Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
139 Cards in this Set
- Front
- Back
|
Minimum parts of POVMR data base
|
General-Signalment, history, physical exam
Problem specific System Degree of evaluation & treatment |
|
|
Components of POVMR
|
Database
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 |
|
|
SOAP
|
Progress notes
Subjective Objective Assessment 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 |
|
|
Shock
|
Inadequate oxygen delivery/ impaired ability of oxygen utilization, to the point that tissue needs are not met
|
|
|
4 Classes of shock
|
Hypovolemic
Relative hypovolemic Cardiogenic Septic |
|
|
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
Oxygenation Vasopressors Blood Transfusions Glucocorticosteroids |
|
|
Ways to restore blood volume in shock
|
IV fluids (when noncardiogenic)
Crystalloids Hypertonic saline Colloids Polymerized hemoglobin |
|
|
Goal of IV fluid administration
|
Increases preload, CO & tissue perfusion
|
|
|
Crystalloids
|
Balanced electrolyte solutions
-LRS |
|
|
Shock dose for crystalloid administration
|
90ml/kg/hr
|
|
|
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 |
|
|
Colloids
|
Albumin, hetastarch, dextrans
Stay in vascular space longer & can be given in lower doses or slow boluses |
|
|
Polymerized hemoglobin
|
Oxyglobin
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
|
|
|
Sepsis
|
Infection w/ systemic inflammatory response
|
|
|
SIRS
|
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
|
|
|
Hyperthermia
|
Any elevation in body temperature above the normal range
|
|
|
Fever
|
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 Fluids 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 |
|
|
FUO
|
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 |
|
|
Anaphylaxis
|
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
|
Histamine
Eosinophilic chemotactic factor Neutrophilic chemotactic factor Arachadonic acid Leukotriences C4, D4, E4 Platelet activating factor Serine porteases Kinins |
|
|
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
Bronchospasms Peripheral vasodilation w/ decreased venous return=hypotension/hypovolemic shock Pruritus 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
|
Epinephrine
IV fluids Corticosteroids Atropine sulfate Aminophylline Antihistaminas |
|
|
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
90ml/kg=dogs 60ml/kg=cats 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
|
Antihistamines
Fast acting corticosteroids |
|
|
Fast acting corticosteroids for local anaphylaxis
|
Inhibit histamine synthesis, limits arachadonic acid metabolism & stabilizes vascular membranes
|
|
|
Wheals
|
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 Diuresis 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
SQ IP IV IO |
|
|
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
|
|
|
Crystalloids
|
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
|
Colostrum
Transplacental Immune serum administration |
|
|
Modes of active immunity
|
Natural infection
Vaccination |
|
|
Advantages of MLVs
|
Fewer doses
Don’t need adjuvants Less hypersensitivity Cheap 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 Immunosuppresion Handling is vital-no sunlight, heat, don’t last long once mixed Disinfectants in multi-use syringes may kill |
|
|
Advantages of inactivated vaccines
|
Stable
Unlikely to cause disease Unlikely to become contaminated |
|
|
Disadvantages of inactivated vaccines
|
Need multiple doses
Short immunity Increased risk of anaphylaxis Expensive Potential reaction to adjuvant Cellular immunity not as good as MLV |
|
|
Intranasal vaccines
|
Local, maybe systemic immunity
MLVs 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
Plasma dextran oxyglobin pentastarch |
|
|
Oxyglobin
|
a colloid w/ oxygen carrying capacity
|
|
|
Indications for colloid administration
|
hypoalbuminemia
hypovolemia ascites pleural effusion shock/trauma |
|
|
Contraindications for colloid administration
|
oliguric renal failure
congestive heart failure coagulopathy Anaphylaxis |
|
|
Plasma as a colloid
|
can't give enough to have significant effect on oncotic pressure
|
|
|
Determining how much fluid to give
|
fluid deficit (% dehydration)
X 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
13-20ml/kg/day not easily measured |
|
|
Sensbile losses
|
Urine output
27-40ml/kg/day easily measured |
|
|
Total maintenance fluid requirement
|
40-60ml/kg/day
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
|
