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139 Cards in this Set

  • Front
  • Back
Minimum parts of POVMR data base
General-Signalment, history, physical exam
Problem specific
Degree of evaluation & treatment
Components of POVMR
Problem list
Plan: Disease & Treatment
Progress notes
Contents of MPL
Master Problem List
ToC-1st page
Problems dated from origin/numerical order from origin
May also contain vaccin., fecal, HW, FeLV or drug information
5 fates of problems on MPL
1. refined w/ new facts
2. combined w/ another problem
3. temporarily inactivated (put off while more serious conditions dealt with)
4. Resolved
5. Removed- was never a problem
Progress notes
Plan (daily plans for disease diagnosis, treatment & client education)
Subjective Assessment POVMR
Observations, that are not easily quantifiable
(i.e. better appetite, looks stronger)
An overall assessment
Objective Assessment of POVMR
Daily physical exam findings
Quantified data: lab results, radiographs, etc
Assessment part of POVMR
Interpretation & explanation of problems at current time
Current differential diagnosis & evaluation of treatment
Daily Plan for Diagnosis
Tests to be performed w/in next 24 hours
Daily Plan for Treatment
List of therapeutic objectives & goals
Treatments to be administered in next 24 hours, including dose, frequency & RoA
Daily Plan for client education
List time of communication, who talk with
Summarize conversation
-update condition, discuss new tests/treatments, update bill
Inadequate oxygen delivery/ impaired ability of oxygen utilization, to the point that tissue needs are not met
4 Classes of shock
Relative hypovolemic
Hypovolemic cause of shock
Inadequate blood volume
Relative hypovolemic cause of shock
Vasodilation & pooling of blood in veins= decreased preload
Cardiogenic causes of shock
Impaired cardiac output
Septic causes of shock
See a combination of hypovolemic, relative hypovolemic & cardiogenic shock due to bacteremia & endotoxemia
Primary means of compensating for shock
Increased sympathetic activity, trying to maintain normal BP increase CO, decrease acidosis, hypoxia,
Initial clinical signs of septic shock
Initial rise in HR & CO
Strong pulses
Bright red mucus membranes
Preserved blood flow to non-essential tissues (skin, GI), but decreased to kidneys & heart
Later clinical signs of septic shock
Present the same as hypovolemic shocks
Consequences of shock
Splenic, venous, arterioular constriction
-↓ BF to viscera
↓ myocardial contractility
Tissue hypoxia-↑vascular permeability
Cellular dysfunction & death-organ failure
Primary goal of shock treatment
Restore adequate delivery of oxygen & nutrients to tissues
Strategies for treatment of shock
Restore blood volume
Blood Transfusions
Ways to restore blood volume in shock
IV fluids (when noncardiogenic)
Hypertonic saline
Polymerized hemoglobin
Goal of IV fluid administration
Increases preload, CO & tissue perfusion
Balanced electrolyte solutions
Shock dose for crystalloid administration
Practical dosing for crystalloid administration
20-30ml/kg as fast as possible and repeated as necessary, then 10-20ml/kg/hr & monitor for overhydration
Effect of Hypertonic saline
3-7% NaCl, a small amount administered causes rapid movement of interstitial fluids back into vascular space
Rapid onset, short-lived effects
Most effective when used in combination w/ colloid
Albumin, hetastarch, dextrans
Stay in vascular space longer & can be given in lower doses or slow boluses
Polymerized hemoglobin
A colloid w/ oxygen carrying capacity
More easily reach tissues with small capillaries/arterioles from vasoconstriction than RBCs
Oxygen in treating shock
Meant to increase (maximize) blood oxygen levels, by using oxygen masks/tents/nasal tubes
Significance of blood transfusions in treating shock
Meant to treat the anemia, causing the shock
Significance of Glucocorticosteroids in treating shock
No proven benenfit, only anecdotal
-stabilizes lysosomal membranes-↓cytokines
May cause vasodilation, so should be given after fluids if given
Significance of NSAIDs in treating shock
Similar effects as glucocorticosteroids
-stabilizes lysosomal membranes-↓cytokines
May cause vasodilation, so should be given after fluids if given
-not a recommended therapy
Uses of GI protectants with shock treatment
Frequently get GI ulceration
So give H2-blockers, proton pump inhibitors to try to prevent
Uses of Antibiotics with shock treatment
Used for septic shock patients
Should be considered for all shock patients, due to risk to bacteria translocating across the intestines
What to routinely monitor in a patient with shock?
TPR, including
-pulse rate & character
-respiratory rate & character
MM color, CRT
Urine output
Lung sounds
Electrolytes, PCV, TP
Other tests that may be useful in monitoring shock?
Pulse Ox
Blood Gas
Blood pressure
Blood glucose
Necessity for Pulse Oximetry in monitoring shock?
To avoid hypoxia & continuous monitoring, but can be difficult to get readings on patients with weak pulses
Necessity for Blood gas in monitoring shock?
To avoid hypoxia
Monitor acid/base balance
Necessity for monitoring systemic BP with shock?
Avoid hypotension (systolic above 90mmHg)
Necessity for monitoring blood glucose with shock?
To avoid hypoglycemia
Infection w/ systemic inflammatory response
Systemic Inflammatory Response Syndrome
Generalized inflammatory response to various stimuli
Septic shock
Shock due to infection w/ resultant hypotension, decreased CO, disrupted BF due to vasoconstriction/vasodilation
Signs of early sepsis
Fever, dark red MM, tachycardia, leukocytosis, thrombocytopenia
Signs of septic shock
Fever/hypothermia, tachycardia, tachypnea, depression, pale MM, weak pulses, hypoglycemia, organ failure
Treatment regimen for sepsis
Aggressive and begun early to prevent more serious complications, treat primary (source) of infection
Antibiotics for sepsis treatment
Should be IV initially, based on suspected pathogen
Oxygen supplementation for sepsis treatment
Improve O2 delivery to tissues, may need transfusion if PCV too low
IV fluids for sepsis treatment
Try to improve tissue perfusion
Prevention of microthrombi formationin sepsis
Give heparin +/- plasma , increases antithrombin III
Importance of enteral feeding in sepsis
Prevents the breakdown of gut mucosal barrier
Any elevation in body temperature above the normal range
Elevation in body temperature because of a change of thermoregulatory set point in the hypothalamus
Heat stroke
A form of nonpyrogenic hyperthermia that occurs when heat-dissipating mechanisms cannot accommodate excessive heat, occurs @ temps >106 w/o signs of inflammation, no change in set point
Malignant hyperthermia
Uncommon, familial nonpyrogenic hyperthermia that occurs
Thermoregulatory center
Anterior hypothalamus w/ peripheral & central thermoreceptors
Treatment of heat stroke
Correct hyperthermia
Supplement O2
Treat other complications & underlying diseases
Methods to correct heat stroke
Clip abdomen, spray/immerse h2o, (not ice-causes peripheral vasoconstriction), fans, stop when body temp reaches 103
Fluid therapy for Heat stroke
Shock dose of crystalloids
Maintenance volume + dehydration status
Fever of Unknown Origin
Temp of @ least 103.5 on @ least 4 of 14 days & illness of 14 days w/o obvious cause
Primary hyperthermia
Temps above 107, usually not a fever
Differentiations of hyperthermias
<103 may be stress or concurrent illness
>104 almost always significant
>107 usually primary hyperthermia
When not to treat fevers
<106 usually not life threatening unless prolonged, actually helps fight infection, limits pathogen replication, enhance leukocyte function, decreases iron avail.=don’t need antipyretics
Treatment of fevers
Antibiotics based on cultures
Fluids, restricted activity
NSAIDs-act at the hypothalamus
Glucocorticoids-only if infectious causes ruled out, b/c cause immunosuppression
Severe local of systemic Type 1 hypersensitivity reaction, acute & can be life threatening
Type 1 hypersensitivity reactions
Requires prior sensitization, & formation of antigen-specific IgE
Subsequent exposures to antigen causes activate ion & degranulation of mast cells-results in anaphylactic reaction
Major mast cell mediators
Eosinophilic chemotactic factor
Neutrophilic chemotactic factor
Arachadonic acid
Leukotriences C4, D4, E4
Platelet activating factor
Serine porteases
Effect of Histamines
H1=sm muscle contraction in bronchi & SI
Pulmonary vasoconstriction, increased vascular permeability, WBC chemotaxis, further mast cells degranulation
H2-bronchial mucus secretion
Effect of arachadonic acid
Metabolized to leukotrienes, prostaglandins, prostacyclins… alter vascular tone & permeability, & WBC chemotaxis
Effect of Serine proteases
Destroy nearby cells,
Complement activation
Increase vascular permeability
Promote further histamine release
Takes longer time than other mediators
Effects of kinins
Increases vascular permeability
Smooth muscle contraction
Prostaglandin release
Stimulates pain receptors
Net effect of Mast Cell mediators
Increase vascular permeability
Peripheral vasodilation w/ decreased venous return=hypotension/hypovolemic shock
Influx of inflammatory cell
Acute anaphylaxis in ruminants
Organ: respiratory tract
Sympt: cough, dyspnea
Path: lung edema, emphysema
Acute anaphylaxis in horses
Organ: Respiratory, intestines
Sympt: cough, dyspnea, diarrhea
Path: edema, emphysema, gi hemorrhage
Actue anaphylaxis in pigs
Organ: Respiratory, GI
Sympt: cyanosis, pruritus
Path: hypotension
Acute anaphylaxis in dogs
Organ: Liver, Gi
Sympt: collapse (hypovolemic) vomit, diarrhea
Path: hepatic congestion, visceral bleeding
Acute anaphylaxis in cats
Organ: Lung, GI, Skin
Sympt: dyspnea, collapse, vomit, pruritus
Path: lung & intestinal edema, eosinophilia
Anaphylatoid reaction
An anaphylactic reaction w/o previous exposure
Emergency management of anaphylaxis
A- airways
B- Breathing
C- cardiovascular support
D- Defibrillate, drugs
Drugs for systemic anaphylaxis
IV fluids
Atropine sulfate
Epinephrine for systemic anaphylaxis
Inhibits further mast cell degranulation, vasoconstriction & bronchodilation
A & B agonist, IM admin.
MOST important initial treatment
IV Fluids for systemic anaphylaxis
Given @ shock doses to counteract hypotension
Can be given w/ crystalloids
Corticosteroids for systemic anaphylaxis
Mainly for the shock
May prevent delayed signs of anaphylaxis
Atropine sulfate for systemic anaphylaxis
To counteract bradycardia & hypotension
Aminophylline for systemic anaphylaxis
For severely dispneic patients to relieve bronchospasms, only used after other, primary treatments administered
Antihistamines for systemic anaphylaxis
Have a very limited effect, b/c histamine is just one of the mediators of anaphylaxis
Drugs for local anaphylaxis
Fast acting corticosteroids
Fast acting corticosteroids for local anaphylaxis
Inhibit histamine synthesis, limits arachadonic acid metabolism & stabilizes vascular membranes
A circumscribed reddened area that is not raised
Indications for fluid therapy
Rehydration, Maintenance of hydration
Expansion of intravascular volume
Maintain/increase plasma oncotic pressure
Correct electrolyte imbalances
Treat specific diseases
Drug delivery
Nutritional support
Skin turgor in hydration assessment
Tented over thoracolumbar area
Looses elasticity w/ dehydration & emaciation
Significance of pulse rate & character in hydration status
Tachycardia & weak pulses detectable when dehydration >8%
Significance of bladder size in hydration status
Dehydrated=should have small bladder
Dehydrated, w/ big bladder= impaired renal function
Clinical signs of dehydrations
<5%= undetectable
5-6%=subtle loss of skin elasticity
6-8%=delayed return of tented skin, dry MM, possible delayed CRT
10-12%=tented skin stands in place, prolonged CRT, sunken eyes, tachycardia, weak pulses
12-15%=hypovolemic shock, near death
Methods for giving fluids
PO fluids
Preferred route, can’t overhydrate, inexpensive
Can’t give to many patients (vomiting, obstructed, shock-need lots of fluids fast)
Can give electrolyte & glucose solutions to help absorption of h2o
SQ fluids
Easy, owner can do @ home, overhydration not a problem, useful for mild dehydrations <5-7%, or maintenance
Can cause/worsen hypothermia
Need to be isotonic, no glucose
IP fluids
Rarely given, except to lab rodents
Indications for IV fluids
Rapidly give large volumes for shock/fluid loss
Diuresis in renal failure
More precise dose & rate needed
Admin. of hypertonic fluids
Contraindications for IV fluids
Need careful monitoring
Overhydration & catheter site irritation/infection
More expensive
Locations of IV catheters
Peripheral veins-isotonic solutions
Central veins-hypertonic solutions & rapid admin
Indications for IO fluids
Easier admin when can’t hit vein, especially small puppies/kittens
Rapid absorption
Can administer same fluids as given IV
Contraindications for IO fluids
Likely damage to the bone
Strong potential for overhydration
Sites for IO fluids
Humerus, femur, anterior tibia, iliac crest
Water w/ Na or glucose
Rapid absorption from vasculature
Significance of glucose in fluids
If given iso-osmolar, quickly hypotonic b/c glucose absorbed/metabolized very rapidly
Characteristics of replacement solutions
Electrolyte concentrations & osmolality similar to plasma=can give large doses rapidly w/o altering plasma electrolytes
Characteristics of maintenance solutions
Electrolyte concentrations similar to what is lost on a daily basis, reduced NaCl, increased K
Alkalinizing fluids
Have lactate or acetate as bicarb, (LRS) preferred in most cases
Acidify fluids
Have lots of Cl (normal saline, Ringer’s)
For vomiting gastric contents
Criteria for use of a vaccination
1. Can cause immune response to a specific disease?
2. Risks of vaccine exceed the benefit
Herd immunity
Produce enough immune animals to decrease the propagation of the agent between individuals
Modes of passive immunity
Immune serum administration
Modes of active immunity
Natural infection
Advantages of MLVs
Fewer doses
Don’t need adjuvants
Less hypersensitivity
Longer immunity
Stimulate cellular & humoral immunity
Disadvantages of MLVs
Reversion to pathogenic form
Can’t be used in pregnant animals
Can be contaminated with other pathogens
Handling is vital-no sunlight, heat, don’t last long once mixed
Disinfectants in multi-use syringes may kill
Advantages of inactivated vaccines
Unlikely to cause disease
Unlikely to become contaminated
Disadvantages of inactivated vaccines
Need multiple doses
Short immunity
Increased risk of anaphylaxis
Potential reaction to adjuvant
Cellular immunity not as good as MLV
Intranasal vaccines
Local, maybe systemic immunity
Reduced shedding of organisms
Oral vaccines
Usually live vaccines in water systems
Local (GI), or systemic immunity
Parenteral vaccines
SQ or IM
Provide systemic immunity
Uses of hypertonic saline
Reserved for shock treatment
of nondehydrated patients
Effect of hypertonic saline
draws water from interstium & intercellular space into vascular space
short-lived, need crystalloid/colloid afterwards
Effects of colloids
large molecules that don't leave vascular space, & draw/hold water into vascular space
Types of colloids
Hetastarch-most used
a colloid w/ oxygen carrying capacity
Indications for colloid administration
pleural effusion
Contraindications for colloid administration
oliguric renal failure
congestive heart failure
Plasma as a colloid
can't give enough to have significant effect on oncotic pressure
Determining how much fluid to give
fluid deficit (% dehydration)
body weight
=volume to give in liters
10kg dog x 7%=.7L
Factors for determining maintenance requirements
Insensible losses
Sensible losses
Insensible losses
Fecal, respiratory
not easily measured
Sensbile losses
Urine output
easily measured
Total maintenance fluid requirement
highest in young & small
lowest in large dogs
Determining rate for administering fluids in chronic loss
should take 24-48 hours
too fast will diures patient
Determining rate for administering fluids in acute loss
replace over 2-6 hours