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26 Cards in this Set

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What is pain?
The conscious experience of an unpleasant sensory or emotional experience associated with actual or potential tissue damage.
What is nociception?
the process of neurotransmission, originating from sensory receptors (nociceptors) which transmits and processes information related to tissue damage.
C fibres, slow & unmyelinated; Ad-fibres, fast, myelinated and small-diameter
What is hyperalgesia?
an exaggerated response to a noxious stimulus.
What is allodynia?
a pain response to a non-noxious stimulus (such as a gentle touch.)
What is peripheral sensitisation?
sensitization of C & A nociceptors, predominantly induced by inflammatory mediators released by tissue damage such that their response threshold is lowered and/or they produce a greater response to the same stimulus.
What is central sensitisation?
The enhanced excitability of spinal nociceptive neurons to result in a hypersensitive and hyperactive nociceptive transmission system. Can be short lived, associated with transient changes in neurotransmitter activity, or long-lived, associated with phenotypic changes in these central neurons.
What is analgesia?
The absence of pain sensation.
What is distress?
Physical and emotional / mental strain or stress.
What is somatic pain?
Somatic pain is easily localized and so often described as acute, aching, stabbing or throbbing. Somatic pain includes cutaneous pain after an operation. Somatic pain can be further classified as superficial (skin) or deep (joints, muscle, or periosteum) in origin.
What is peripheral pain?
Either visceral (thoracic/abdominal) or somatic (joints, muscles, or periosteum.) Visceral pain is poorly localized and frequently described as cramping or gnawing. May be also reffered pain to cutaneous sites far from site of injury.
What is neuropathic pain?
The result of trauma, inflammation, or sensitization of peripheral nerves or spinal cord. Neuropathic pain is described as burning, lacerating, and intermittent, and is often poorly responsive to treatment.
What is idiopathic pain?
Persistent pain in the absence of an identifiable organic substrate. Idiopathic pain is often excessive and associated with emotional stress or behavioral abnormalities.
What are the physiological signs of pain?
Inc blood pressure, inc heart rate, inc peripheral vasoconstriction - identifiable by pale mucus membranes, inc respiratory rate, possible muscle splinting, inc catabolic processing, dec food / water intake, dec voiding, dec grooming, and/or altered behavior: obtunded, defensive, protective, and/or needy. CAUTIONARY NOTE: these signs may be related to other factors such as concurrent disease, drug therapy, other stressors and are not reliable indicators used in isolation. Additionally, animals may hide all signs of pain; when in doubt it must be assumed to have similar pain responses as humans.
What is multimodal analgesia?
The simultaneous administration of a combination of analgesic agents (opiods, NSAIDs, and alpha2-agonists) with different modes of action and different side effects which may act synergistically and achieve optimal analgesia with less risk/side effects than large doses of a single drug.
What is pre-emptive analgesia?
Administration of an analgesic agent prior to noxious stimulation.
What are the 3 modes of ventilation?
Spontaneous, Controlled (artificial, aka IPPV), and "sighing".
What is IPPV?
Intermittent Positive Pressure Ventilation: controlled by manual compression of a rebreathing bag or by a mechanical ventilator. Positive: R & Vt are determined by the anaesthetist, overriding the risk of hypoventilation from anaesthtically reduced chemoreceptor sensitivity. Manual ventilation is only feasible in small animals, small food animals <100kg+/-, foals and calves. Large animals require mechanical ventilators.
When is IPPV not appropriate for use?
When an animal has: preexisting lung damage / disease, a V/Q discrepancy, respiratory alkalosis, hypothermia, reduced cardiac output.
What are the causes of tissue hypoxia?
1) Decreased atmospheric FIO2: N2O, inc FICO2, diethylether, N2;
2) low Tidal VA: dec r, dec Vt, inc Vd;
3) Alveolar, bad V/Q: hypovolaemia, positional, disease, pregnancy;
4) Haemoglobinaemic: dec CaO2, aneamia;
5) Stagnant / low Qt: over dose, cardiac disease, polycythaemia;
6) Histotoxic, low DO2: DNP, HCN, left-shift ODC;
7) Demand inc V02: pyrexia, hyperthyroidism, inc work

NOTE to remember: many problems are additive, ex: anemia = high starting kPa
What is oxygenation?
Oxygen delivery:

DO2 = Qt x CaO2
ie,
DO2 = Qt x [SaO2 x 1.31 x (Hb) + 0.03]/7.2kPa

where Qt=cardiac output, SaO2 = haemoglobbin saturation based on PaO2 saturation.... resulting in normal curve plus or minus...
How do anaesthetics affect fluid deficits?
"Decompensate" - ie, incapacitate compensatory mechanisms, depress cardiac output, derange blood-gases, exacerbate pH changes, impair renal function, increase respiratory water losses (low FiH2O); also, surgery imposed H2O deprivation, 3rd space losses, gross haemorrhage, evaporation from wound, blood sequestration in tissues then removed (ex spay), urinary losses.
What are the types of shock?
Hypovolaemic: reduced ECBV,
Cardiogenic: inadequate CO,
Vasculogenic: low BP due to inappropriate vascular tone,
[Neurogenic],
[Anaphylactic]
Define the term: hypotonic.
Water lost in excess of electrolytes (pure water).
What are the clinical signs of hypotonic /free water loss? How can they be corrected?
Skin tenting,
Increased haematocrit & TSP,
Oliguriga,
Impaired mentation,
“Shock” (eventually)
1. tachycardia,
2. hypotension

Treatment: 5% dextrose solution, ie. "isotonic water"
What are the clinical signs of isotonic loss? How can they be corrected?
Fluid & Electrolyte losses: 1:3 IV:ISF (ie, ECF volume changes!)

Clinical signs:
i. Tachycardia,
ii. Tachypnoea,
iii. Prolonged CRT,
iv. Pale m2,
v. Δ mentation,
vi. Oliguriga,
vii. Weak pulse,
viii. Cold extremities,
ix. NO THIRST!
x. at 10-20% ECBV
xi. 57-75 ml/kg = dog
xii. “shock” (24-48 hrs)
e. Treatment:
i. IV crystalloids / polyelectrolyte solutions
a. replace x3-4 to refill ECF
What are the clinical signs of intravascular loss? How can they be corrected?
c. Clinical signs:
i. Hypovolaemia, rapid onset:
1. Tachycardia,
2. Tachypnoea,
3. Prolonged CRT,
4. Pale m2,
5. Δ mentation,
6. Oliguriga,
7. Weak pulse,
8. Cold extremities

Treatment: replace like w/ like - Blood / plasma if possible! Colloids if not.