General Vet Med Midterm

Front 1

what is another name for fever?

Back 1

pyrexia

Front 2

define pyrexia

Back 2

elevation in core body temp that occurs due to a changed thermoregulatory set point in the hypothalamus

Front 3

define hyperthermia

Back 3

elevation in core body temperature that occurs without a change in the hypothalamic set point

Front 4

what are two major etiologies of hyperthermia

Back 4

1. heat stroke
2. malignant hyperthermia

Front 5

what is heat stroke?

Back 5

form of non-pyrogenic hyperthermia that occurs when heat-dissipating mechanisms of the body cannot accommodate excessive heat

Front 6

what is malignant hyperthermia?

Back 6

uncommon, familial non-pyrogenic hyperthermia that occurs secondary to some anesthetic agents (e.g. halothane) and muscle relaxants

Front 7

balance between heat load and heat-dissipating mechanisms

Back 7

thermal homeostasis

Front 8

what are the two major components of thermal homeostasis?

Back 8

1. heat load
2. heat dissipation

Front 9

what are two major sources of heat load?

Back 9

1. environmental heat
2. heat generated by metabolism and exercise

Front 10

what are four ways the body can dissipate heat?

Back 10

1. radiation
2. convection
3. conduction
4. evaporation

Front 11

what internal mechanism causes the hypothalamus to change its set point temperature?

Back 11

thermoreceptors sense change in ambient or core body temperature

Front 12

what are six ways in which an animal will thermoregulate to elicit heat loss due to a signal from the hypothalamus?

Back 12

1. panting
2. vasodilation
3. postural change
4. seek cold environment
5. perspiration
6. grooming

Front 13

what are the two basic ways that the body will elicit heat gain in response to a signal from the hypothalamus?

Back 13

1. increased production of heat
2. decreased loss of heat

Front 14

what are three physiological responses by which the body will produce heat in response to a signal from the hypothalamus?

Back 14

1. catecholamines
2. thyroxine (↑metabolism)
3. shivering

Front 15

what are four ways the body can decrease loss of heat?

Back 15

1. vasoconstriction (maintain core body temp)
2. piloerection
3. postural changes
4. seek warm environment

Front 16

what type of chemical stimulates fever?

Back 16

prostaglandins

Front 17

what is the pathophysiologic pathway by which fever is initiated?

Back 17

exogenous pyrogens → endogenous pyrogens → bind to vascular epithelium in the hypothalamus → stimulate prostaglandin release → ↑thermoregulatory set point

Front 18

what are six examples of exogenous pyrogens?

Back 18

1. infectious agents
2. antigen-antibody complexes
3. bile acids
4. drugs
5. tissue inflammation
6. necrosis

Front 19

upon stimulation by exogenous pyrogens, what is the source and composition of the endogenous pyrogens released into the blood?

Back 19

cytokines released from leukocytes (IL-1, IL-6, IFN-β, IFN-γ, TNF-α)

Front 20

what type of exogenous pyrogen can directly activate the hypothalamus, thus bypassing the endogenous pyrogenic pathway?

Back 20

microbial toxins

Front 21

what is the second-messenger responsible for changing the setpoint in the hypothalamus?

Back 21

cAMP

Front 22

what are six undesirable potential consequences of fever?

Back 22

1. increase metabolic demands
2. muscle catabolism
3. suppressed erythropoiesis
4. increased fluid and caloric needs
5. DIC
6. shock

Front 23

what are two ways in which fever is directly protective to the body?

Back 23

1. inhibit viral replication
2. cytotoxic or cytostatic to microbial pathogens

Front 24

what are five indirect ways in which fever is protective to the body?

Back 24

1. ↓iron uptake by microbes
2. ↑microbial death within phagocytes
3. ↑lymphocyte transformation and activation
4. ↑granulocytic mobility
5. improve monocytic oxidative metabolism

Front 25

what is FUO

Back 25

fever of unknown origin

Front 26

in veterinary medicine, what conditions are required to diagnose a FUO?

Back 26

- fever of sufficient duration to rule out common, simple, or self-limiting causes
- initial tests do not reveal specific cause
- failure to respond to short course of antibiotics

Front 27

what should a client be warned about when the patient is diagnosed with a FUO?

Back 27

- time consuming and frustrating
- may need additional tests
- may need to repeat tests
- can become expensive
- 10-15% cases are undiagnosed

Front 28

what are some potential rule-outs for FUO?

Back 28

- disease from travel
- recent vaccination
- heartworm, FeLV/FIV
- medication
- response to therapy
- Hx of other illness, Sx
- subtle signs of illness (pain, lameness)
- illness in other pets or humans in household

Front 29

in a physical exam, what is
- the max temperature that may be due to stress?
- the max temperature of a fever?

Back 29

- stress: up to 103 °F
- fever ≤ 106 °F

Front 30

what is the next step if all diagnostic tests performed still yield an FUO?

Back 30

therapeutic trial

Front 31

what are six undesirable outcomes of a therapeutic trial for an FUO?

Back 31

1. exacerbate undiagnosed disease
2. continued progression of an undiagnosed disease
3. drug toxicity/side effects
4. induction fo antibiotic resistance
5. interfere with future diagnostics
6. expensive

Front 32

in a therapeutic trial for a FUO using corticosteroids:
- indications for glucocorticoids
- contraindications
- complications
- how long will therapy take to resolve clinical signs?

Back 32

- indicated for immune-mediated disease
- contraindicated if infection cannot be ruled out
- may mask clinical signs and may complicate Dx of neoplasia
- if immune-mediated FUO, pyrexia and clinical signs usually resolve in 24-28 hours

Front 33

how is mild-to-moderate fever initially treated?

Back 33

since fever may have beneficial effects, ensure adequate fluid therapy and nutritional support. If this does not work, consider antipyretics.

Front 34

why should you not cool an animal with a fever?

Back 34

because the thermoreceptors will tell the hypothalamus that the body temp is lower and the fever could be worsened by elevation of the hypothalamic set point

Front 35

what are three side effects to consider when using antipyretics?

Back 35

1. hypothermia
2. impairment of host immune defenses
3. other side effects such as GI, renal, hepatic, etc.

Front 36

when using NSAIDs as antipyretics, what (two) drug types should they not be combined with?

Back 36

1. don't mix multiple NSAIDs
2. don't use with corticosteroids

Front 37

give five examples of commonly-used NSAID antipyretics

Back 37

1. salicylates (aspirin)
2. carprofen
3. deracoxib
4. meloxicam
5. fibrocoxib

Front 38

what is the only NSAID that can be used in cats?

Back 38

Meloxicam labeled SC, off-label for oral

Front 39

if an animal is in heat stroke:
- what temperature can lead to tissue and organ damage over time?
- what temperature will lead to death in a few minutes?

Back 39

- >107 °F causes tissue and organ damage
- >110 °F for a few minutes causes death

Front 40

what are two common effects on the CNS due to heat stroke?

Back 40

1. thermal injury to cerebral vascular endothelium
2. parenchymal thrombosis and hemorrhage associated with DIC

Front 41

what are four consequences of CNS parenchymal thrombosis and hemorrhage (associated with DIC) during heat stroke?

Back 41

1. neuronal injury and cell death
2. cerebral edema
3. cerebellar dysfunction
4. damage to thermoregulatory center (predisposition to subsequent hyperthermic episodes)

Front 42

what are two major GI/hepatic effects of heat stroke?

Back 42

1. direct thermal injury to GI cells and hepatocytes
2. ischemic from prolonged splanchnic hypotension

Front 43

as a result of heat stroke, what are two common outcomes of splanchnic ischemia?

Back 43

1. hepatocellular necrosis and cholestasis
2. GI ischemia and ulceration

Front 44

if GI ischemia and ulceration result from heat stroke, what are three ways in which GI flora can cause disease?

Back 44

1. bacterial translocation
2. endotoxemia
3. sepsis

Front 45

what are two major renal effects of heat stroke?

Back 45

1. acute renal failure fron tubular necrosis
2. pre-renal azotemia

Front 46

what are four pathophysiologic mechanisms by which heat stroke can cause acute renal failure due to tubular necrosis?

Back 46

1. direct thermal injury to tubular epithelium
2. hypoxia due to hypovolemia
3. microthrombi associated with DIC
4. nephrotoxicity from myoglobin released via rhabdomyolysis

Front 47

why does heat stroke cause hypovolemia?

Back 47

direct thermal damage to the heart causes necrosis of the myocardium, and a downward spiral of arrhythmia → ↓CO → hypoperfusion → ischemia → more necrosis

Front 48

what are three CV clinical signs on diagnosis of hyperthermia?

Back 48

-initially tacky, HYPEREMIC mucous membranes that may become ashen and pale with prolonged CRT
- initially, tachycardia with bounding pulses; may turn into thready pulses, arrhythmias
- petechiations, ecchymosis

Front 49

what are four characteristics of a CBC in a patient with hyperthermia?

Back 49

1. ↑hemoconcentration due to dehydration
2. hemolytic anemia with schistocytes and nRBC
3. leukocytosis/leukopenia due to inflammation and/or sepsis
4. thrombocytopenia due to consumption (DIC), ↑loss in GI tract, and thermal injury to megakaryocytes

Front 50

what are three non-pharmaceutical ways to correct hyperthermia?

Back 50

1. clip thick hair coats
2. spray or immerse in cool water, then cool with fan
3. cool water lavage or enemas

Front 51

if treating an animal for hyperthermia, at what temperature do you discontinue treatment?

Back 51

103 °F

Front 52

what is POVMR?

Back 52

Problem Oriented Veterinary Medical Record

Front 53

in a POVMR, what is the definition of a Problem?

Back 53

anything that might interfere with the animal's well being and MIGHT require further evaluation and treatment

Front 54

when stating a Problem in a POVMR, in how much detail do you define that problem?

Back 54

at the highest level of refinement, but not overstated

Front 55

in a POVMR, in what two basic ways are problems recorded?

Back 55

1. a temporary problem list
2. a master problem list

Front 56

what accompanies a temporary problem list?

Back 56

initial plan

Front 57

what are the four components of a temporary problem list/initial plan?

Back 57

1. problem
2. rule outs
3. Dx plan
4. Rx plan

Front 58

in what order are problems listed on a master problem list?

Back 58

from the most important problem to the least important problem?

Front 59

how often is a temporary problem list/initial plan updated?

Back 59

at least daily

Front 60

what are the four major components of a master problem list?

Back 60

1. table of contents
2. problems dated from origin
3. numerical order from origin
4. may contain vaccination, tests, and drugs dispensed information

Front 61

for a problem in the POVMR, what are the five fates of a problem?

Back 61

1. refined with accumulation of tests
2. combined with another
3. temporarily inactivated
4. resolved
5. removed - in error, was never a problem

Front 62

in a POVMR, what would two problems be combined?

Back 62

when further assessment determines these problems are caused by the same thing, a refinement of the problem list

Front 63

what method is used to rule out diseases when refining the problem?

Back 63

bifurcation

Front 64

what is used to detail the progress of a problem?

Back 64

a SOAP

Front 65

what does SOAP stand for?

Back 65

Subjective, Objective, Assessment, Plan

Front 66

in making a SOAP
- how do you record multiple problems?
- what are good practices to allow others to easily read the document?

Back 66

- each problem is recorded separately and referenced by number from the Master Problem List
- be concise, use phrases and abbreviation, write legibly

Front 67

what are three basic components of the Subjective portion of a SOAP?

Back 67

1. historical
2. overall assessment
3. observations not easily quantified (e.g. "stronger, better appetite")

Front 68

what are two basic components of the Objective portion of a SOAP?

Back 68

1. daily physical exam findings
2. Quantified data (e.g. lab results, radiographic findings, ECG, neuro exam)

Front 69

what are four common components of the Assessment portion of a SOAP?

Back 69

1. interpretation and explanation of problem at this time period
2. current differential diagnosis
3. evaluation of treatment plan
4. how this case differs from a typical case

Front 70

what are the three components of a Daily Plan on a SOAP?

Back 70

Diagnosis (Dx), Treatment (Rx), and Client Education (CE)

Front 71

what is recorded on a SOAP Daily Dx Plan?

Back 71

1. what tests will be performed in the next 24 hours
2. a box for initials and time check offs

Front 72

what is recorded on a SOAP Daily Rx Plan?

Back 72

1. a list of therapeutic objectives and goals
2. what treatments will be administered in the next 24 hours (including dose, frequency, and route of administration)
3. a box for initials and time check offs

Front 73

what is recorded on a SOAP Daily CE?

Back 73

1. list time of communication
2. person talked with
3. summarize conversation (update condition, discuss new Dx tests or Rx, update bill)

Front 74

what are the three basic components fo shock?

Back 74

1. inadequate systemic oxygen and nutrient delivery
2. impaired utilization of oxygen
3. poor tissue perfusion

Front 75

when in shock, what three pathophysiological mechanisms result in poor tissue perfusion?

Back 75

1. vasoconstriction
2. decreased cardiac output
3. vasodilation

Front 76

what are the three basic forms of shock?

Back 76

1. hypovolemia
2. distributive
3. cardiogenic

Front 77

what are the two subtypes of hypovolemic shock?

Back 77

1. hemorrhagic
2. relative

Front 78

what is distributive shock and what are two major etiologies?

Back 78

- vasodilation, effectively removing blood from circulation
- sepsis or anaphylaxis

Front 79

basically, what causes cardiogenic shock?

Back 79

decreased cardiac output

Front 80

what comprises the compensatory response to hypotension with hypovolemic shock?

Back 80

- sympathetic activation, RAAS, ADH: vasoconstriction, ↑cardiac contractility, fluid retention
-redistribution of blood flow toward heart, brain and lungs, and away from splanchnic and skin

Front 81

what are the three core areas of circulation during hypovolemia?

Back 81

brain, heart, lungs

Front 82

at what point does shock occur in hypovolemia?

Back 82

when compensation is inadequate or excessive and results in impaired tissue perfusion

Front 83

how can compensatory mechanisms contribute to the clinical signs of hypovolemic shock

Back 83

among other reasons, vasoconstriction may impair the blood flow to some organs

Front 84

what is the basic pathogenesis leading to hypovolemic shock?

Back 84

primary disease → compensated shock → decompensated shock

Front 85

what are some clinical signs of compensated hypovolemic shock?

Back 85

- may be subtle
- tachycardia
- bounding pulses
- tacky and/or pale mucous membranes
- prolonged CRT

Front 86

what are some clinical signs of early decompensated hypovolemic shock?

Back 86

- tachycardia progressing to bradycardia
- bounding pulses progressing to weak pulses
- pale mucous membranes
- cold extremities
- depression
- oliguria

Front 87

what is the basic goal in the treatment of hypovolemic shock? What is the basic means for doing this?

Back 87

restore adequate oxygen delivery by restoring blood volume (resuscitation)

Front 88

when resuscitating from hypovolemic shock, what are three positive outcomes of restoring blood volume?

Back 88

1. increase preload →
2. increased CO →
3. increased tissue perfusion

Front 89

what is the shock dose of IV crystalloid for the dog and the cat?

Back 89

dog: 90 ml/kg
cat: 60 ml/kg

Front 90

when giving IV crystalloids to treat hypovolemia
- how often do you assess response?
- despite the typical "shock dose" of crystalloid, how much should be given?

Back 90

- assess every 10-15 minutes
- titrate to effect

Front 91

what are three common clinical signs that represent a positive response to IV fluids administered for hypovolemia?

Back 91

1. decreased HR
2. improves pulse character
3. improved mucous membrane color and CRT

Front 92

hypertonic saline
- concentration
- mechanism of action
- time to effect
- duration of action
- typical dose

Back 92

- 7% NaCl
- water from interstitial and intercellular space to intravascular space
- maximum effect in 5-10 minutes
- short-lived effect
- smaller volume than isotonic (4-5 ml/kg)

Front 93

when are colloids indicated in shock?

Back 93

- hypoproteinemia (to avoid ascites/pleural effusion)
- lack of response to initial crystalloid administration

Front 94

when are vasopressors and/or positive inotropes indicated in hypovolemia?

Back 94

- poor response to volume replacement
- severe hypotension or oliguria

Front 95

administration of vasopressors to treat hypovolemia:
- what type of drug is used?
- what is the desired effect?
- what are two examples of drugs to use?

Back 95

- α-adrenergic drugs
- increases effective circulating volume
- norepinephrine, high dose dopamine

Front 96

administration of positive inotropes to treat hypovolemia:
- what type of drug is used?
- what is the desired effect?
- what is an example of a commonly used drug?

Back 96

- β1 agonist
- increased contractility → increased CO
- dobutamine (also has weak β2 effect)

Front 97

rank the major effect (dominant neurotransmitter action) of dopamine administration depending on dose from low dose to high dose

Back 97

- low: dopaminergic
- β-adrenergic
- high: α-adrenergic

Front 98

when is oxygen delivery indicated in shock?

Back 98

always

Front 99

how can hypothermia be detrimental to treatment of shock and what are two ways to warm the patient?

Back 99

it impairs vascular response to fluids
1. passive warming (e.g. Bair Hugger)
2. warm IV fluids

Front 100

for patients in shock, when is blood transfusion indicated? What is the goal?

Back 100

- indicated when PCV < 20-25%
- goal is to maintain a PCV above 25%`

Front 101

what are four "other" supportive treatments used for shock?

Back 101

1. bicarb to treat acidosis if present after volume replacement
2. GI protectants (H2 blockers such as cimetidine, ranitidine, famotidine) to treat/prevent GI ulceration
3. antibiotics for septic shock, GI hemorrhage, and translocation due to decompensatory shock
4. analgesia - opioids preferred

Front 102

list some things that should be monitored during treatment of shock

Back 102

- TPR
- BW (watch for fluid overload)
- MM color, CRT
- urine output
- lung sounds
- electrolytes, PCV, TP
- BP (keep > 60)

Front 103

what is the definition of sepsis?

Back 103

systemic inflammatory response to infection

Front 104

what is the definition of bacteremia?

Back 104

presence of bacteria in the blood

Front 105

what term is associated with a generalized, excessive inflammatory response to various stimuli?

Back 105

systemic inflammatory response syndrome (SIRS)

Front 106

what are four common risk factors for sepsis?

Back 106

1. localized infection
2. immunosuppression
3. invasive devices (e.g. catheters)
4. surgery

Front 107

in sepsis, what is the initial cause for the pathogenesis of clinical signs

Back 107

dying cells and bacterial antigens stimulate the host inflammatory response

Front 108

in sepsis, what is the pathogenesis resulting from activation of the host inflammatory response?

Back 108

1. ↑capillary permeability
2. vasodilation
3. activation of coagulation cascade → thrombosis
4. decreased cardiac function
5. multiple organ failure

Front 109

what are five clinical signs of early sepsis

Back 109

1. depression
2. fever
3. tachycardia
4. red mucous membranes
5. rapid CRT

Front 110

what are two clinical signs that differ between early hypovolemia and sepsis?

Back 110

1. hypovolemia: pale MM; sepsis: red MM
2. hypovolemia: prolonged CRT; sepsis: rapid CRT

Front 111

describe the cardiovascular effects of early septic shock

Back 111

- peripheral vasodilation predominates:
- skin, GI tract
- brick-red mucous membranes, strong pulses
- vasoconstriction to kidney, heart
- ↑HR, ↑contractility

Front 112

what are seven clinical signs of septic shock that has progressed beyond early stages?

Back 112

1. fever or hypothermia
2. tachycardia
3. tachypnea
4. depression
5. weak pulses
6. slow CRT, pale MM
7. organ failure

Front 113

with chronic bacteremia, describe the severity of clinical signs. What are four clinical signs of chronic bacteremia?

Back 113

- clinical signs are often mild
1. fever (intermittent)
2. lameness (polyarthritis)
3. vomiting
4. depression

Front 114

what are three important laboratory tests to perform in sepsis, and what information do they provide?

Back 114

1. CBC - consistent with inflammation +/- hemoconcentration
2. urinalysis - bacteruria can occur in sepsis without clinical signs of UTI; culture the urine in suspected sepsis
3. blood chemistry - hypoalbuminemia (liver involvement); elevated liver enzymes; hyperbilirubinemia; hypoglycemia

Front 115

in searching for the origin of infection that may be causing sepsis, where are seven places to look?

Back 115

1. gingiva
2. urinary tract
3. respiratory tract
4. abdomen
5. reproductive tract
6. cardiac valves
7. GI tract

Front 116

in diagnosing sepsis, what are three places that are important to culture?

Back 116

1. primary site
2. urine
3. blood

Front 117

how do you determine the initial antibiotic to use when treating sepsis?

Back 117

determine from the likely organisms at the primary site of infection, or from a Gram stain/cytology.

Front 118

in antibiotic treatment of sepsis:
- route of administration
- dosage
- spectrum

Back 118

- administer IV
- use a high dose
- use a broad spectrum initially and refine as Dx is refined

Front 119

what are five aspects of treating sepsis?

Back 119

1. antibiotics
2. IV fluids
3. treatment for shock if present (vasodilation predominates)
4. treat complications (DIC, organ failure, hypoglycemia)
5. nutritional support

Front 120

what percentage of the body weight is water? What percentage of body weight is blood volume?

Back 120

- 60% of body weight is water
- 7% of body weight is blood volume

Front 121

what are seven indications for fluid therapy?

Back 121

1. rehydration
2. maintenance of hydration
3. expansion of intravascular volume
4. maintain or increase plasma oncotic pressure
5. correct electrolyte imbalances
6. diuresis
7. treat specific diseases

Front 122

what are five common etiologies for fluid loss?

Back 122

1. PU/PD
2. vomiting/diarrhea
3. hemorrhage
4. fluid sequestration (e.g. pleural effusion or ascites)
5. lack of intake

Front 123

at what percentage dehydration is potentially lethal?

Back 123

10%

Front 124

what are six ways to assess hydration status?

Back 124

1. skin turgor
2. mucous membranes
3. pulse rate and character
4. CRT
5. urinary bladder
6. body weight

Front 125

under what percentage dehydration is "undetectable"?

Back 125

< 5%

Front 126

what are clinical signs for 5-6% dehydration?

Back 126

subtle loss of skin elasticity

Front 127

what are clinical signs for 6-8% dehydration?

Back 127

delayed skin tent, dry MM

Front 128

what are clinical signs for 10-12% dehydration?

Back 128

long skin tent, dry MM, slow CRT, sunken eyes, tachycardia, weak pulses

Front 129

what are clinical signs for 12-15% dehydration?

Back 129

hypovolemic shock

Front 130

an animal presenting with subtle loss of skin elasticity is what % dehydrated?

Back 130

5-6%

Front 131

an animal presenting with delayed skin tent, dry MM is what % dehydrated?

Back 131

6-8%

Front 132

an animal presenting with long skin tent, dry MM, slow CRT, sunken eyes, tachycardia, and weak pulses is what % dehydrated?

Back 132

10-12%

Front 133

an animal presenting with hypovolemic shock is what % dehydrated?

Back 133

12-15%

Front 134

what are five routes of fluid administration?

Back 134

1. oral
2. SC
3. intraperitoneal
4. IV
5. intraosseous

Front 135

what are four advantages of oral fluid therapy?

Back 135

1. most physiologic route
2. no risk of overhydration
3. reduce electrolyte loss in diarrhea
4. inexpensive

Front 136

what are two disadvantages of oral fluid therapy?

Back 136

1. not for vomiting, GI obstruction, NPO
2. slow absorption

Front 137

why do oral electrolyte solutions contain glucose

Back 137

because they are co-transported

Front 138

what are three advantages of SC fluids?

Back 138

1. simple and economical
2. minimal risk of overhydration
3. OK for mild dehydration

Front 139

what are three disadvantages of SC fluids?

Back 139

1. cannot correct moderate/severe dehydration
2. vasoconstriction impairs absorption
3. cellulitis possible

Front 140

SC fluids:
- concentration?
- how much K+ maximum?
- how much glucose?

Back 140

- isotonic
- K+ content up to 35 mEq/L
- no glucose

Front 141

why is glucose not used in SC fluids?

Back 141

- potential for infection
- glucose absorbed quickly, so solution will become hypotonic

Front 142

what are three advantages of IV fluids?

Back 142

1. rapid administration possible
2. shock, diuresis, drug administration
3. hypertonic fluids OK

Front 143

what are four disadvantages of IV fluids?

Back 143

1. IV catheter required
2. monitoring
3. risk of overhydration
4. expense

Front 144

where is an IV catheter placed for isotonic solutions?

Back 144

peripheral vein: cephalic or saphenous

Front 145

where is an IV catheter placed for hypertonic solutions?

Back 145

jugular vein

Front 146

how often must an IV catheter be changed?

Back 146

every 72 hours

Front 147

what are three advantages of intraosseus fluids?

Back 147

1. use when other routes are inaccessible
2. rapid placement
3. rapid fluid absorption

Front 148

what are three disadvantages of intraosseous fluids?

Back 148

1. infection, growth plate damage
2. risk of overhydration
3. may require pump

Front 149

what is the difference between a replacement crystalloid solution and a maintenance solution?

Back 149

replacement may be given rapidly without detremental effects; maintenance is given to maintain fluid balance after replacement fluids have restored balance

Front 150

maintenance solutions:
- electrolyte concentrations
- comment on Na and Cl concentrations
- comment on K+
- other additives
- these are used in patients with what status of hydration?

Back 150

- electrolyte concentrations are similar to those lost in normal animal (urine, GI secretions)
- less Na and Cl than replacement (~ 40 mEq/L vs. 130-150 in replacement)
- more K+ than replacement solutions
- dextrose added to maintain isotonicity
- use in adequately hydrated patient

Front 151

at what rate is hypertonic saline administered?

Back 151

over 5-10 minutes (4-8 ml/kg)

Front 152

give five examples of colloid solutions

Back 152

1. dextrans
2. hetastarch
3. pentastarch
4. albumin
5. plasma

Front 153

what is the advantage of using colloids over hypertonic crystalloids?

Back 153

they expand the intravascular volume for a longer period of time vs. hypertonic solutions

Front 154

what are four indications for using colloids?

Back 154

– Hypovolemia combined with:
• Hypoalbuminemia
• Fluid accumulations (ascites, pleural effusion, edema)
• Increased capillary permeability
– Inadequate response to crystalloid
– Shock
– Hypotension during anesthesia

Front 155

what are three general aspects of a fluid therapy plan?

Back 155

1. fluid volume
2. rate of administration
3. type of fluid

Front 156

how do you calculate fluid defecit?

Back 156

1. estimate dehydration %
2. defecit volume = % dehydration x BW (kg)

Front 157

what is the maintenance fluid volume requirement in the average patient?

Back 157

50 ml/kg/day

Front 158

what are the two types of losses of fluid volume in a normal patient, where these originate, and amount of each?

Back 158

1. insensible losses - fecal, respiratory, cutenaous - about 20 ml/kg/day
2. sensible losses - urinary - about 30 ml/kg/day

Front 159

what are three components used to calculate fluid volume in a fluid replacement plan?

Back 159

1. fluid deficit
2. maintenance requirement
3. ongoing losses (e.g. vomiting, excess urination, diarrhea)

Front 160

how is a total fluid maintenance requirement calculated? How does animal morphology and age affect this value? What is the average range of maintenance requirement for dogs and cats?

Back 160

- parallels basal energy requirements (1 mL/kcal)
- small and young animals have a higher fluid requirement per kg BW
- average is 40-60 ml/kg/day in dogs and cats

Front 161

what are five ways in which pathologic ongoing losses of fluids can occur?

Back 161

1. diarrhea
2. vomiting
3. polyuria
4. 3rd space loss (e.g. ascites)
5. bleeding

Front 162

what three questions should be answered when determining rate of fluid administration?

Back 162

1. what was the rate of fluid loss?
2. what is the magnitude of loss?
3. what is the current circulatory status?

Front 163

over what time period should fluids be restored in:
- chronic loss?
- acute loss?
- shock?

Back 163

- chronic loss: 24-48 hr (usually 24 hr)
- acute loss: 2-6 hr
- shock: 15-60 min (dog, 90 ml/kg/hr; cat, 60 ml/kg/hr)

Front 164

why are fluids replaced more slowly in chronic loss?

Back 164

because rapid administration results in diuresis, not rehydration

Front 165

which type of fluid should be used when:
- patient has diarrhea and vomiting from the duodenum (as well as stomach)?
- patient is only vomiting gastric contents?

Back 165

- diarrhea + SI vomitus: standard replacement electrolyte solution
- gastric contents only: normal saline is ideal (due to metabolic alkalosis with hyponatremia and hypochloremia)

Front 166

what are three etiologies in which fluid retention will complicate fluid replacement? In these cases, what type of fluid should be used?

Back 166

1. heart/hepatic failure
2. hypoalbuminemia
3. effuision/edema
- use low sodium fluid or colloid except heart failure

Front 167

when monitoring fluid therapy, how often should you give a complete physical examination?

Back 167

2x per day

Front 168

what are six clinical signs of overhydration?

Back 168

1. serous nasal discharge
2. chemosis (edema of the conjunctival tissue)
3. cough, dyspnea, crackles, ↑respiratiory rate
4. edema, ascites
5. shivering, restlessness
6. diarrhea, vomiting

Front 169

what are four causes of overhydration?

Back 169

1. excessive fluid adminstration
2. oliguria
3. hypoproteinemia
4. imparied cardiac output

Front 170

if a dehydrated patient also presents for CRF, how does that change your fluid replacement plan?

Back 170

- give fluids faster (fluid defecit + 6hr of maintenance over 6 hr)
- put on 2x maintenance
- diurese

Front 171

what are four parameters to monitor in a patient on fluid therapy?

Back 171

1. PCV, total solids
2. BW
3. urine output (1 ml/lb/hr)
4. central venous pressure if
- fluid administration ≥ 90 ml/kg/hr for > 1 hr
- low urine output
- questionable cardiac function

Front 172

how does weight gain/loss correlate with fluid excess/deficit?

Back 172

A gain or loss of 0.5 kg should be considered an excess or deficit of 500 ml of fluids

Front 173

what is considered a normal urine output?

Back 173

1-2 ml/kg/hr

Front 174

what are five possible reasons for inadequate hydration despite fulid therapy?

Back 174

1. calculation error
2. underestimation of fluid deficit
3. ongoing losses
4. rate of infusion to ohigh (diuresis rather than rehydration)
5. technical problems with the catheter

Front 175

why should oxygen supplementation be avioded in hyperthermia?

Back 175

may contribute to overheating

Front 176

what are two ways to treat DIC in hyperthemic patients?

Back 176

1. transfusion
2. heparin

Front 177

in the hyperthemic patient, what are four ancillary treatments to prevent further complications?

Back 177

1. treat DIC aggressively
2. prevent bacterial translocation & sepsis from GI (a/b and GI protectants)
3. correct hypoglycemia
4. correct acid/base and electrolyte abnormalities

Front 178

what type of drugs are contraindicated in hyperthermic patients and why?

Back 178

NSAIDs, because they alter the hypothalamic set point

Front 179

when treating for hyperthermia, what two drugs may be used to treat hypotension after resuscitation?

Back 179

1. dopamine
2. dobutamine (β1 agonist)

Front 180

what is the average prognosis for severe hyperthemia? What determines the prognosis?

Back 180

- guarded
- depends on length of time animal was hyperthermic, amount of organ damage, and response to intensive supportive care

Front 181

what are some poor prognostic indicators for hyperthemia?

Back 181

- delayed admission (> 90 minutes)
- coma or neuro degen
- hyopthermia on presentation
- persistent hyperglycemia
- ARF
- DIC
- refractory hypotension
- hyperbilirubinemia
- ventricular arrhythmias
- persistent hypoproteinemia
- dyspnea, pulmonary edema

Front 182

what drugs are used to treat primary immune mediated polyarthritis?

Back 182

immunosuppressive doses of corticosteroids

Front 183

what is anaphylaxis?

Back 183

a severe local or systemic Type I hypersensitivity reaction

Front 184

what type of antibodies mediate anaphylaxis?

Back 184

IgE

Front 185

how does IgE stimulate an anaphylactic reaction?

Back 185

antigen cross-links IgE on mast cells, causing degranulation

Front 186

what is the pathogenesis of a skin sensitization that leads to anaphylaxis?

Back 186

antigen binds to dendritic cells → dendritic cells presents antigen to Th-cells in LN → B cell clonal expansion and enter the blood stream → B cells secrete IgE, which binds to mast cells → 2nd antigen exposure causes degranulation of mast cells by cross-linking of IgE

Front 187

what are four major physiological effects of histamine release?

Back 187

1. No production (vasodilation)
2. enhances leukocyte chemotaxis
3. stimunates arachadonic acid metabolites (e.g. prostaglandins/leukotrienes)
4. potentiates further mast cell degranulation

Front 188

what are the effects when histamine stimulates:
- smooth muscle?
- exocrine secretions?
- vasculature?

Back 188

- smooth muscle contraction (bronchi & SI); pulmonary vasoconstriciton
- bronchial mucus, rhinorrhea, lacrimation, salivation, gastric acid, pepsin
- Wheal formation (swollen lump on the skin), edema, pruritis

Front 189

what are the major organs of anaphylaxis in:
- ruminants?
- horses?
- swine
- cats?
- dogs?

Back 189

- ruminants: respiratory tract
- horses: respiratory tract and intestine
- swine: respiratory tract and intestine
- cats: lung and respiratory tract
- dogs: liver and GO tract

Front 190

what are five common causes of anaphylaxis?

Back 190

1. vaccines
2. blood products
3. venom
4. food
5. drugs (e.g. a/b, opiates, NSAIDs)

Front 191

what are the ABC's of energency life support?

Back 191

A- airways
B- breathing
C- cardiovascular support

Front 192

what is the pharmaceutical first line of treatment for anaphylaxis? What routes of administration?

Back 192

ephinephrine
- IV or intratracheal (diluted and 2x IV dose)
- IM, SC in less severe presentations
- CRI

Front 193

what are four drug types used when treating systemic anaphylaxis?

Back 193

1. epinephrine
2. IV fluids (shock dose or to effect) - crystalloids, or colloids if needed
3. immunosuppressive levels of fast-acting corticosteroids
4. antihistamines IM; IV DOSES CAN CAUSE HYPOTENSION (not very useful during acute phase)

Front 194

when treating systemic anaphylaxis, what drugs are used to treat:
- refractory hypotension?
- persistent bradycardia?
- respiratory distress?

Back 194

- refractory hypotension: dopamine CRI
- persistent bradycardia: atropine
- respiratory distress: inhaled bronchodilators (e.g. albuterol); oxygen; early elective intubation

Front 195

why should patients with localized anaphylaxis be monitored carefully?

Back 195

because it can be systemic

Front 196

what are two drugs used to treat localized anaphylaxis?

Back 196

1. antihistamines (e.g. diphenhydramine)
2. corticosteroids (e.g. dexamethasone)