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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Clinical signs of dysnatremia

A
  1. obtundation
  2. disorientation
  3. head pressing
  4. seizures
  5. coma
  6. death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How to calculate plasma osmolality?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What molecule contributes most to plasma osmolality?

A

Sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treating Hyponatremia

A
  • hypertonic slaine treatment until clinical signs begin to diminish
  • diuretic therapy w/ furosemide/ mannitol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Psuedohyponatremia

A
  • does not require treatment

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pseudohyperkalemia

A
  • thrombocytosis (platelet degranulation leads to K release)
  • Japanese Breeds w/ hemolysis of RBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical signs of Hypokalemia

A
  • muscle weakness (cervical ventroflexion)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Pseudohyperchloremia
- KBr administration, the Br will falsely read as Chloride on the machine
26
Treatment of hypochloremic met alkalosis
- 0.9% NaCl to help kidney eliminate bicard
27
Treatment of hyperchloremic met. acidosis
- LRS, fluids w/ low [Cl]
28
Calcium functions in the body
- coagulation - cardiac contractility - muscle contraction
29
Causes of Hypocalcemia
- Eclampsia (puerperal tetany) - CKD - pancreatitis - iatrogenic (blood transfusions)
30
Clinical signs of hypocalcemia
mild: none moderate: facial pruritis, muscle tremors, 'tetany' severe: seizures, obtundation, cardiac dysrrhythmias, death
31
Treatment of hypocalcemia
IV calcium fluids
32
Hypercalcemia causes acronym
HARD IONS
33
3 main types of shock
1. Vasoconstrictive 2. Metabolic 3. Vasodilatory/ Distributive
34
What are the 6 perfusion parameters
1. Mentation 2. CRT 3. mucous membrane color 4. extremities temp 5. peripheral pulse quality 6. heart rate
35
Hypovolemic Shock (pathogenesis)
- decreased venous return -> dec preload -> dec SV -> dec CO -> dec tissue perfusion
36
Causes of Hypovolemic shock
- hemorrhage - ongoing water losses - third space losses
37
Common Causes of obstructive shock
- GDV - cardiac tamponade - tension pneumothorax - thrombus - space occupying lesions
38
Causes of Cardiogenic Shock
- poor contractility - HR too low or too high - valvular insufficiency
39
T/F: All types of vasoconstrictive shock can be treated isotonic fluids
F: cardiogenic shock cannot be treated with isotonic fluids
40
Most common cause of vasodilatory shock
- Septic shock
41
Shock resuscitation goals
- O2 therapy | - vascular access or intraosseus catheters
42
Isotonic fluids Shock dose
Dogs: 80-90mL/kg Cats: 40-60mL/kg
43
When to use hypertonic saline
- large animals w/ hypovolemic shock | - treat cerebral edema
44
Contraindications of hypertonic saline
- cardiogenic shock - hypernatremic - dehydrated patients Max rate = 4mL/kg over 5 min.
45
Colloids fucntion
- increase plasma oncotic pressure
46
indications for colloids
- hypovolemic shock - obstructive shock - septic shock - shock w/ hypoalbuminemia
47
Contraindications for colloids
- cardiogenic shock - acute kidney injury - coagulopathy (interferes w/ vWF)
48
2 sources of heat production
- basal metabolic rate (dec w/ shock and inc w/ disease) | - increased muscle activity (excercise, resp distress)
49
Forms of heat loss
- convection (through air) - conduction (direct contact) - radiation - evaporation (humidity dependent)
50
Factors affecting heat loss
- body SA/ mass - insulation (BCS) - external temperature - relative humidity
51
Heat stress vs Heat stroke
Heat stress: lethargy, weakness, vomiting, diarrhea, tremors | Heat stroke: evidence of CNS dysfunction +/- liver dysfunction
52
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
53
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
54
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
55
Prognosis for hyperthermia (neg indicators)
- seizures - nRBC - hypoglycemia - DIC - AKI
56
Primary vs Secondary Hypothermia
Primary - exp. to low environmental temps | Secondary - d/t disease, drugs, surgery, etc
57
Physiological effets of hypothermia
- bradycardia (SA node is temp dependent) - initial vasoconstriction, then loss - dysrhythmias - hypovolemia from cold diuresis - coagulopathy in sever hypothermia
58
Rewarming (passive vs active)
Passive: reduce heat loss, blankets Active: applies exogenous heat, forced air blanket, IV warm fluids
59
Complications w/ rewarming
- can causes vasodilation -> hypotension | - counter by administering fluids during rewarming
60
Therapeutic hypothermia
- used post CPR | - during great vessel occlusion
61
Drowning (aspiration rate)
- 90% of patients aspirate fluids into lungs while 10% do not, but rather die of hypoxia from laryngospasm
62
Dysnatremia from drowning
Hypernatremia in salt water | Hyponatremia from fresh water
63
Canine blood typing
- roughly 13 subtypes | - DEA 1 and DAL have very high incidence w/ no naturally occurring antibodies
64
Feline blood typing
either A, B, or AB
65
What would happen if you give A blood to a B type cat?
- it will kill the cat
66
What would happen if you give B blood to an A type cat?
- cat would just get sick, but most likely would not die
67
Indications for cross-matching blood types
- unknown transfusion hx - >7 days since first transfusion - unknown donor type - if donor DEA7 type unknown
68
What is the Major Cross-match
- donor RBCs mixed w/ recipient serum
69
What is the Minor Cross-match
- donor serum mixed w/ recipient RBCs
70
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
71
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
72
Fresh Frozen Plasma (contents, indications, pros, cons)
Contents - clotting factors, albumin, vWF Indications - coagulopathy, vWD, hypoalbuminemia Cons - expensive, adverse rxns
73
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
74
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
75
Cryopoor Plasma (contents, indications, pros, cons)
Contents - does not contain 5, 8, vWF | Indications - VIt-K dependent coagulopathy, hypoproteinemia
76
Acute hemolytic transfusion reaction
- intra/extra vascular hemolysis - IgM/G mediated reaction - clinical signs (restlessness, vomiting, hypotension, collapse, hemoglobinemia/uria, vasodilatory shock, AKI)
77
T/F: cats are more resistant to anticoagulant rodenticides than dogs.
T
78
MOA of Anticoagulant rodenticides
- prevents activation of Factors 2, 7, 9, 10 (vit. k dependent clotting factors)
79
What elevates first w/ anticoag rodenticides (pt or ptt)
PT elevates first because Factor 7 has the shortest half life
80
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
81
Treatment of anti-coag rodenticides (asymptomatic patient)
- induce vomiting + activated charcoal | - vit k1 therapy
82
Treatment of anti-coag rodenticides (symptomatic patient)
- provide clotting factors via transfusion - O2 therapy - Vit. K1 therapy
83
T/F: cats are more susceptible to bromethalin rodenticides than dogs
T
84
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
85
Diagnosis of bromethalin rodenticides
detection of metabolite in fat, brain, liver, or baits | vacuolar myelinopathy from the edema
86
Treatment of bromethalin rodenticides
- control CNS signs - *no antidote* - prognosis is v poor
87
Cholecalciferol toxicity (clinical signs)
- anorexia, vomiting, diarrhea, PU/PD, ECG changes
88
Cholecalciferol toxicity (Diagnosis)
- clinical signs - hx of exposure - metastatic calcification
89
Cholecalciferol toxicity (Treatment)
- decontam. if possible | - monitor serum [Ca] and treat hypercalcemia if necessary
90
What is the first course of action on an animal coming in for potential toxicity?
- make sure they are stable/ stabilize the patient
91
Ethylene Glycol (MOTA)
- metabolites bind to Ca to form Calcium oxylate crystals --> AKI - parent compound is slightly CNS depressing
92
Ethylene Glycol (clinical signs, phase 1-3)
Phase 1 - CNS depression Phase 2 - severse acidosis, inc RR Phase 3 - AKI + renal failure
93
Ethylene Glycol (diagnosis)
- detection of parent compound | - very elevated kidney [Ca]
94
Ethylene Glycol (treatment)
- prevent metabolism of EG into metabolites w/ ethanol or fomepizole (inactivate alcohol dehydrogenase)
95
Xylitol (Clinical Signs)
- emesis, lethargy - hypoglycemia - elevated liver enzymes and bilirubin - coagulopathy, thrombocytopenia
96
Xylitol (diagnosis)
- hx of exposure | - relevant clinical signs
97
Xylitol (Lesions)
- gross hemorrhage | - microscopic hemorrhage, acute hepatic necrosis
98
Xylitol (treatment)
- decontamination - emesis, AC not useful - treat hypoglycemia - treat coagulopathy - hepatoprotectants
99
Methylxanthines (clinical signs)
- vomiting and diarrhea - hyper-reflexia, - tachycardia, possible PVCs Mainly cardio and CNS excitability (over-caffeinated)
100
Methylxanthines ( Diagnosis)
- alkaloids in tissues, urine, or stomach contents
101
Methylxanthines (Treatment)
- decontamination - control seizures - treat tachycardia and PVCs - B-blockers such as metaprolol
102
Amanitin (target organ)
- liver
103
Amanitin (MOA)
- bind eukaryotic DNA-dependent RNA polymerase II which inhibits RNA elongation essential for transcription
104
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
105
Amanitin (clin-path findings)
- HIGH [AST] - hypoglycemia - coagulopathy
106
Amanitin (treatment)
- AC - IV fluids, correct hypoglycemia - antiemetics
107
Cycad Palms (target organ)
- gi and hepatic necrosis
108
Kalanchoe (target organ)
- cardiac glycoside (like oleander)
109
Easter Lily (target organ)
- kidney/ nephrotoxic
110
Philodendron (target organ)
- insoluble Ca-oxylates (mechanical irritation)
111
Acetaminophen (target organ)
Cats - RBCs d/t formation of methemoglobin | Other - hepatotoxic
112
Acetaminophen (Clinical Signs)
- methemoglobin ( cyanosis, resp distress) - heinz body anemia - hematuria and hemoglobinuria - Edema of face and paws
113
Acetaminophen (Diagnosis)
- History, clinical presentation, detection of drug in plasma
114
Acetaminophen (treatment)
- N-acetylcysteine is antidotal by binding directly to toxic metabolite
115
SSRIs (MOA)
- inhibits re-uptake of serotonin
116
SSRIs (Seratonin Syndrome Signs)
- agitiation, vocalizaiton - vomiting, tremors - hyperthermia, transient blindness
117
SSRIs (treatment)
- decontamination - counter clinical signs such as tachycardia, hypertension, tremors - counter w/ cyprohepatine
118
Amphetamines (Clinical Signs)
- sympathomimmetic toxidrome - CNS overstimulation (hyperexcitability, agitation, tachycardia, hyperthermia) - rarely depression, weakness, bradycardia
119
Amphetamines (treatment)
- control clinical signs --> mainly tremors/ seizures induing hyperthermia
120
Amphetamines (Diagnosis)
- urine samples
121
Albuterol (clinical signs)
- tachycardia v common - VPCs less common - hypokalemia (can be concerning)
122
Albuterol (treatment)
- w/ propanolol for tachycardia and hypokalemia
123
Cannabis (clinical signs)
- CNS signs ( CNS depression, ataxia, disorientation, mydriasis) - urinary incontinence - emesis
124
Cannabis ( Diagnosis)
- hx of exposure | - delta9-THC in urine
125
Cannabis (treatment)
- decontamination | - no antidote
126
Opioid Toxicity (clinical signs)
- emesis, defecation, salivation, CNS depression, miosis, ataxia - Severe: resp. depression, constipation, hypothermia, coma, death
127
Opioid Toxicity (treatment)
- Naloxone
128
Opioid Toxicity (species sensitivity)
- cats are super sensitive
129
pRBC administration volume
pRBC (Volume) = 90 * BW * ( change in PCV/ donor PCV)
130
Treating Acute Hemolytic Transfusion Reaction
- 0.1 mg/kg dexamethasone | - fluid therapy for vasodilatory shock