Week 4 Flashcards
(145 cards)
1
Q
What is surrounding the eye?
A
Densest collagen in the body on the outside- sclera and cornea anteriorly
2
Q
What is the most common eye injury we will see?
A
Mechanical injury- transfer of kinetic force to the eye. Blunt (closed eye injury, remains intact) or sharp trauma (eye ruptures). Penetrating injury doesn’t always get through the cornea or sclera or it can perforate.
** coup and countre coup injury can occur in the eye as well
3
Q
A
Chemosis- the swelling of the conjunctiva (surrounds the sclera)– conjunctiva is full of lymphatics and conjunctiva. Chemosis is a non- specific response to injury.
4
Q
A
Conjunctival haemorrhage (can occur with chemosis)
5
Q
A
Blepharospasm
6
Q
A
Epiphora- either overproduction of tears or inadequate drainage
7
Q
A
Corneal oedema- endothelium is important in maintaining the transparancy of the cornea because it pumps fluids out. Can be localized or diffuse.
8
Q
What happens to the eye with this type of trauma?
A
May see a rim of pigment left behind on the rim, you will see the angles change– you are impeding the drainage of the aqueous humour–> intra-occular pressure rises–> cause deformation of the eye–> can cause serious problems at the junction between the cornea and the sclera.. very sensitive to shear forces–> ANGLE RECESSION, ANGLE TEARING = HAEMORRHAGE
9
Q
A
Hyphaema- pressure dropping, which causes this problem. The amount of blood in the eye can impede the oxygenation of the tissues. Gradually drains out but can block the drainage and cause problems with pressure.
(Closed eye blunt trauma)
10
Q
A
Corneal blood staining
11
Q
A
Traumatic cataract- effect on the lens, damaging anterior lens capsule from blunt trauma, star burst opacity. Closed eye blunt trauma. Cataract= clouding of the lens (lens is made of epilthelial cells- if you get damage to the equilibrium, fibres can break down– leading to loss of transparency– age and increasing density– cataract is a pathological phenomenon where fibres are degrading– can be focal or diffuse… some cataracts are breed related, and found in specific parts of the lens)
12
Q
A
Lens luxation from blunt trauma (closed eye). Rupture of zonula fibres… can be forwards (through the pupil into the anterior chamber- sitting in the chamber blocking fluid flow- eye has no lymphatic drainage- it relies on the flow of aqueous humour from the ciliary body– if you block the angles– serious problems of pressure and hypoxia) or backwards (into vitreous). Posterior chamber is in front of the lens- between the iris and the lens.
13
Q
What is the picture? What is flare?
A
Rubeosis iridis (won’t see most of the time because their eyes are brown- the delicate fine vessels are not supposed to be there)
Anything that causes hypoxia in the eye causes blood vesselts to proliferate due to release of VEGF and other factors.
Flare= protein leakage in the aqueous humour
(Closed eye blunt trauma)
14
Q
When can retinal atrophy occur?
A
* Blunt trauma can actually transmit a shock wave through the vitreous (it is a gel)- and can shear the photoreceptor segments. The shock wave of the vitreous body can damage soft tissue. It can repair. You may never know it happened in veterinary medicine. Sometimes it doesn’t repair. If the choroid is damaged (supplies nutrition to the retina) then the retina will atrophy
15
Q
Possible consequences of blunt eye trauma
A
16
Q
A
Iris Prolapse
17
Q
A
Ruptured globe- most common site of rupture is the temporal limbus (versus nasal– different directional terms due to horses and cattle can’t use lateral and medial).
** if you rupture the eye- the fluid will come out and it can take the uvea out with it. It can take the iris out as well since it is floating around. Entire intra-occular contents can be expelled- you don’t need a big hole either (e.g. 3 mm hole in humans).
** loss of barrier of epithelium = loss of protection for infection… plugging the whole with the uvea does not protect against infection– it does not replace the cornea in that regard
18
Q
What can penetrating injury cause?
A
* Penetrating injury is usually more focused- energy in a pointed way that may or may not perforate the eye
** oedema
** can carry the epithelium in with the object
19
Q
A
Epithelialisation- epithelium travels inside the eye with the penetrating object. You can culture your own epithelium– it just grows and covers the eye- the normal restrainst to growth are not present. If some of the fibrous stroma also gets in… or fibrous membranes- live behind the iris– you can then get granulation tissue…. they contract in the skinw hich is good BUT in the EYE, the tissues deform… and then can cause RETINAL DETACHMENT
20
Q
A
Retinal detachment
21
Q
A
Grass seed- moved around in the eye- gets to the back of the eye, bumps up against the orbit and optic n. May not see damage much from the front. lt also takes bacteria in with it. Which completely wrecks the tissues. Can end up full of pus. Common injury in young dogs– cat clawing especially.
Endopthalmitis or Panopthalmitis
22
Q
How are immune responses different in the eye?
A
You can’t afford to have a normal immune response in the eye. Sequestered from the immune system (other parts of the body too). You can’t disrupt the delicate balance of the eye system. It means though that when things get in there, they can go wild. It also means that proteins and antigens that get in the eye are “foreign” from the eyes point of view. You can get a lens induced uviitis- not infectious, can be completely sterile but still wreck the eye because of its own proteins.
23
Q
Open eye trauma- penetrating injury
A
* Cyclitic (ciliary body) membrane- impede production of vitreous humour and the eye becomes hypotonic (fluid mechanics)
* traumatic injury to the lens of a cat may cause a focal post traumatic lens sarcoma (neoplasm) derived from the lens epithelium (name is off)- more common in the US so possibly a genetic component
24
Q
Capacity of regeneration and repair in the eye
A
Cornea is the only part that can regenerate
* Repair:
* Retina: Muller cells, retinal pigment epithelium (only possible with these two types of cells)
* Lens: epithelium- limited
* Uvea- limited
* Sclera- limited
(function is rarely restored back to normal, which sometimes does not matter)
25
Retina repair
Muller cells, retinal pigment epithelium (only possible with these two types of cells)
\*\* get a glial scar, a spot with no vision, but rarely clinically significant. Can keep the retina in place if it is falling off.
26
Lens repair
Cataracts & luxation- you can take it out or leave it in- no repair will occur (the arrows are cataracts)
\*\* need organization for transparency- otherwise you lose vision
27
28
Corneal Wound Healing Cascade
(similar to skin)
\*\*Epithelial sliding--\> keratocyte death--\>swelling of fibres--\> inflammatory cell infiltration--\> keratocyte transformation to fibroblasts and myofibroblasts--\> wound contracture--\> remodelling
Below: don't need to know, just extra information:
\* Epithelial injury release of cytokines--\> keratocyte apoptosis/ necrosis--\> lacrimal gland-tear growth factor response/ early epithelial healing--\> keratocyte proliferation and migration--\>Myofibroblast differentiation and migration--\> Myofibroblast/ keratocyte cytokine production (TGF beta, etc.)--\> Myofibroblast collagen, gag, etc. production--\> inflammatory cell infiltration- monocyte differentiation to fibroblast--\> collagenase, metalloproteinase, etc. production and stromal remodelling--\> epithelial surface closure hyperplasia--\> myofibroblast apoptosis/ necrosis myofibroblast transdifferenatiation--\> inflammatory cell apoptosis/ necrosis--\> keratocyte return to normal state
29
Corneal vascularisation
30
Cerebral oedema- sometimes you cannot tell grossly. Chronic can appear dry. Coning in the myelencephalon.
31
Vasogenic oedema- Bovine Malignant Catarrhal Fever (in Bali- a lymphoproliferative virus- Gamma herpes
\*\*cuffing of blood vessels in inflammatory disorders of the brain as well
\*\* water from the blood stream around the blood vessel around the white matter (white matter is easy for oedema fluid to dissect through)
\*\* can also see lymphocytes
\*\* Vasogenic oedema- around trauma lesions as well as inflammation, around tumours, abscesses, infarcts
\* Vitamin B 1 deficiency can affect the endothelial cells and therefore the brain as well.
\*\* foot processes help to insulate around the capillaries
32
Oedema dissecting through so many oligodendricytes die off- astrocytes swell and they grow extra processes
33
For example, Mulberry heart disease with pigs- vitamin E and/ or selenium deficiency, not enough antioxidants-- damages lots of tissues including vascular endothelium. If pigs survive for \> 24 hours then they develop vasogenic oedema. Spectacular lesions in the frontal gyri of the brian.
Encephalomalacia (oedema and necrosis are two causes of softening of the brain)
34
Pulpy kidney disease (enterotoxaemia). The bacterium, Clostridium perfringens type D, can build up when there is a sudden change to a low-fibre, high-carbohydrate diet. This can occur when sheep are moved onto lush, rapidly growing pasture or cereal crops, or when sheep are fed grain.
\* C. perfringens type D usually inhabits the instestines without problems, but with the change in diet, it multiplies and produces a toxin
\*\*Used to be a blood vessel- haemorrhage and coagulated fibrin. Devastating condition in the brain. Mainly sheep get this.
35
Focal symmetrical encephalomalacia
\* Pulpy kidney disease (C. pirfringens type D)
\* Damage to particular areas with the brain- no one knows why
\* Usually symmetrical- around the brain stem, and other areas
36
Annual Rye grass toxicity- peracute vasogenic oedema
\* nematode on see heads--\> secondary bacterial infection of where the nematode was--\> bacteria produce toxin that damages blood vessels
37
Cerebral oedema is usually what kind?
Vasogenic
38
Hydrostatic Oedema
\* Hydrocephalus headed foals in Werribee lab- hydrocephalus due to obstruction usually- accumulated CSF associated with increased pressure- ependyma lining the CSF system has a permeable membrane. Pushes straight through ependyma and into the white matter. Contributes to the atrophy.
\*Same thing happens with obstructive block of central canal forcing CSF into white matter
39
Cytotoxic oedema
\* Oedema accumulating within cells
\* Chronic hepatitis- hepatic encephalopathy (particularly ammonia)- toxins because the liver isn't working properly. Astrocyte nucleus swelling--\> cytoplasm swelling--\> intracellular oedema aka cytotoxic oedema, can also see extracellular oedema with it
40
Phalaris toxicity- high mortality in sheep in AUS, NZ, South Africa and California.
\* spectacular astrocytic swelling
\* Plants contain four types of indole alkaloids
Can cause Sudden Death Cardiac Syndrome (toxin affecting the autonomic innervation of the heart), Polioencephalomalacia-like Sudden Death Syndrome (peracute ammonia toxicity due to impairment of hepatic urea cycle enzymes), Subacute to Chronic Staggers Syndrome (repeated exposure)
41
What is osmotic oedema?
Brain is hyperosmolar compared to the blood. Water is dragged out of the blood stream and CSF into the brain and into neurons. Uncommon.
\*Most likely to occur in pigs
\* Indirect salt poisoning- hypernatraemia due to dehydration
\* brain is manufacturing osmotic molecules- therefore becoming hyperosmolar
\* when they hydrate the pigs, blood sodium level drops quickly, brain tries to export the ions- but can't do it quickly- therefore it becomes hyperosmolar relative to the blood- therefore water is dragged into the brain
42
Osmotic Cerebral oedema, cerebral cortical necrosis, microscopically eosinophils
43
\* what is this?
\* what neurons are most susceptible to hypoxia?
Stroke (uncommon in domestic animals)
Cerebral hypoxia- a microscopic infarct in the medulla would cause death, elsewhere may not
\* 3-4 minutes neurons can survive without oxygen
\*\* neurons that are most vulnerable to hypoxic injury are the neurons that use glutamate as a neurotransmitter (bombarded by excess glutamate release = switches on intracellular death cascade that releases free radicals and proteases)
44
Causes of Excitotoxic Injury
Shrunken shrivelled coagulative necrosis neurons due to excessive glutamate release or another cause:
\* hypoxia
\* thiamine deficiency
\* hypoglycaemia
\*lead poisoning
\* organomercurial poisoning
\* prolonged seizure activity
\* chronic traumatic encephalopathy
\* dementia pugilista
45
Cerebral infarct (astrocyte processes filled in or collapsed space with astrocytes along the edges)
46
Strokes
\* Guttural pouch fungal infection affecting carotid artery - septic, fungal, or bland emboli
\* Cardiomyopathy with thrombosis
\* feedlot cattle- bacteria can cause thrombosis in the brain
47
Cerebral infarcts
48
These animals have infections in their CNS. What are the odds these animals will recover fully? Why? Why is the CNS so vulnerable?
\* poor as it does not repair- if you wipe out neurons you've lost them
\* brain stem and the medulla can kill you, even a small lesion
\* do not have a big population of surveillance cells like you do in the GIT or lungs, for example
\* lack of space- once you get an inflammatory reaction, oedema, etc. no space to accomodate increased mass
\* infectious agent in the CSF, it is rapidly dispersed all around the system-- once it is in the CSF it can cross the ependyma into the parenchyma
\* Virchow Robin Spaces (perivascular spaces)- invaginations- it can penetrate around those spaces deeper into the underlying spinal cord.
\* Easily disperses through white matter
\* Fibrin and pus in the ventricular system you can cause obstructive hydrocephalus
49
How can bacteria get into the CNS?
Haematogenous, tracking up nerves (Rabies or ulcer in the oral cavity can let Lysteria in along axons), penetrating trauma, guttural pouches (bacteria from infection nearby), cerebral abscesses from a grass awn under an eyelid--along optic nerve to cranial vault, otitis interna, vertebral osteomyelitis direct extension to involve the meninges, aspergillosis can extend from the nasal cavity or paranasal sinuses
50
Properties of an ideal anaesthetic
\* should render the patient unconscious
\* Should also provide: analgesisa, muscle relaxation, minimal cardiorespiratory depression
\* Induction and recovery rapid and smooth
\* Depth of anaesthesia easily titrated
\* non irritant and non toxic
51
What do most anaesthetic agents do in regards to receptor interaction?
Inhibiting excitatory receptors: glutamate NMDA, 5HT, Ach
\* many anesthetic agents enhance effects on inhibitory receptors (GABA, glycine)
52
What are some of the effects of anesthetics?
\* depression of brain function (eye ball rotation- nystagmus, pupil dilation/ constriction, more)
\* changes in HR and BP and the baroreflex (capacity to respond to falling blood volume is blunted due to overall depression of cardiovascular function at the level of the cardiovascular center)
\* Respiratory depression (O2 sat, RR)
\* muscle relaxation
53
What are the stages of anesthesia?
Stage 1: amnesia, euphoria
Stage 2: "excitement": delirium, resistance to handling
Stage 3: "surgical anaesthesia": unconsciousness, regular respiration, decreasing eye movement
Stage 4: "medullary depression": respiratory arrest, cardiac depression and arrest
54
How do you know what stage of anaesthesia you're in?
55
What is an ASA score?
Health status prior to anaesthesia
1-5, 1 is good health prior to anaesthesia- 5 is poor health
56
What are the risks to anaesthesia?
57
Analgesic vs. Local anaesthetic
Analgesic- targets pain pathways
vs.
Local anaesthetic- non- specifically inhibits periphernal nerve pathways (motor, sensory autonomic)
58
Advantage of inhaled anaesthetics
\* no need for injection
\* you can rapidly back it off if you need to lift the stage
\* how well they work depends on the solubility of the particular agent- 2 types are important: solubility in blood vs. solubility in liquid
59
What is solubility?
\* expressed as a partition coefficient
\* how much is in the blood (alveolar air??)
\* how much is in lipid (lipid soluble in order to get into the brain)
\* some are more lipid soluble then others-- this means more risk for drug accumulation in the fat compartment over time with a fat animal
60
Factors that determine speed of induction and recovery
\* Ventilation rate is important: Breathing more rapid- stop the flow of anaesthetic agent then they will wake up quickly
\* Cardiac output- changes the speed to which the anaesthetic gets to the brain
\* Brain has a large portion of the blood supply- therefore concentration in the brain closely tracks concentration in the blood
\* Low blood solubility--\> more rapid equilibration between phases, more rapid induction, more precise control, more rapid elimination and recovery
\*\* if more solube- takes longer to reach equilibrium- you need more drug into the blood- a bigger sink, will be bound there more by forces that hold the drug in the blood (what solubility means)-- a less soluble drug will equilibrate more readily-- so this is what you want!!
61
What is the problem with a high lipid solubility?
\* gradual accumulation in body fat-- redistribute from the brain, through muscle tissue, to the fat... so in a fat patient potentially a longer hangover e.g. problems with recovery
62
What is dose dependent on? Where does the anaesthetic flow in the body?
Flow rate and dose dialed on the vaporizer.
63
What are wash-in and wash-out curves?
tell us about the concentration in the arterial blood (FA) as a ratio over the concentration in inspired air (FI)
\* curves on the right are mirror images (wash-out curves)
\* Sevoflurane equilibrates much more quickly than the other two-- why?? It is less soluble. Blood gas partition coefficient is much lower
64
What are some other factors in anaesthetic uptake and elimination?
\* greater dose to alveolar compartments= deeper faster
\* as the patient lightens, they will breathe faster and increase the rate of anaesthetic wash- in to the lungs
\* as they become deeper, ventilation will reduce and this leads to less anaesthetic coming into the lungs
65
What makes a good inhalation anaesthetic?
\* induction and recovery are rapid
\* depth of anaesthesia are easily adjusted
66
What is Minimal alveolar concentration (MAC)?
\* Amount of anaesthetic to prevent movement to surgical incision in 50% of healthy patients
\* consequence- always having to titrate the dose
\* attempts to provide equipotency of different anaesthetics (compare one to another)
\* can measure the alveolar compartments but not what is in the brain
67
Nitrous Oxide as an anaesthetic
\* low potency (MAC 100%)-- which would kill-- do not use \> 70% nitrous oxide because it will reduce available oxygen concentration (carrier gas anaesthetic)
\* low solubility--\> rapid onset and offset
\* good analgesic but not enough as sole anaesthetic even with generous premedication
\* Will expand closed air spaces e.g. pneumothorax, middle ear effusions
68
Halothane as an anaesthetic
\* Relatively soluble in blood and lipid
\* Increased risk of arrythmia because it sensitizes myocardium to catecholamines
\* Halothane hepatitis (rare)
\* Spontaneous abortion
\* Decreases CO, BP, and organ perfusion
\* 20-30% metabolized in liver
\*\* Adrenaline + Halothane may cause ventricular fibrillation/ cardiac arrest
69
Malignant hyperpyrexia
\* especially in pigs
\* Halothane can cause
Newer agents are weak triggers
Uncontrolled hyperthermia--\> acidosis leading to death
70
Isoflurane
\* Less soluble than halothane
\* less cardiodepressive
Less than 1% metabolized
71
Sevoflurane
\* puts them to sleep in 2-3 breaths
\* Similar to isoflurane
\* less soluble
\* less irritant to airways
\* less smell (mask inductions)
\* not gentle! will go down very fast
72
Methoxyflurane
\* slow induction and recovery
\* up to 50% metabolized (much longer hangover period) BUT good analgesia, which is why it is still used
\* good analgesia but very slow anaesthetic
NOT COMMON
73
Analgesia and Anaesthesia-- one for both??
Most volatile anaesthetics do not have alagesic properties
74
What are advantages of injectable anaesthetics?
Disadvantages?
\* rapid induction through excitement phase
\* need little equipment
\* lend themselves to combination use
Disadvantages:
\*once administered can't be withdrawn
\* elimination can be more prolonged
\* require access to a vein
75
What is pharmaceutics?
The chemical composition of the drug: pH, preservatives, storage temperature
e.g. Thiopentone pH 10.5- irritant & cremaphor vehicle to solubilize the drug-- therefore may lead to histamine release
76
Distribution and redistribution
\* head is the active side
\* tissues with a higher proportional blood flow receive a greater proprotion of drug initially but will also lose it rapidly
\* animals wake up because it redistributes away from the brain
\* the blood flow to the brain is autoregulated (fixed)
77
What happens with CO drops?
Proportion of blood that goes to the brain actually changes
\* If CO halves, then 20% of drug bolus hits the brain
78
What is important about thiopentone?
Do not mix with other drugs in the same syringe-- it will precipitate out
79
Pregnancy and neonates and anaesthetics
80
What are the classes of injectable anaesthetics?
81
Barbiturates
\* derivatives of barbituric acid
\* Activity and duration of action depends on substitutions
\* oxybarbiturates
\*thiobarbiturates
\* inhibitory- increasing binding of GABA to its receptor
\*\* ultra- short acting: thiopentone and methohexitone
\* short acting: pentobarbitone
\* Long acting: phenobarbitone (seizure control and occasionally for sedation)
82
Barbiturates- effects
Not analgesics
\* decrease cerebral blood flow, cerebral oxygen consumption, medullary centres: thermoregulation, respiratory, vasomotor, vagus
83
Termination of effects of thiobarbiturates due to redistribution
vs. oxybarbiturate termination
\* brain conc. tracks closely to blood conc.
Ultimately distro into fat
\* termination of effect depends not on metabolism or excretion but on REDISTRIBUTION
\*\* this is in contrast to oxybarbiturates which termination depends on hepatic metabolism-- hepatic enzyme induction, elimination is species dependent
84
Thiobarbiturates clinical use-- and contraindications
main risk: extravascular depostion, without fail result in sloughing of tissue if you don't take steps to remedy
Precautions:
\* thin patients- less redistribution to fat
\* obese patients (may require a relatively overdose)-- not necessarily stay asleep for longer, but will have a longer hangover
\* hepatic dysfunction (metabolized in liver)
\* respiratory depression
\*tissue irritant, strictly IV
85
What are dissociative anaesthetics?
Dissociates higher and lower brain centres (much lower effect at the lower brain centres)
\* Phencyclidine derivatives: Ketamine, Tiletamine
86
Ketamine mechanism of action
\* specific antagonist at glutamate NMDA receptor
\* Antagonist at ACh muscarinic receptor
\* Agonist at opioid receptors
\* A schedule 8 drug (restricted)- dependence
\*\*IV anaesthetic agent with ANALGESIC properties, problem is restricted\*\*
87
Ketamine CNS effects
\* produces dysphoria- dissociating between thalamus and cortex
\* can increase cerebral blood flow- therefore can cause ICP-- not a drug to use if suspected head trauma
\* Cataleptic state
\* Hallucinations and emergence reactions
\* GOOD ANALGESIC
\* NOT a good muscle relaxant (orthopedic or abdominal surger you would need good muscle relaxant)
88
Propofol
\* Unrelated to other anaesthetics (not a class)
\* Major advantage: short duration of action and rapid recovery
\* Useful for induction/ short procedures or outpatient cases
\* Disadvantage: Formulated as emulsion (with soya bean oil and glycerol) exists as an oil at room temperature-- bad thing because it is a good medium for growing bugs.. so need to be careful and throw out what you haven't used at the end of the day
\* rapidly metabolized
Effects:
\* GABA- mimetic
\* equivalent to thiopentone in CV and resp effects: apnoea following rapid injection
\* Myocardial depression, vasodilation and hypotension
\* Rapid metabolism means little accumulation of drug--- the only real difference from thiopentone
89
When should you use Propofol?
\* Induction of anaesthesia
\* Short procedures or outpatient cases (but is cardio depressant for a bit of time)
\* Decreases cerebral blood flow (head trauma)-- therefore good for head trauma patients
90
Steroid anaesthetics
Neuroactive steroids- acting at the level of the CNS-- modulating activity of GABA
\* Alphaxalone/ alphadolone
\* Alphaxalone has twice the acitivity of alphadalone
\* Alphadalone included to improve solubility
\* act by modulation of GABA activity
\* less CV and resp depression than other anaesthetic agents
\* reduces cerebral O2- consumption more than reduced blood flow should indicate
\*\* Peanut allergies caused it to be discontinued with human anaesthetists- still can cause swelling in cats-- probably also an allergic reaction to cremaphor vehicle-- Alfaxan CD does not have the same hazard but problem is right now it is covered by a patent so really expensive 20x thiopentone
91
Benzodiazepines- effects & mechanism of actions
\* E.g. diazepam (valium), midazolam, temazepam, zolazepam
\* Actions on CNS: hypnotic, sedative, anxiolytic, anticonvulsant, skeletal muscle relaxant, amnesic
92
Pharmacological effects of benzodiazepines & clinical uses
\* CV- minimal effects
\* Skeletal muscle--\> relaxation
\* so used with ketamine to provide muscle relaxation
\*\* Anxiolytic--\> behavioural modifiers
\*hypnotics
\* premedicants
\* anaesthesia induction
\* Anticonvulsants (status epilepticus)
\* Appetite stimulation (Cats)
93
Balanced anaesthesia
Combination of drugs: hypnotic, analgesic, anaesthetic and neuromuscular relaxant drugs to achieve optimal anaesthesia with smooth rapid recovery. (prevent wind up)
\* rend the patient unconscious
\* provide analgesia, muscle relaxation, minimal cardiorespiratory depression
\* Induction of anaesthesia easily titrated
\* nonn irritant and non toxic
94
Which anaesthetics provide analgesia?
ketamine, nitrous oxide, and methoxyflurane
95
What might you use for balanced anaesthesia?
96
What do local anaesthetics do?
Stop the impulse along the nerve fibre- not changing anything in the CNS or periphery.
97
What are the anatomic considerations of local anaesthesia?
Easier to block pain fibres than motor bifres because smaller/ unmyelinated fibres are easier to block! (Myelinated fibres are only blocked at nodes of Ranvier, so harder to block)
\*\* therefore motor fibres are blocked at higher doses because they are myelinated and the opposite is true for pain fibres
98
Local anaesthetic agents are sodium channel blockers, how is this helpful functionally?
Drug has to be hydrophilic OR msut enter through an open sodium channel.
Advantage because active nociceptive pathways-- more APs transmitted-- then more likely to be transmitted due to open channels
99
Why do you need a higher dose in inflammed tissue?
If tissue is inflamed, tissue becomes more acidic, therefore higher proprotion of drug being ionized. Becomes imp. when providing local anaesthesia to a cow with a teat that is inflammed. NEED A HIGHER DOSE.
100
Ester vs. Amide linked local anaesthetics duration of action
Ester- metabolized faster in tissue and plasma therefore short acting e.g. procaine, cocaine
Amides- metabolized in the liver, so longer acting e.g. lignocaine, bupivicaine
101
What factors influence absorption and potential toxicity?
102
What are the systemic effects of local anaesthetics?
103
What local anaesthetics are used in veterinary medicine? Where are they most useful?
104
What do neutrophils in CSF mean?
What if it is lymphocytic or plasmocytic?
Monocytes or macrophages?
Most likely bacterial infection- and you would culture it
\* lymphocytic or plasmocytic- screening serological testing for most likely viral culprits, but sometimes it could be protozoa (toxoplasma), fungal infections, or lymphoma (monomorphic lymphocytes), some viruses (EEE, WEE, and VEE)-- EEE is neutrophil rich
\* sometimes dominated by monocytes or macrophages-- call this granulomatous, if accompanied by neutrophils then pyogranulomatous lepto(xxx)., GME, if it is a cat it could be FIP, occasionally fungus (but start with most logical)
105
106
perivascular cuff- Perivascular cuffs are regions of leukocyte aggregation in VRS, usually found in patients with viral encephalitis. VRS are extremely small and can usually only be seen on MR images when dilated.
\*\* pigs always throw eosinophils out
107
Normal on the right
Bacterial leptomeningitis- most common
\* some degree of accompanying encephalitis
\* increased vascular permeability and oedema
108
Bacteraemia and localization in the brain
Strabisimus
The bacteria would go everywhere- the better vascularized
Some degree of polyarthritis
\* endophthalmitis
\* heart valves, lungs, hepatitis
\*\* odds are already stacked against them and then it also goes to the brain
109
Bacterial- can tell by petechial haemorrhage- also cannot follow blood vessels because extra layer
\*\* pus
\* sulci (valleys) exudate will pool
110
111
Tracking in ventricular system, exceptional clogging from bacterial infection-- obstructs CSF outflow which will kill rapidly due to ICP
112
If blood is swarming with bacteria- Septic Thromboembolism
Histophilus somni
\*\* this picture is larger septic thromboembolism so on the outside
113
If colonies are smaller, they tend to get stuck at the grey/ white junction-- in the hypothalamic parts of the brain-- this baby survived long enough for micro abscesses to form
114
3 common immune mediated diseases with no infectious agent present
1. GME- granulomatous meningoencephalitis (if spinal cord involvement meningoencephalomyelitis)
- large perivascular cuffs, gradually expanding space occupying mass, females more commonly affected then males
- cause UNK- triggering antigen???- T cell mediated delayed type hypersensitivity reaction
- some localized lesions- may think you're dealing with a tumour, can be diffuse-- if cerebral hemisphere involvement = seizures
- treatment: corticosteroids- ultimately a death sentence
2. Nectrotizing meningoencephalitis- inflammatory involving the brain and the meninges- not as common but much more devastating. Often asymmetric cavitating lesions of the cerebral cortex. Some dogs get necrosis of the brain stem. Trigger UNK. Predominantly involving grey matter of cerebral cortex therefore most clinical signs would be seizure (which can also exacerbate due to excitotoxic injury in the neurons).-- presented due to seizure or behavioural changes. Histo: pleocytosis, inflammatory CSF as well. Rapidly progressive- if do nothing, dead in weeks, at most a few months.
3. Steroid-responsive Meningitis-arteritis in Dogs- Lesion is Intense arteritis (Beagle Pain syndrome)- Boxers & GSPs- sudden onset of pain of any manipulation of the head or neck due to intense inflammation of the meninges. Febrile, depressed, anorexic, Trigger UNK but believed to be immune mediated. Tx: corticosteroids. (can affect other arteries but clinical signs related to the meningeal arteries)
115
Pathogenesis of TSE
Prion--\> lymphoid tissues--\> lymphoid organs (white pulp of the spleen)--\> peripheral axons--\> astrocytes--\> neurons
\* hypermetria
\* ataxia
\* spongiform- holes in axons, dendrites, and nerve cell bodies but no immunereaction whatsoever... amyloid plaques
116
Thiamine (B1) Deficiency
Polioencephalomalacia
\* blind
\*+/- nystagmus
\*ataxia
Thiamine is involved in neurotransmission, oligodendrictye metabolism, ATP development in neurons
\* later stage- seizure, recumbent
\* vitamine B in a ruminant from bacteria in the rumen, therefore most common reason is to upset the ruminal flora- can be sudden-- urea molasses as nitrogen supplements can upset the flora in the stomach. (common in ruminants)
\* excess sulfates or sulfides can inactivate thiamine
\* bracken fern (also dew fern and horse tail) contains thiaminase-- horses develop thiamine deficiency
\* Clinical signs: brain swelling (vasogenic cerebral oedema), neuronal necrosis in the grey matter of the cerebral cortex
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Any animal, especially ruminant with neurological disease, what do you immediately?
Give it vitamin B1
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What is unique about tetanus grossly?
\*No lesions
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Organophosphate poisoning
Overstimulation of target receptor by ACh due to inactivation of cholinesterase
\* i.e. muscle tremors
\* no lesions
\* clinical diagnosis- exposure, there is an assay
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Phalaris Toxicity
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pyoencephalon
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Listeria monocytogenes penetrates damaged oral mucosa and ascends axons of trigeminal nerve--\> trigeminal neuritis and ganglioneuritis--\> unilateral microabscessation in the medulla oblongata with inflammation of the overlying leptomeninges +/- extension into the adjacent pons or rarely the cranial cervial spinal cord
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Bite wound on pig tails can be portals of entry for bacteria- suppurative infections can track up the spinal cord in the epidural space.
\*\* same in the skull wherever nerves are coming out- are potential routes of entry
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Routes of entry- bilateral severe chronic otitis externa. White layer of the dura peeled off the bone.
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Brain Abscess- slow growing which is why it takes so long to see
\* likely haematogenous, can start from the ear, or if it is at the front- obliterating the olfactory lobe- paranasal sinuses or back of the nasal cavity- extension of infection through the cribiform plate
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What viruses are neurotropic?
Bovine herpes virus 1, Rabies, Distemper, Feline Panleukopaenia, FIP etc.
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Could see this is in Canine Distemper, for example
Microglia orbiting around nerve cell body- neuronalphargic nodule
\*\* Can tell it is a virus- have to search for clues to which one
(the picture here with one inclusion body in a neuron- could mean Rabies)
\* if there is a lot of demyelination- few viruses that do so- Distemper, Caprine Arthritis Virus, Visna (Lenti Virus)
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What are the two most common fungal infections in Australia?
Cryptococcus (cats) and Aspergillos (dogs)
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Aspergillosis
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Cryptococcus neoformans
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What are the big protozoa in AUS that infect the CNS?
Toxoplasma gondii
Neospora caninum
Sarcocystis species
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Visceral larval migrans- large metazoan (multicellular) parasites can produce CNS disease by aberrant larval migration in normal hosts or migration in aberrant hosts (therefore a massive inflammation, more intense reaction in aberrant hosts vs. normal hosts)
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Hytadid cyst of a tape worm
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What are the key horomones secreted by the posterior pituitary?
Oxytocin and ADH (anti-diuretic hormone)
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What are the functions ADH?
\* acts on renal collecting ducts to increase water reabsorption from urine (binds on principal cells)
\* Increases vascular resistance (binds on smooth muscle)
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What are the functions of oxytocin?
\* Cause contraction (uterus during pregnancy)
\* Mammary gland (milk let down)
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What are the hormones the anterior pituitary releases?
\* Thyroid stimulating hormone (TSH)
\* Adrenocorticotropic hormone (ACTH)
\* Prolactin (PRL)
\* Lutenizing hormone (LH)
\* Follicle Stimulating Hormone (FSH)
\* Growth hormone (GH)
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Functions of growth hormone?
\* Responsible for postnatal somatic growth
- increasing the number of cells (hyperplasia)
- increasing the size of cells (hypertrophy)
\* acute metabolic effects: mobilizes fat and conserves glucose, lipolysis in adipose tissue, inhibition of glucose uptake by muscle, stimulation of gluconeogenesis by hepatocytes
\* growth promoting: GH causes release from liver of IGF1, stimulations differentiation and prolif of cells, role for local autocrine IGF 1 release, causes bones to grow in length
\*\* broad ranging anabolic effects
\* it does not work alone- insulin like growth factor 1 (IGF-1): GH causes the release of IGF-1 in local tissues- mediates the effects of GH
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What do each of these do?
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Pituitary Dwarfism
Hyposecretion of GH during growth years
\* Genetic predispotion, tumours, infarcts and infections
\* causes slow bone grwoth and early epiphyseal plates closure
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Gigantism
\*hypersecretion of GH (early in life) results in gigantism
\* abnormal increase in length of bones
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Acromegaly
\* caused by a GH secreting tumour of the anterior pituitary
\* PU/PD
\*Feline acromegaly also- protrusion of the mandible (prognathism)
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Stimulation of GH release vs. Inhibition
\* stimulation: exercise, level of fatty acids, sugar, dietary protein, stress, ghrelin (stomach hormone), more
\* inhibition: high carbohydrate, negative feedback (IGF-I & GH)
