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BVMS 3 > Module 14 Wk 1 > Flashcards

Module 14 Wk 1 Flashcards

1
Q

(Small Animal Emergencies: Triage and Patient Stabilisation)

Explain how to perform a triage exam

A
  • Stable vs. immediate care (CPA/Shock)
  • Based on vital signs- AirwayBreathingCirculation
  • Includes brief history (presenting complaint), CPR code status and brief focused physical exam
  • Traffic light system Red: Critical Unstable Amber: Urgent/potentially unstable Green: Stable
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2
Q

Explain how to perform a primary survey and concept of ABCDE

A
  • Goal of a primary summary is to identify and stabalise life threatening problems
  • ABCDE stands for AirwayBreathingCirculationDemnorEntire body
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3
Q

Explain the difference between a primary and secondary survey

A

In a primary survey, it’s quick, whereas in a secondary survey, you are doing a full clinical examination, body weight, detailed history, and giving the client an estimation of the visit. In this secondary survey, you want to fully understand the patient’s condition and develop a comprehensive diagnosis and treatment plan.

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4
Q

Describe common emergency stabilisation measures and evaluate their suitability in an individualpatient

A
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5
Q

Describe options for vascular access in the emergency patient

A
  • IV should be obtained asap in all critically ill patients for fluids and drugs.
  • In patients unable to breathe this may need to be delayed to allow for stabiliation in O2 therapy so options include
  • Peripheral venous catheter – cephalic/saphenous
  • Central venous catheter- jugular
  • PICC- peripherally inserted central catheters
  • Intraosseous catheter- prone to infection
  • Venous cutdown
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6
Q

Describe an emergency database

A
  • PCV/TS
  • Blood glucose
  • Lactate
  • BUN/Creatinine
  • Blood smear
  • Venous blood gas and electrolytes
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7
Q

(Management of shock)

Define shock

A
  • An imbalance between O2 supply and demand in the cell
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8
Q

Identify different types of shock

A
  • Hypovolaemic
  • Haemorrhagic
  • Disruptive
  • Cardiogenic
  • Hypoxic
  • Obstructive
  • Metabolic
  • (overlap of different types of shock)
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9
Q

Recognise the major indications for fluid therapy and identify clinical cases where fluid therapy may be required

A

The compensatory mechanisms in shock lead to dehydration, volume loss (hypovolemia or blood loss) and 3rd space loss so need fluid therapy to restore circulation and perfusion

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10
Q

T/F Fluid is a goal directed therapy

A

True - It is a goal directed therapy

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11
Q

What is the fluid rate for dogs?

A

Dogs: 10-20ml/kg IV

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12
Q

What is the fluid rate for cats?

A

Cats: 5-10 ml/kg IV

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13
Q

What route would you use when treating a patient with fluids?

A
  • venous access
  • intraosseous access - good in puppies or kittens as difficult to get access
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14
Q

What are the two types of fluid you can use?

A
  • hypertonic crystalloids shift fluids into the intravascular space, increasing vascular volume rapidly. Has anti-inflam effects and reduces ICP
  • colloids are larger molecules that do not cross the vascular endothelium. They have a high Colloid osmotic pressure, which expands and maintains intravascular volume. For shock, a smaller volume than crystaloids is required. They have controversial benefits.
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15
Q

What are the different types of drugs that help treat shock?

A
  • Vasopressors
  • Intropes
  • Vitamins can treat oxidative stress.
  • steroids
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16
Q

What does a Vasopressors do? What can you treat with them?

A

They cause vasoconstriction and reduce the intravascular space optimising volaemia. Could treat septic and distributive shock.

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17
Q

What do Intropes do? What can you use them to treat?

A

They decrease systolic function of the heart. Can use to treat septic shock.

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18
Q

Explain how monitoring of clinical signs, physiological and laboratory data assist in the diagnosis and treatment of shock

A

It is really important as it gives you an indication of the severity of the shock the patient is suffering from. You should monitor HR, RR, MM colour, CRT, Mentation, Pulses, and extremities (temp).

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19
Q

Discuss common complications which may occur as a result of fluid therapy

A
  • when treating haemorrhagic shock, an excess of fluid will exacerbate bleeding
  • when treating obstructive shock, there is a risk of hypervolaemia after correction.
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20
Q

What are the consequences of shock?

A
  • reperfusion injury
  • Dilated coagulopathy
  • SIRS
  • MODS
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21
Q

(Evaluation and Emergency Management of the Trauma Patient - Thoracic trauma)

Describe the major causes of hypoxaemia following an RTA

A
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22
Q

Outline the various options for management of pneumothorax

A

The goal is to re-expand the collapsed lung. Along with this we want to improve the venous return and cardiac output. Pleural drainage may be required via thoraconcentesis tube. If unresolved, it may need an exploratory thoracotomy.

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23
Q

Methods of providing supplemental oxygen

A
  • Intubation
  • Ventilation
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24
Q

Recognize the clinical manifestations of traumatic brain (primary and secondary) injury and raised Intra-cranial pressure

A
  • Primary Injury is immediate result. This type of injury includes concussion, contusion and laceration resulting in heamatoma formation and brain compression.
  • secondary injury is hours or days after trauma. This type of injury is caused by a combination of intracranial and systemic insults leading to neuronal cell death.
  • raised intracranial pressure is where the volume of the intracranial contents exceed compensatory mechanisms resulting in brain herniation if not identified and treated.
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25
Q

Describe how you would assess the severity of a TBI

A
  • Level of consciousness
  • Brain-stem reflexes (pupil size, PLRs and eye movement)
  • Limb movements
  • Respiratory pattern
  • Blood pressure and heart rate
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26
Q

Describe how you would manage a TBI

A
  • You want to ensure there is adequate oxygenation. You want to avoid and/or correct factors that predispose to secondary brain injury. Along with this you wany to address raised ICP.
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27
Q

What steps would you take if there is clinical eveidence of ICH in your patient?

A
  • Reduce cerebral oedema with hyperosmolar therapy
  • Mannitol
  • Hypertonic saline (NaCl 7.5%)(2-4 ml/kg IV over 10 minutes)
  • Reduce Cerebral Metabolic rate
  • Anaesthesia, barbiturate therapy, hypothermia
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28
Q

When using Mannitol and Hypertonic saline to treat Intra-cranial heamorrhage what would the dose and rate be?

A
  • Mannitol 0.5-1 g/kg IV over 20. minutes
  • Hypertonic saline - 2-4 ml/kg IV over 10 minutes
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29
Q

(Evaluation and Emergency Management of the Trauma Patient - Acute abdomen Abdominal Trauma)

What is a Heamoabdomen?

A
  • Heamoabdomen - Where there is a precence of heamorrhagic effusion in the peritonial cavity.
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30
Q

What is a uroabdomen?

A

Uroabdomen - Where there is leakage of ureine into the peritoneal or retroperitoneal. This causes a loss of integrity of the urinary system.

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31
Q

How might a heamoabdomen clinically manifest

A

With a Heamoabdomen clinically the patient will present shocked/collapsed, having arrythmias/pulse defects.

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32
Q

How might a uroabdomen clinically manifest

A

With a Uroabdomen the patients bladder may or may not be palpable, urination may or may not be present.

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33
Q

Outline the potential consequences of abdominal trauma and their diagnosis

A

Sepsis peritonitis - peritonitis resulting from and identifiable source of intraperitoneal infection, typically bacterial in origin and most commonly a result of leakage of the GI tract.

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34
Q

Understand the principles governing the medical management of abdominal trauma.

A

In both heam and uro medical management is essential before any surgical correction.

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35
Q

Understand the principles governing the surgical management of abdominal trauma.

A

Surgical management is what comes after medical managment, This is where surgical intervention is used to try solve and explore the trauma.

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36
Q

How would you manage a heamoabdomen?

A

Initially, you want to manage the shock and control the source of bleeding. Fluid should be hypotensive or low volume. Blood transfusion can aid along with oxygen therapy.

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37
Q

(Imaging the Emergency Patient)

List the main common traumatic injuries.

A
  • Pneumothorax
  • Pulmonary contusion
  • Pleural effusion (fluid)
  • Ascites
  • Diaphragmatic rupture
  • Fracture/luxations
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38
Q

Whats the difference between over exposed and under exposed?

A
  • Over-exposed is where it is too dark, there is a lack of contrast.
  • Under-exposed is where it is too white with too little differentiation.
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39
Q

What are common traumatic lesions to the thoracic wall?

A
  • Diaphragm rupture
  • Ribs
  • Dislocation of sternum
  • Flail chest
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40
Q

What are 3 common intrathoracic traumatic lesions?

A
  • Pneumothorax
  • Pulmonary contortion
  • Pneumomediastinum- cervical, pharyngeal?
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41
Q

What might you see on a radiograph of a patient who has pneumothorax?

A
  • Heart raised from the sternum
  • retraction of lung lobes
  • increased lung opacity
  • Blebs within the pulmonary tissue
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42
Q

What is the stand-out thing you see on a radiograph of a patient who has tension pneumothorax?

A

Heart raised from sternum

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43
Q

What is a pulmonary contusion?

A

It is a bruise on the lung which is the same opacity as soft tissue.

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44
Q

What would you see on a radiograph of a patient with pleural effusion?

A
  • Loss of cardiac silhouette on DV and if very severe you’ll see it on lateral
  • Retraction of lung lobes where there is visible soft tissue in plural spaces, outlines of lungs with leaf or scalloped edges.
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45
Q

T/F if pleural effusion is acute lungs will have scalloped edges?

A

Flase they will have leaf edges.

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46
Q

What can be seen on a radiograph of a patient with a diaphragmatic rupture?

A
  • Abdominal Organs in the thoracic cavity
  • Loss of diaphragmatic line
  • Increased opacity
  • Pleural effusion
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47
Q

What does FAST help detect?

A
  • abdominal fluid
  • Pericardial fluid
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48
Q

Describe what you would see on a radiograph of a patient with peritoneal effusion

A
  • Organs not visible
  • Loss of serosal detail
  • presence of peritoneal fluid
  • presence of peritoneal gas
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49
Q

What is GDV?

A

Gastric dilation and Volvulus is where the stomach is rotated and shaped like a smurf or popeye, and the small intestines are dilated, all causeing functional paralysis of SI.

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50
Q

(Anaesthetic risk and pre-anaesthetic assessment)

Describe the ASA physical status classification system

A

This is a 5 grade system.
- Grade 1 is a healthy patient
- Grade 2 is described as a mild, fully compensated, systemic disease.
- Grade 3 is where a severe systemic disease functionally affects the patient.
- Grade 4 is where a severe systemic disease is a constant threat to the patients life.
- Grade 5 is a moribund patient that is not expected to survive with or without treatment

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51
Q

Identify groups of patients at increased risk of anaesthetic mortality/morbidity based on signalment

A
  • Age - older animals and very young animals
  • Breed - brachycephalic and breeds that have unexpected responses to drugs
  • Body weight - increased
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52
Q

Recognize major disease categories which increase anaesthetic risk and explain how these risks could be reduce

A
  • cardiovascular and Respiratory are the main two

These can be reduced by
- Taking a full history
- abnormalities from this?
- can we stabilise these?
- Doing pre-op blood
- if there was anything from this?
- Can we do anything to limit the risk?

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53
Q

(Clinical pharmacology of analegesics)

Whats is the mechanism of Opioid analgesics

A

They activate opioid receptors to reduce neuronal excitability

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54
Q

What are the effects + side effects of Opioid Analgesics

A
  • analgesic
  • sedative
  • dysphoria/euphoria
  • respiratory depression
  • Nausea
  • Reduced gut motality
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55
Q

T/F Opiod analgesics have poor oral bioavailability?

A

True

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56
Q

What would you use opioid analgesics for?

A
  • To relieve pain
  • To provide sedation
  • To reduce required dose of general ana
  • To treat diarrhoea
  • To control coughing
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57
Q

What patients would you take caution using opioid analgesics with?

A
  • existing hypoventilaition
  • increased ICP
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58
Q

Describe the mechanism of action of NSAIDs

A

They inhibit the production of prostaglandins and thromboxanes by cyclo-oxygenase enzymes.

59
Q

What effects do NSAIDs have?

A

Analgesia and anti-inflammatory, antipyretic.

60
Q

What side effects can NSAIDS have?

A
  • Dyspepsia, GIT ulceration
  • Renal toxicity
  • Hepatic toxicity
  • Effects on platelet function
61
Q

What would you use NSAIDs for?

A
  • Pain management
  • Management of inflammatory disorders
  • Management of pro-thrombotic states
  • Management of specific tumours
62
Q

When should you not use NSAIDS with what patients?

A
  • Gastrointestinal tract disease, especially GI ulceration
  • Acute or chronic renal disease
  • Impaired hepatic function
  • Haemostatic disorders
  • Patients concurrently treated with steroids
  • Breeding, pregnant or lactating animals
  • Patients with unstable asthma
63
Q

What is the mechanisms of action of a local anaesthetic?

A

They block sodium channels, preventing the initiation and conduction of action potentials.

64
Q

What are the effects ans side effects of local anaesthetics?

A
  • Analgesia via blocking neuronal transmission
  • Antidysrythmic action
  • CNS toxicity - twitching seizures, coma
  • CVS toxicity - Bradycardia, hypotension
65
Q

what can affect the effects of local anaesthesia?

A
  • The activity can be altered by tissue PH
  • Ionisation can slow the onset.
66
Q

How might you use local anaesthesia?

A
  • topical application
  • inflitration
  • instillation into cavity wound
  • peripheral nerve block
  • epiduralblock
  • IV regional ana (beir block)
  • IV infusion
67
Q

T/F most contraindications of local anaesthetic is to do with technique rather than drugs?

A

True bro

68
Q

What is the only local ana that can be administered IV?

A

Lidocaine NEVER bupivacaine

69
Q

What are the noval routes of administration?

A
  • oral transmucosal - absorbed through buccal mucosa
  • transdermal - through skin
70
Q

(Approach to suspected poisoning)

Describe how you would prevent further absorption of toxins.

A
  • irrigation of eyes - irrigate the eye for at least 15 mins with saline/water
  • skin - wash/clip hair, prevent grooming.
  • GI - emetics, gastric lavage, absorbants, enemas or surgical removal.
71
Q

What are contraindications to emetics?

A
  • Neurological dysfunction
  • Corrosive ingestion
  • Predisposed to aspiration - Megaoesophagus, laryngeal paralysis, brachy?
  • Time post ingestion (>4 hours) ? - Paracetamol vs raisins
  • Prior vomiting
72
Q

Apomorphine is a recommended emetic in dogs; talk about it (administration, effect, pros and cons and reversal)

A
  • Administration IV, SC or via the conjunctiva
  • It acts via dopamine receptors in the chemorecpetor trigger zone
  • Its expensive
  • Its not a controlled drug
  • can cause sedation so reveers with naloxone if required.
73
Q

Dexmedetomidine/Medetomidine/Xylazine are recommended emetic in cats; talk about it (administration, effect, pros and cons and reversal)

A
  • Its moderately effective
  • causes sedation and cardiorespiratory depression
  • you need atipamezole to reverse
74
Q

What kind of patients should you consider around gastric lavage?

A

Neurological patients.

75
Q

What is the main absorbant we use in vet med around toxins?

A

Activated charcoal - It binds toxins and stops further absorption

76
Q

What kind of toxin migh IV fluids help with?

A
  • Theobromine (chocolate) because it increases renal elimination
  • Lilies and raisins because it supports the kidneys
77
Q

What might IV lipid emulsion help with?

A
  • Lipophilic toxins
  • Toxins with a short halflife
78
Q

What are the clinical signs of a patient who has ingested paracetamol less than 24hrs?

A

Less than 24hr
- cyanosis/muddy brown mucous membranes
- Tachycardia, tachypnoea, lethargy
- facial and paw oedema
- vomiting
- anaemia

79
Q

What are the clinical signs of a patient who has ingested paracetamol more than 24hrs?

A

More than 24hrs
- liver failure
- icterus - jaundice
- seizures/coma
- renal failure
- haematuria

80
Q

How to treat a paracetamol toxicity?

A
  • Emetics if less than 2hrs post ingestion
  • Absorbents
  • Supportive care such as IVFT, O2, blood products
  • Antidotes
81
Q

What antidotes can you use with paracetamol toxicity?

A
  • N-acetylcysteine
  • S-adenosylmethionine
  • Ascorbic acid (vit C)
  • Cimetidine (dogs)
82
Q

What are the clinical signs of a patient who has injected slug bait?

A
  • Hyperaesthesia
  • Tremors
  • Seizures
  • Hyperthermia
  • liver failure after 2-3days occasionally
83
Q

How would you treat a patient who has ingested slug bait?

A
  • Treat regardless of dose ingested
  • Emetics if asymptomatic and observe
  • Activated charcoal
  • If seizures: Diazepam (propofol if non-responsive) +/- gastric lavage
  • Methocarbamol
  • IVFT and nursing care
84
Q

what are the effects of a patient injestion Rodenticides?

A
  • it slowly absorbed from GIT
  • It blocks vit K activition so there is a depletion of clotting factors, so there is a defect in secondary haemostasis
85
Q

What are the clinical signs of a patient that has ingested Rodesnticides

A
  • Lethargy
  • Body cavity haemorrhage -Haemothorax (dyspnoea), Haemoabdomen
  • Epistaxis
  • GI bleed - melaena / haematemesis
  • Joint pain
  • Anaemia
86
Q

How would you treat a patient who has ingested rodenticides ?

A
  • When they are asymptomatic, treat with activated charcoal and emesis.
  • When symptomatic, there should be immediate support via o2 +/- transfusion
87
Q

What are the clinical signs of a patient who has ingested antifreeze less than 12hrs?

A
  • neurological signs
  • GI signs
  • Acidosis
88
Q

What are the clinical signs of a patient who has ingested antifreeze 12hrs to 24hrs ago?

A
  • Cardiopulmonary signs - tachypnoea, tachycardia, acidosis, pulmonary oedema, shock
89
Q

What are the clinical signs of a patient who has ingested antifreeze 24-72 hours ago?

A

Renal - swollen/painful kidneys

90
Q

How would you treat a patient that has ingested Antifreeze?
(Emetics, activated charcoal, drugs, Fluid, antidotes?)

A
  • Emetics probs won’t be useful unless they present very quickly
  • Activated charcoal is not useful
  • Diazepam for seizures
  • Need to correct acidosis
  • IVFT - monitor urine output and electrolytes
  • Antidotes
91
Q

What antidotes can you use to treat antifreeze toxicity? and what will it do?

A

20% ethanol or 4-methyl pyrazole - if less than 12hrs will block alcohol dehydrogenase and allow renal excretion of the ethylene glycol unmetabolised

92
Q

How would you treat patient who has ingested a toxic amount of chocolate?

A
  • Emesis, activated charcoal
  • Enhance urinary excretion via IVFT, urinary catheterisation
  • Continuous ECG and seizure monitoring
  • Arrthymias (treat if clincally sig.)
  • Symptomatic treatment of tremors/seizures and GI signs
93
Q

What clinical signs can a patient ingesting a grape/raisin display?

A
  • GI - vomiting, diarrhoea, abdominal pain
  • Acute renal failure from 24-72hr
94
Q

(Clinical Pharmacology of sedatives)

what is a tranquiliser?

A

It relieves anxiety without drowsiness

95
Q

What is a Neuroleptic?

A

A tranquiliser used in treatment of psychoses

96
Q

Whats is a sedative?

A

It is a calming effect with drowsiness

97
Q

what is a hypotic?

A

It induces sleep

98
Q

List the main drugs used as sedatives

A
  • Phenothiazines
  • Butyrophenones
  • Alpha2-adrenoceptor agonists
  • Benzodiazepines
99
Q

Describe the mechanism of action of phenothiazines?

A

A non-selective dopamine anatagonism

100
Q

What effects can Phenothiazines have?

A
  • Cardi - vasodilation causing hypotension and anti-arrhythmic action
  • Resp - minimal
  • GI - Reduced gut motality, reduce secretion of saliva
  • Hypothermia
  • Penile prolapse
  • Mild antihistamine activity
101
Q

Describe the Pharmokenetics of phenothiazines

A
  • IM (IV, SC)
  • oral gels/tablets
  • slow onset and long duration
102
Q

T/F phenothiazines are metabolized in the liver?

A

Trueeee pat

103
Q

What would you use phenothiazines for in practice?

A
  • pre-med prior to genral
  • sedation
  • motion sickness
  • calming effects
104
Q

What are the contra-indidcation of using phenothiazines?

A
  • Hypervolemia
  • Breeding stallions - penis
  • Lower doses recommened in giant, brachycephalic and herding breeds.
105
Q

What is the mechanism of action of butyrophenones?

A

They are also dopamine anatgonsist

106
Q

What side effects do Butyrophenones have?

A
  • Vasodilation and hypotension
  • occasionally hallucinations
107
Q

What is the butyrophenone, Azaperone, used for and how?

A
  • sedation, pre med or behavioural modification
  • Administered deep IM
108
Q

Whats is the butyrophenone Hypnorm made up of, used for and administered?

A
  • Fluanisone and fentanyl
  • used for sedation and pre-med
  • Administered IM or IP
109
Q

What is the mechanism of action of alpha2-adrenoceptor agonists?

A

They activiate adrenergic receptors within the sympathetic NS

110
Q

Describe what effect alpha2 have on pre-synaptic a2, Post-synaptic A2 and post-synaptic a1 receptors

A
  • At pre-synaptic a2 they reduce noradrenaline release (sympatholytic)
  • At post-synaptic a2 they mimic noradrenaline (sympathomimetic)
  • At post-synaptic a1 they also mimic noradrenaline (sympathomimetic)
111
Q

Side effects?????

A
112
Q

Describe the pharmokenetics of Alpha2s

A
  • Administered via IM, IV, SC or epidurally
  • Oral route but high first pass metabolism
  • oral transmucosal route may be useful in agressive patients
113
Q

Why would you use Alpha2’s clinically?

A
  • Sedation/Pre-med
  • Analgesia
  • Offset ketamine hypertonicity
  • Reduce anxiey/fera in dogs with noise phobia
114
Q

What are the contradiction of using Alpha2’s?

A

You should be mindful of patients with cardivascular disease or poor health

115
Q

List the types of Alpha2’s

A
  • Xylazine
  • Detomidine
  • Romifidine
  • Medetomidine
  • Dexmedetomidine
116
Q

What a2 agonist has the most pharmalogical effect?

A

Xylazine < detomidine/medetomidine < romifidine

117
Q

What Alpha 2 agonist causes less ataxia?

A

Romifidine

118
Q

What Alpha2 causes uterine contraction?

A

Xylazine

119
Q

T/F Xylazine causes vomiting in dogs and cats more than medetomidine?

A

True queen

120
Q

What is the main difference between medetomidine and Dexmedetomidine?

A
  • Dexmedetomidine is more potent
  • Dexmedetomidine may have slightly shorter duration
  • Otherwise very similar
121
Q

What is Zenalpha?

A

It is a combination of medetomidine and peripheral alpha2 antagonist.

122
Q

What are the two Benzodiazepines?

A

Diazepam
Midazolam

123
Q

What is Benzodiazepines mechanism of action?

A

The potentiate activity of inhibitory neurotransmitter GABA

124
Q

What are effects and side effects of Benzodiazepines?

A
  • Anxiolytic action - but may get paradoxial excitment in helathy patients so better sedation in sicker patients
  • minimal cadriovascular and resp depression so well suited to sicker patients
  • Anticonvulsant properties
  • muscle relaxation
125
Q

Describe the pahrmacokenetics of Benzodiazepines

A
  • Administered by IV, (IM) or orally
  • They have a rapid onset and short duration
  • Metabolised via liver
126
Q

Why would you clinically use benzodiazepines?

A
  • Premed/hypnosis of sick animals
  • Prevention/treatment of seizures
  • Muscle relaxation
  • To induce eating (cats)
  • Occasionally to modify behaviour or reduce anxiety
127
Q

what are the contra-indications of Benzodiazepines?

A
  • Hepatic encephalopathy (portosystemic shunts)
  • Early pregnancy (teratogenic)
128
Q

(Prescribing & dispensing: responsibilities & controlled drugs)

What are the problems associated with the mobile dispensary?

A
  • Temperature - Min-max thermometer, Data logger preferred
    and Portable refrigeration unit.
  • Public access
  • Stock rotation
  • Drug waste
129
Q

What should you report if there is problem with animal medicines?

A
  • Suspected adverse reactions AND lack of efficacy
  • Reactions to authorised veterinary medicines AND human medicines
  • Reactions in animals AND also people handling drugs
130
Q

List the Schedules of controlled drugs and give examples

A
  • schedule 1 - greatest potential harm
  • schedule 2 - must be stored in a fixed locked place, info required on the prescription, prescription valid for 28days, use must be recorded and signed by a vet
  • schedule 3 - info required on the prescription, prescription only valid for 28days, invoice retained for 2 years
  • schedule 4 - prescription only valid for 28days, invoices retained for 2 years
  • schedule 5 - invoices retained for 2 years
131
Q

List the requirements for a controlled drug written prescription

A
  • Declaration that CD is prescribed for an animal or herd under the veterinarian’s care
  • Name & address of owner, plus name of animal to whom the CD is to be administered
  • Name & form of drug
  • Amount of product prescribed in both words & numbers - For example: Twenty (20) capsules
  • Strength of preparation
  • Dose to be administered and the route (take as directed or take as required is not acceptable)
  • Prescribing vet’s MRCVS registration number
132
Q

Describe the destruction of out of date schedule 2 CDs

A
  • must be denatured
  • disposed of as pharmacological waste
  • witnessed by a vet, police or VMD inspector
133
Q

Describe what to do with waste of schedule 2 CD’s

A
  • Some breakages are inevitable
  • Clear up using an appropriate spill kit - SOP
  • Dispose of waste in appropriate containers - Pharmaceutical waste
  • Record in a register that the ampoule has been broken
  • Counter sign
134
Q

(Choosing appropriate premedication and sedation)

What are the aims of premedication?

A
  • To produce a calming effect or sedation
  • To provide analgesia
  • To reduce doses of other agents required
  • To ‘smooth’ induction and recovery
  • To counteract unwanted effects of other anaesthetic drugs
135
Q

What do anticholinergics do?

A
  • They block the effects of acetyl choline at receptors
  • They block parasympathetic effects
136
Q

T/F atropine and glycopyrrolate are examples of anticholinergics?

A

True

137
Q

Give examples of Acepromazine combinations

A
  • ACP and buprenorphine
  • ACP and methadone
138
Q

Give examples of Alpha2 combinations

A
  • Medetomidine and butorphanol
  • Dexmedetomidine and methadone
139
Q

Give examples of Alfaxalone combination

A
  • Alflaxalone and butorphanol
  • Alflaxalone and midazolam
140
Q

Give examples of ketamine combinations

A
  • Midazolam and Ketamine IM (cats)
  • Alpha 2 and opiod and ketamine
    CANT USE ALONEEE
141
Q

T/F sedation is essential for pre-ana medication?

A

False - * Sedation is not essential for pre-anaesthetic medication. If the animal is calm/handleable and If the effects of sedatives are undesirable.

142
Q

In a young healthy, very lively dog who is to be castrated, what would you use to pre-med and sedate?

A
  • Route = would be IM due to being difficult to handle
  • Sedation = Medetomidine (alpha2) is the best option, and combining it with ketamine is also good sedation, even at a lower dose.
  • Opiod - Buprenorphine is a good analgesia here. Pethidine is also a full new agonist, which will provide good anaesthetic but has a short duration; however, since it’s a castration, it will be okay!
143
Q

In a 3yr old CKCS witha grade 5/6 systolic heart murmour, mitral disease who is to have a patella luxation, what would you use to pre-med and sedate?

A
  • Route = IV as small doses of drugs needed
  • Sedation = not in this case
  • Opiod = Buprenorphine good here downside its not easy to top up during surgery

BVMS 3 (10 decks)

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