necrosis

98
Q

Xylitol (treatment)

A
  • decontamination - emesis, AC not useful
  • treat hypoglycemia
  • treat coagulopathy
  • hepatoprotectants
99
Q

Methylxanthines (clinical signs)

A
  • vomiting and diarrhea
  • hyper-reflexia,
  • tachycardia, possible PVCs
    Mainly cardio and CNS excitability (over-caffeinated)
100
Q

Methylxanthines ( Diagnosis)

A
  • alkaloids in tissues, urine, or stomach contents
101
Q

Methylxanthines (Treatment)

A
  • decontamination
  • control seizures
  • treat tachycardia and PVCs
  • B-blockers such as metaprolol
102
Q

Amanitin (target organ)

A
  • liver
103
Q

Amanitin (MOA)

A
  • bind eukaryotic DNA-dependent RNA polymerase II which inhibits RNA elongation essential for transcription
104
Q

Amanitin (Clinical Disease)

A
  • 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
105
Q

Amanitin (clin-path findings)

A
  • HIGH [AST]
  • hypoglycemia
  • coagulopathy
106
Q

Amanitin (treatment)

A
  • AC
  • IV fluids, correct hypoglycemia
  • antiemetics
107
Q

Cycad Palms (target organ)

A
  • gi and hepatic necrosis
108
Q

Kalanchoe (target organ)

A
  • cardiac glycoside (like oleander)
109
Q

Easter Lily (target organ)

A
  • kidney/ nephrotoxic
110
Q

Philodendron (target organ)

A
  • insoluble Ca-oxylates (mechanical irritation)
111
Q

Acetaminophen (target organ)

A

Cats - RBCs d/t formation of methemoglobin

Other - hepatotoxic

112
Q

Acetaminophen (Clinical Signs)

A
  • methemoglobin ( cyanosis, resp distress)
  • heinz body anemia
  • hematuria and hemoglobinuria
  • Edema of face and paws
113
Q

Acetaminophen (Diagnosis)

A
  • History, clinical presentation, detection of drug in plasma
114
Q

Acetaminophen (treatment)

A
  • N-acetylcysteine is antidotal by binding directly to toxic metabolite
115
Q

SSRIs (MOA)

A
  • inhibits re-uptake of serotonin
116
Q

SSRIs (Seratonin Syndrome Signs)

A
  • agitiation, vocalizaiton
  • vomiting, tremors
  • hyperthermia, transient blindness
117
Q

SSRIs (treatment)

A
  • decontamination
  • counter clinical signs such as tachycardia, hypertension, tremors
  • counter w/ cyprohepatine
118
Q

Amphetamines (Clinical Signs)

A
  • sympathomimmetic toxidrome
  • CNS overstimulation (hyperexcitability, agitation, tachycardia, hyperthermia)
  • rarely depression, weakness, bradycardia
119
Q

Amphetamines (treatment)

A
  • control clinical signs –> mainly tremors/ seizures induing hyperthermia
120
Q

Amphetamines (Diagnosis)

A
  • urine samples
121
Q

Albuterol (clinical signs)

A
  • tachycardia v common
  • VPCs less common
  • hypokalemia (can be concerning)
122
Q

Albuterol (treatment)

A
  • w/ propanolol for tachycardia and hypokalemia
123
Q

Cannabis (clinical signs)

A
  • CNS signs ( CNS depression, ataxia, disorientation, mydriasis)
  • urinary incontinence
  • emesis
124
Q

Cannabis ( Diagnosis)

A
  • hx of exposure

- delta9-THC in urine

125
Q

Cannabis (treatment)

A
  • decontamination

- no antidote

126
Q

Opioid Toxicity (clinical signs)

A
  • emesis, defecation, salivation, CNS depression, miosis, ataxia
  • Severe: resp. depression, constipation, hypothermia, coma, death
127
Q

Opioid Toxicity (treatment)

A
  • Naloxone
128
Q

Opioid Toxicity (species sensitivity)

A
  • cats are super sensitive
129
Q

pRBC administration volume

A

pRBC (Volume) = 90 * BW * ( change in PCV/ donor PCV)

130
Q

Treating Acute Hemolytic Transfusion Reaction

A
  • 0.1 mg/kg dexamethasone

- fluid therapy for vasodilatory shock

VET 433a - Small Animal Stream 1 (10 decks)

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